Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY  

Background: During bipolar (BIP) radiofrequency (RF) ablation using two catheters in humans, each catheter is placed in separate cardiac chambers or spaces. We developed a contact force-controlled experimental preparation, and compared measurements made with two catheters placed in a single bath (SB), versus each catheter placed in separate baths, in order to assess the preparation-dependent differences in the results of BIP-RF ablation.
Methods: In the SB experiments, a porcine heart was placed in the center of the bath, while in the dual-bath (DB) experiments, it was placed between two half baths communicating through windows.
Results: The initial impedance was greatest (110.5 +/- 7.2 Omega) with the BIP-DB, followed by the BIP-SB (92.0 +/- 5.6 Omega) and the unipolar (UNIP) DB (84.9 +/- 4.7 Omega) configurations. During 50-W ablation for 60 seconds at a 20-g contact force, the root mean square voltage was 75.7 +/- 2.5 V in the BIP-DB, 68.0 +/- 2.1 V in the BIP-SB, and 66.8 +/- 2.0 V in the UNIP-DB. The mean surface lesion diameters were similar among the three configurations. However, the endocardial lesion depth was 5.60 +/- 0.56 mm with the BIP-DB, 4.71 +/- 0.64 mm with the BIP-SB, and 4.24 +/- 0.58 mm with the UNIP-DB configuration. On average, the endocardial lesions were significantly deeper than the epicardial ones.
Conclusions: BIP ablation created much deeper lesions as compared to UNIP ablation. Lesion depth could be different depending on experimental preparation, and contact force-controlled DB preparation may be a much more appropriate model for studying the effects of BIP ablation. (PACE 2017; 40: 223-231)

DOI： 10.1111/pace.12993

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BACKGROUND Catheter ablation of the renal artery can be performed without apparent angiographic stenosis. This suggests that renal nerve function can be attenuated with minor structural damage to the renal artery.
OBJECTIVE To clarify this hypothesis, we examined the relationship between electrical nerve stimulation (ENS)-induced blood pressure (BP) response and severity of histological injury of the renal artery using an acute canine model of renal artery ablation.
METHODS An irrigation catheter was inserted into the renal arteries of 8 dogs, and radiofrequency current was delivered at 15, 20, or 25 W. ENS was applied to each artery before and after ablation.
RESULTS Before ablation, ENS increased the BP and heart rate from 145 15/86 13 to 189 21/111 19 mm Hg and from 116 9 to 130 6 beats/min, respectively. Heart rate variability indices and serum catecholamine levels were elevated concomitantly. After ablation, the ENS -induced increase in BP and heart rate were markedly attenuated after 15 W ablation and those were nearly completely inhibited after 20 or 25 W ablation. An increase in heart rate variability indices and serum catecholamine levels became insignificant regardless of the applied energy. Renal artery angiograms revealed stenotic lesions only after 25 W ablation procedures. Histological studies showed mild to moderate injury of the arterial wall and autonomic nerves caused by 20 and 25 W ablation procedures, whereas only minor changes caused by 15 W ablation.
CONCLUSION Functional renal autonomic nerve ablation is potentially performable with the guidance of ENS.

DOI： 10.1016/j.hrthm.2016.04.021

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Radiofrequency (RF) catheter ablation of the renal artery is therapeutic in patients with drug-refractory essential hypertension. This study was designed to examine the role of the renal autonomic nerves and of RF application from inside the renal artery in the regulation of blood pressure (BP). An open irrigation catheter was inserted into either the left or right renal artery in 8 dogs. RF current (17±2 watts) was delivered to one renal artery. Electrical autonomic nerve stimulation was applied to each renal artery before and after RF ablation. BP, heart rate, indices of heart rate variability, and serum catecholamines were analyzed. Before RF ablation, electrical autonomic nerve stimulation of either renal artery increased BP from 150±16/ 92±15 to 173±21/105±16 mm Hg. After RF ablation, BP increased similarly when the nonablated renal artery was electrically stimulated, although the rise in BP was attenuated when the ablated renal artery was stimulated. Serum catecholamines and sympathetic nerve indices of heart rate variability increased when electrical autonomic nerve stimulation was applied before RF ablation and to the nonablated renal artery after RF ablation, although it changed minimally when the ablated renal artery was stimulated, suggesting interconnectivity between afferent renal nerve stimulation and systemic sympathetic activity. Renal artery angiogram showed no apparent injury after RF ablation. In conclusion, electrical stimulation of the renal arterial autonomic nerves increases BP via an increase in central sympathetic nervous activity. This response might be used to determine the target ablation site and end point of renal artery RF ablation. © 2012 American Heart Association, Inc.

DOI： 10.1161/HYPERTENSIONAHA.111.00095

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BACKGROUND Previous studies have showed that the interval between the peak and the end of the T wave (Tp-e) is a marker of transmural dispersion of ventricular repolarization.
OBJECTIVE We studied the relationship between (a) the Tp-e on local pseudo transmural electrograms (pseudo transmural Tp-e) or limb leads of body surface electrocardiogram (surface Tp-e) and (b) the intracardiac left ventricular (LV) repolarization during a drug-induced QT-interval prolongation.
METHODS Using open-chested canine intact hearts treated by anthopleurin-A, transmural LV electrograms were recorded via needle electrodes placed in the basoanterior, midanterior, apicoanterior, basolateral, midlateral, and apicolateral LV wall. Recovery time (RT) was calculated as an index of local repolarization at each transmural unipolar electrode.
RESULTS This model showed slower heart rate-dependent heterogeneous distribution of ventricular repolarization both along the basal to apical axis and along the transmural axis. RT was longer at the LV apex than at the base and longer in the lateral than in the anterior wall during the slower heart rate. A high correlation was found between surface Tp-e and total LV dispersion. In contrast, pseudo transmural Tp-e correlated with transmural RT dispersion. The shortest RT in the heart roughly corresponded to the peak, as did the longest RT with the end of the T wave on the surface electrocardiogram.
CONCLUSION During drug-induced QT-interval prolongation with a large apicobasal and anterolateral dispersion of ventricular repolarization, the Tp-e in the limb leads expresses spatial (total) distribution of repolarization in the whole left ventricle.

DOI： 10.1016/j.hrthm.2011.11.046

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The aim of this study was to determine whether or not the coexistence of sustained ST-segment elevation and abnormal Q waves (STe-Q) could be a risk factor for electrical storm (ES) in implanted cardioverter defibrillator (ICD) patients with structural heart diseases.
In all, 156 consecutive patients received ICD therapy for secondary prevention of sudden cardiac death and/or sustained ventricular tachyarrhythmias were included. Electrical storm was defined as epsilon 3 separate episodes of ventricular tachycardia (VT) and/or ventricular fibrillation (VF) terminated by ICD therapies within 24 h. During a mean follow-up of 1825 1188 days, 42 (26.9) patients experienced ES, of whom 12 had coronary artery disease, 15 had idiopathic dilated cardiomyopathy, 6 had hypertrophic cardiomyopathy, 4 had arrhythmogenic right ventricular cardiomyopathy, 4 had cardiac sarcoidosis, and 1 had valvular heart disease. Sustained ST-segment elevation and abnormal Q waves in epsilon 2 leads on the 12-lead electrocardiography was observed in 33 (21) patients. On the KaplanMeier analysis, patients with STe-Q had a markedly higher risk of ES than those without STe-Q (P 0.0001). The multivariate Cox proportional hazards regression model indicated that STe-Q and left ventricular ejection fraction (LVEF) (30) were independent risk factors associated with the recurrence of VT/VF (STe-Q: HR 1.962, 95 CI 1.243.12, P 0.004; LVEF: HR 1.860, 95 CI 1.202.89, P 0.006), and STe-Q was an independent risk factor associated with ES (HR 4.955, 95 CI 2.699.13, P 0.0001).
Sustained ST-segment elevation and abnormal Q waves could be a risk factor of not only recurrent VT/VF but also ES in patients with structural heart diseases.

DOI： 10.1093/europace/eur386

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OBJECTIVES We sought to identify the triggers of ventricular tachyarrhythmia (VTA) in experimental models of long QT type 2 (LQT2) and long QT type 3 (LQT3) syndromes.
BACKGROUND Most adverse cardiac events occurring in the long QT type 1 syndrome are related to sympathetic nerve activity. In contrast, various factors may trigger VTA in patients with LQT2 and LQT3.
METHODS The mode of onset of VTA and therapeutic effects of the potassium-adenosine triphosphate channel opener nicorandil were compared in canine models of LQT2 and LQT3, using three induction protocols: 1) bradycardia produced by atrioventricular block (BRADY); 2) programmed ventricular stimulation; and 3) electrical stimulation of the left stellate ganglion (left stellate stimulation [LSS]). Transmural unipolar electrograms were recorded, and the activation-recovery interval (ARI) was measured.
RESULTS Ventricular tachyarrhythmias developed during BRADY in all six experiments in the LQT3 model, but in none of the six experiments in LQT2. Programmed ventricular stimulation induced VTA in two experiments of the LQT2 model, but in none of the LQT3 experiments. Stimulation of the left stellate ganglion induced VTA in three experiments in LQT2 and in two experiments in LQT3. Nicorandil caused greater shortening of ARI and greater attenuation of transmural ARI dispersion in the LQT2 model than in the LQT3 model. After treatment with nicorandil, a single VTA was induced in the LQT2 model by LSS, whereas in the LQT3 model, VTA remained inducible by BRADY in four experiments and LSS in one experiment.
CONCLUSIONS An abrupt increase in sympathetic activity appeared arrhythmogenic in both models. Nicorandil attenuated the heterogeneity of ventricular repolarization and suppressed the induction of VTA in the LQT2 model, but had a limited therapeutic effiect in the LQT3 model. (C) 2002 by the American College of Cardiology Foundation.

DOI： 10.1016/S0735-1097(02)01975-7

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INTRODUCTION: Cold saline application through an irrigation catheter may induce reversible inhibition of submyocardial excitation, which may be used to identify in advance an ideal site for radiofrequency (RF) energy delivery around delicate areas. METHODS: An open irrigation catheter was positioned vertically or parallel with 10-g contact on coronary perfusing porcine hearts and the contacted myocardium was cooled by cold saline at 4°C (20 mL/min). A temperature electrode was inserted 2 mm below the myocardial surface (intra-myocardial temperature at approximately 2 mm below the surface [Temp-BS]). Pacing threshold inside the ventricular wall was measured using an eight-pole electrode plunge needle inserted 5-8 mm close to the ablation catheter, and percent increase of the pacing threshold by the cold saline application (%increase-PT) was calculated. RESULTS: During cooling, pacing at 10 V from the myocardial surface interrupted constant capture in 7/10 experiments in vertical and in 9/10 experiments in parallel ablation catheter contact. Minimum Temp-BS was not different in both catheter contact positions (25.9 ± 4.0°C in vertical vs. 25.4 ± 2.6°C in parallel). Large % increase-PT on the surface myocardium decreased as the myocardial depth became deeper, and > 150% increase was at a depth approximately 2-3 mm from the surface and > 120% increase around 6-7 mm from the surface. After cessation of cold saline application, the increased %increase-PT recovered to the pre-cooling values. CONCLUSIONS: Cold saline application through an irrigation catheter reversibly inhibited submyocardial excitation. This simple method may have the potential to pre-determine the ideal ablation site in sensitive areas of the heart, although further studies and technological adjustments are required before clinical use.

DOI： 10.1111/pace.15104

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INTRODUCTION: Unipolar radiofrequency (RF) ablation using half-normal saline irrigation (UNIP-HNS) and bipolar RF ablation using normal saline irrigation (BIP-NS) are effective to treat arrhythmias from inside thick myocardium. However, differences between these two ablations when using a long application time had not fully been studied. METHODS: UNIP-HNS, BIP-NS and unipolar RF ablation using normal saline irrigation (UNIP-NS) were applied for 120 seconds (30 W and 20-g contact) to porcine endocardial wall (≧15.0 mm thickness). RESULTS: All ablations (30 applications each in UNIP-HNS and BIP-NS, and 20 applications in UNIP-NS) were successfully accomplished without steam-pop. Total impedance decline was largest in BIP-NS followed by UNIP-HNS and UNIP-NS. UNIP-HNS created larger surface lesions and greater maximum lesion width under the surface than those by UNIP-NS and BIP-NS. Endocardial lesion depth in UNIP-HNS and BIP-NS were deeper than that in UNIP-NS, but with no difference between UNIP-HNS and BIP-NS, when selecting non-transmural lesions. Similar results were obtained when all lesions (non-transmural and transmural) were included and endocardial lesion depth of the transmural lesions (13/30 applications of BIP-NS) was estimated as 50% of the myocardial thickness. Lesion length in the transverse myocardial wall (endocardial plus epicardial lesions) was greatest in BIP-NS. CONCLUSIONS: Longer application time ablation (30 W) targeting the thick myocardium was performable in UNIP-HNS and BIP-NS. Since a transmural lesion and/or a deeper lesion into the myocardial wall are created, BIP-NS is preferable if two ablation catheters can be positioned on either side of the target.

DOI： 10.1016/j.ipej.2024.11.003

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BACKGROUND: The coagulation response during vascular injury with uninterrupted administration of direct oral anticoagulants has not been elucidated. OBJECTIVE: Our aim was to evaluate differences in coagulation responses after vascular injury between uninterrupted direct thrombin inhibitor and direct factor Xa inhibitor recipients. METHODS: Patients scheduled for catheter ablation for atrial fibrillation were randomly assigned to receive dabigatran or apixaban in this prospective, randomized, comparative, parallel-group study. Venous blood was collected 3 times: 180 minutes after taking the anticoagulant on the day before the procedure, before vascular punctures of the ablation procedure, and 10-15 minutes after the start of vascular punctures. RESULTS: Forty-two patients were enrolled. The prothrombin fragment 1+2 level, the primary end point, was much larger after vascular puncture in the uninterrupted dabigatran recipients (median, 83 pmol/L; interquartile range, 56-133 pmol/L) than in the uninterrupted apixaban recipients (median, 1 pmol/L; interquartile range, -3 to 19 pmol/L; P < .001). Antithrombin levels decreased after vascular puncture in dabigatran recipients, and both protein C and antithrombin levels decreased after vascular puncture in apixaban recipients. CONCLUSION: Unlike uninterrupted apixaban, uninterrupted dabigatran does not inhibit thrombin generation in response to vascular injury.

DOI： 10.1016/j.hrthm.2024.07.017

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Language：English   Publisher：(一社)日本循環器学会  

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INTRODUCTION: During radiofrequency (RF) ablation, impedance monitoring has been used to avoid steam-pop caused by excessive intramyocardial temperature (IMT) rise. However, it is uncertain why the impedance decline is related to steam-pop and whether the impedance decline is correlated to IMT. METHODS: Twenty-one bipolar ablations (40 W, 30-g contact, 120 s) were attempted for seven perfused porcine myocardium. Immediately after ablation, a temperature electrode was inserted into the mid-myocardial portion, and the recovery process of impedance and its correlation to IMT were assessed. RESULTS: Transmural lesion was created in all 21 applications but steam-pop occurred in 5/21 applications with large impedance decline. In the 16 applications without steam-pop, impedance and IMT soon after ablation were 97.2 ± 4.0 Ω and 66.1 ± 4.8 °C, respectively. Reasonably high linear correlation was demonstrated between the maximum IMT after ablation and impedance differences before and after ablation. Recovery processes of the decreased impedance and the elevated IMT fit well to each equation of the single exponential decay function and showed symmetric shapes with no statistical difference of time constant (100.1 ± 34.5 s in impedance vs. 108.7 ± 27.3 s in IMT) and half-time of recovery (144.5 ± 49.8 s in impedance vs. 156.9 ± 39.4 s in IMT). Recovered impedance after ablation (104.8 ± 3.9 Ω) was 5.1 ± 2.0 Ω smaller than that before ablation (109.9 ± 2.7 Ω), suggesting several factors other than IMT rise participate in impedance decline in RF ablation. CONCLUSIONS: Recovery of impedance and IMT after ablation well correlated, which supports the usefulness of impedance monitoring for safe RF ablation.

DOI： 10.1016/j.ipej.2023.12.001

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INTRODUCTION: Radiofrequency (RF) catheter ablation induces excitation recoverable myocardium around durable core lesions, and its distribution may be different depending on energy delivery methods. METHODS AND RESULTS: In coronary perfusing porcine hearts, pacing threshold through the ventricle was measured using eight-pole (1-mm distance) needle electrodes vertically inserted into myocardium before, within 3 min after and 40 min after 40 W ablation with 10-g catheter contact (Group 1: irrigation catheter for 15 s, Group 2: irrigation catheter for 40 s, Group 3: nonirrigation catheter for 15 s, Group 4: nonirrigation catheter for 40 s). Ablation was accomplished in all 12 ablations in Groups 1-3 whereas in 8/12 ablations in Group 4 because of high-temperature rise. Within 3 min after ablation, 10.0 V pacing uncaptured electrodes were distributed from the surface to inside the myocardium, and its depth was deeper in 40 s than in 15 s ablation. 40 min after ablation, excitation recovery at one or more electrodes below the durable lesion was observed in all Groups. Excitation recovery electrodes were also observed on the surface in Group 1 but not the other Groups. Accordingly, the number of excitation-recovered electrodes were larger in Group 1 than the other Groups. CONCLUSIONS: Regardless of the ablation methods, excitation recoverable myocardium was present around 1.0 mm below the durable lesions. Lesions created by short application time using an irrigation catheter may have included large excitation recoverable myocardium soon after ablation because of the presence of reversible myocardium on well-irrigated myocardial surfaces.

DOI： 10.1111/jce.15873

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Language：Japanese   Publisher：(公財)日本心臓財団  

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BACKGROUND: Inappropriate shocks delivered by subcutaneous implantable cardioverter-defibrillators (S-ICDs) are most frequently caused by cardiac oversensing. However, the predictors for oversensing of S-ICD remain unclear. OBJECTIVE: We aimed to investigate the predictors for oversensing of S-ICD, especially clinical impact of an electrocardiographic (ECG) change. METHODS: We retrospectively enrolled 99 consecutive patients who underwent S-ICD implantation between 2013 and 2021. Oversensing events were defined as inappropriate charge of the capacitors induced by cardiac or noncardiac signals other than tachycardia. RESULTS: During a median follow-up period of 34 months (interquartile range 20-50 months), 11 of 99 patients (11%) experienced 34 oversensing events and 4 patients (4%) received inappropriate shocks during their events. Six patients exhibited ECG changes (bundle branch block, 3; ventricular pacing, 1; inverted T wave, 1; poor R-wave progression, 1) during the follow-up period. Oversensing events were observed in 4 of 6 patients with ECG change (67%), and 3 patients underwent S-ICD removal because of inevitable shock. Contrastingly, of the remaining patients without ECG change, all 7 patients who experienced oversensing events could continue using S-ICD with the reprogramming sensing vector and/or restriction of excessive exercise. Logistic regression analysis showed that lower voltage of Sokolow-Lyon ECG (V1S + V5R) was the predictor of oversensing in patients without ECG change. When the cutoff value was 2.1 mV, the sensitivity, specificity, positive predictive value, and negative predictive value were 85.7%, 62.7%, 15.7%, and 98.1%, respectively. CONCLUSION: Unavoidable oversensing resulting in S-ICD removal is caused by ECG change. Oversensing in patients without ECG change can be managed.

DOI： 10.1016/j.hrthm.2022.05.037

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DOI： 10.1111/jce.15684

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BACKGROUND: The incidence of electrical storm (ES) is significantly higher during the daytime. However, the association between nocturnal ventricular tachyarrythmias during ES and prognosis remains unclear. Therefore, this study aimed to investigate the clinical characteristics and outcomes of ES with midnight ventricular tachyarrythmias. METHODS: We included 48 consecutive patients who had an implantable cardioverter-defibrillator or cardiac resynchronization therapy defibrillator implanted between 2010 and 2020 and those who had experienced the onset of an out-of-hospital ES episode. According to the midnight (0:00 a.m.-6:00 a.m.) occurrence of ventricular arrythmia events consisting of ventricular tachycardia (VT) and ventricular fibrillation (VF), we divided them into two groups (with-midnight group: n = 27, without-midnight group: n = 21). The clinical characteristics and outcomes of the two groups were compared. RESULTS: The patients in the with-midnight group were mostly males, had longer QRS duration, and longer corrected QT-interval than those in the without-midnight group (p < .05). The incidence of all-cause death, especially heart failure death, was higher in the with-midnight group than in the without-midnight group (p < .01). Multivariate analysis showed that the presence of midnight VT/VF during ES was the only independent risk factors for heart failure death (HR = 18.9, 95%CI = 1.98-181, p = .011). CONCLUSIONS: The presence of midnight VT/VF during ES might be associated with the poor prognosis. The loss of a sympathetic circadian pattern of VT/VF distribution during ES might suggest advanced stages of the cardiac disease.

DOI： 10.1111/pace.14592

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DOI： 10.1161/CIRCEP.121.010392

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Antimitochondrial antibodies (AMA) are serum autoantibodies specific to primary biliary cholangitis and are linked to myopathy and myocardial damage; however, the presence of AMA as a risk factor for ventricular tachyarrhythmias (VTs) has remained unknown. This study aimed to elucidate whether the presence of AMA-related noncardiac diseases indicates VTs risk.This cohort study enrolled 1,613 patients (883 females) who underwent AMA testing to assess noncardiac diseases. The incidence of VTs and supraventricular tachyarrhythmias (SVTs) from a year before the AMA testing to the last visit of the follow-up were retrospectively investigated as primary and secondary objectives. Using propensity score matching, we extracted AMA-negative patients whose covariates were matched to those of 152 AMA-positive patients. In this propensity score-matched cohort, the incidence of VTs and SVTs in the AMA-positive patients were compared with that in AMA-negative patients.The AMA-positive patients had higher estimated cumulative incidence (log-rank, P = 0.013) and prevalence (5.9% versus 0.7%, P = 0.020) of VTs than the AMA-negative patients. The presence of AMA was an independent risk factor for VTs (hazard ratio, 4.02; 95% CI, 1.44-20.01; P = 0.005). Meanwhile, AMA were associated with atrial flutter and atrial tachycardia development. In AMA-positive patients, VTs were associated with male sex, underlying myopathy, high creatine kinase levels, presence of chronic heart failure or ischemic heart disease, left ventricular dysfunction, presence of SVTs, and the electrocardiographic parameters indicating atrial disorders.The presence of AMA-related noncardiac diseases is an independent risk factor for VTs.

DOI： 10.1536/ihj.22-075

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Language：Japanese   Publisher：(公財)日本心臓財団  

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BACKGROUND: Remote monitoring (RM) has been shown to reduce all-cause mortality in patients with implantable cardioverter-defibrillators or cardiac resynchronization therapy defibrillators (ICD/CRT-D). Not all devices transmit an alert for antitachycardia pacing (ATP) therapy, and it is unknown whether differences of RM alert affect the outcomes of electrical storm (ES). METHODS: We enrolled 42 patients with ICD/CRT-D whose out-of-hospital ES were detected by RM between 2013 and 2020. We divided their 54 episodes into two groups (ATP-alert-on; 22, ATP-alert-off; 32), and clinical outcomes were compared between the two groups. RESULTS: In 35 of 54 episodes of ES, ventricular tachycardia (VT) could be terminated within 24 h of ES onset just by ATP (ATP-alert-on: 14, ATP-alert-off: 21); however, many patients subsequently received shock delivery for VT. Among the 35 episodes, only in ATP-alert-on group, seven patients were prompted to visit our hospital without ICD shock through confirmation of ES by ATP-alert. Episodes that led to shock delivery 24 h or longer after the ES onset were significantly less common in the ATP-alert-on group (ATP-alert-on: 1/14, ATP-alert-off: 9/21, p = .03). Although there were no significant differences in the number of shock deliveries between episodes in the two groups, the number of ATP deliveries were significantly fewer in the ATP-alert-on group (12[7-26] vs. 29[16-53] in ATP-alert-off group, p = .03). Multivariate logistic regression analyses showed that the only ATP-alert significantly reduced ATP deliveries (HR = 0.14, 95%CI = 0.04-0.57, p = .003). CONCLUSION: Remote monitoring with an ATP-alert function during electrical storm may reduce appropriate ICD therapy through prompting early review.

DOI： 10.1111/pace.14334

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

BACKGROUND: Anti-tachycardia pacing (ATP) delivered from an implantable device is a useful tool to terminate ventricular tachycardia (VT). But its real-world efficacy for those patients having multiple VTs with varying VT rates has not been fully studied. METHODS: Using the Nippon-storm study database, efficacy of patient-by-patient basis ATP programing for Japanese patients having both non-fast (120-187 bpm) and fast VT (≥188 bpm) was assessed. According to the useful criteria of ≥50% success termination by ATP, patients were divided into three subgroups; success ≥50% for both non-fast and fast VT (both useful), ≥50% only for non-fast VT (non-fast VT useful), or ≥50% for neither non-fast nor fast VT (neither useful). RESULTS: During a median follow-up of 28 months, ATP terminated 184 of the 203 non-fast VT episodes (91%) and 86 of the 113 fast VT episodes (76%) in all 41 patients. In the patient-by-patient analysis, efficacy of ATP was not different between non-fast and fast VT in most of the patients (36/41 = 88%); 32 patients were in the both useful and four other patients in the neither useful. Neither ischemic nor non-ischemic structural heart disease was associated with the ATP efficacy, whereas LVEF more than 37.0% and non-prescribed amiodarone were characteristics of the patients classified into the both useful. CONCLUSIONS: ATP well terminated both non-fast and fast VT occurring in individual Japanese patients with various structural heart diseases in the real-world device treatment and this finding further supports ATP programing for all device tachycardia detection zones in most patients with multiple VTs.

DOI： 10.1002/joa3.12572

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DOI： 10.1002/joa3.12491

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INTRODUCTION: The local conduction delay has been deemed to play an important role in the perpetuation of ventricular fibrillation (VF) in Brugada syndrome (BrS). We evaluated the relationship between the activation delay during programmed stimulation and cardiac events in BrS patients. METHODS: This study included 47 consecutive BrS patients who underwent an electrophysiological study and received implantable cardiac defibrillator therapy. We divided the patients into two groups based on whether they had developed VF (11 patients) or not (36 patients) during the follow-up period of 89 ± 53 months. The activation delay was assessed using the interval between the stimulus and the QRS onset during programmed stimulation. The mean increase in delay (MID) was used to characterize the conduction curves. RESULTS: The MID at the right ventricular outflow tract (RVOT) was significantly greater in patients with VF (4.5 ± 1.2 ms) than in those without VF (2.2 ± 0.9 ms) (p < .001). A receiver operating characteristics curve analysis indicated that the optimal cut-off point for discriminating VF occurrence was 3.3 with 88.9% sensitivity and 91.3% specificity. Furthermore, patients with an MID at the RVOT ≥ 3.3 ms showed significantly higher rates of VF recurrence than those with an MID at the RVOT < 3.3 ms (p < .001). The clinical characteristics, including the signal-averaged electrocardiogram measurement and VF inducibility were similar between the two groups. CONCLUSION: A prolonged MID at the RVOT was associated with VF and maybe an additional electrophysiological risk factor for VF in BrS patients.

DOI： 10.1111/jce.15065

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AIMS: Although shortening of the corrected QT interval (QTc) is a key finding in the diagnosis of short QT syndrome (SQTS), there may be overlap of the QTc between SQTS patients and normal subjects in childhood and adolescence. We aimed to investigate electrocardiographic findings for differentiation of SQTS patients. METHODS AND RESULTS: The SQTS group comprised 34 SQTS patients <20 years old, including 9 from our institutions and 25 from previous reports. The control group comprised 61 apparently healthy subjects with an QTc of <360 ms who were selected from 13 314 participants in a school-based screening programme. We compared electrocardiographic findings, including QT and Jpoint-Tpeak intervals (QT and J-Tpeak, respectively), those corrected by using the Bazett's and Fridericia's formulae (cB and cF, respectively) and early repolarization (ER) between the groups. QT, QTc by using Bazett's formula (QTcB), QTc by using Fridericia's formula (QTcF), J-Tpeak, J-Tpeak cB, and J-Tpeak cF were significantly shorter in the SQTS group than in the control group. On receiver operating characteristic curve analysis, the area under the curve (AUC) was largest for QTcB (0.888) among QT, QTcB, and QTcF, with a cut-off value of 316 ms (sensitivity: 79.4% and specificity: 96.7%). The AUC was largest for J-Tpeak cB (0.848) among J-Tpeak, J-Tpeak cB, and J-Tpeak cF, with a cut-off value of 181 ms (sensitivity: 80.8% and specificity: 91.8%). Early repolarization was found more frequently in the SQTS group than in the control group (67% vs. 23%, P = 0.001). CONCLUSION: A QTcB <316 ms, J-Tpeak cB < 181 ms, and the presence of ER may indicate SQTS patients in childhood and adolescence.

DOI： 10.1093/europace/euab097

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DOI： 10.1253/circj.CJ-20-0637

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DOI： 10.1253/circj.CJ-66-0196

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Andersen-Tawil syndrome (ATS) is an inherited disorder characterised by the triad of ventricular arrhythmias (VAs), periodic paralysis and dysmorphic features. A 31-year-old woman diagnosed with ATS caused by a KCNJ2 mutation (p.R228ins) was urgently admitted to our hospital following an episode of syncope during exercise. Electrocardiography revealed frequent premature ventricular complexes and non-sustained ventricular tachycardias (VTs) with pleomorphic QRS patterns. During the intravenous flecainide test (30 mg), the frequent VAs were inhibited completely. After oral flecainide (100 mg) was started, VAs, except for a brief bigeminy, were suppressed during the exercise test. On 24-hour Holter recordings, the VAs decreased from 50 133 to 13 363 beats/day (-73%). Sustained VT and syncope were not observed during a 3-year follow-up period. Intravenous flecainide challenge test may be useful in predicting the efficacy of oral flecainide treatment for patients with ATS.

DOI： 10.1136/bcr-2019-229628

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：W.B. Saunders  

Objective: To investigate the prevalence and outcomes of asymptomatic coronary artery disease (CAD) in patients with the first episode of ischemic stroke. Methods: Patients admitted to our hospital between November 2001 and January 2009 for the episode of an acute ischemic stroke/transient ischemic attack were included. Stress-Tl-201 scintigraphy was performed and followed by coronary angiography (CAG). The prevalence and risks for asymptomatic CAD, and long-term outcomes were studied. Results: Of 1309 patients, only 15 (1.1%) patients presented with a history of CAD. Excluding 406 patients because of severity, systemic infection, early transfer to another hospital, or a refusal to participate, myocardial scintigraphy was performed in 903 patients (mean age, 72 ± 10 years, male 63.9%), and myocardial ischemia was diagnosed in 214 patients (23.7%). Of these patients, 76 patients underwent CAG, and showed significant stenosis (&gt
75%) of a coronary artery in 61 (80.3%) patients. The risk factors for positive scintigraphy findings and CAG were high-grade premature complexes via Holter monitoring (P &lt
.0001), enlarged left ventricle (P =.0051) and wall motion abnormalities (P =.0014) observed on echocardiography, and carotid artery stenosis observed in magnetic resonance angiography imaging (P &lt
.0001). During the follow-up periods of 83 ± 47 months and of 91 ± 47 months, 17.2% of scintigraphy-positive and 2.8% of scintigraphy-negative patients developed episodes of myocardial ischemia, respectively (P &lt
.001). Conclusions: Symptomatic CAD was rare in Japanese patients with the first episode of ischemic stroke, but asymptomatic CAD was identified by stress Tl-201 myocardial scintigraphy in one-quarter of the patients. Positive scintigraphy was associated with asymptomatic CAD and future cardiac events.

DOI： 10.1016/j.jstrokecerebrovasdis.2018.10.035

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DOI： 10.1016/j.jacc.2017.10.076

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier Ltd  

In an 86-year-old woman who had been treated for sick sinus syndrome, the small high-frequency current delivered by pacemaker in order to measure the minutes ventilation for utilizing the rate-response mode was transiently over-sensed on the Holter electrocardiogram. Although her pacing system was working appropriately, the numbers of the paced beats on the automatic Holter analysis were undercounted (from &gt
60% to &lt
5%) during the over-sensing periods because these currents were recognized as multiple pacing spikes. Physicians need to pay attention to such multiple pacing spike markers, because these can be a cause of unreliable results of the Holter analysis. &lt
Learning objective: Paying attention to multiple pacing spike markers on Holter electrocardiogram is clinically important in patients treated by a rate-response pacemaker. This is because (1) this does not imply the malfunction of the pacemaker system, and (2) results from automatic Holter analysis would not be reliable during the period when these multiple pacing markers were recorded.&gt

DOI： 10.1016/j.jccase.2017.08.007

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

Background: Patients with repetitive ventricular tachyarrhythmias so-called electrical storm frequently require antiarrhythmic drugs. Amiodarone is widely used for the treatment of electrical storm but is ineffective in some patients. Therefore, we investigated the efficacy of stepwise administration of nifekalant, a pure potassium channel blocker, and mexiletine for electrical storm.
Methods: This study included 44 patients with repetitive ventricular tachyarrhythmias who received stepwise therapy with nifekalant and mexiletine for electrical storm. Nifekalant was initially administered, and mexiletine was subsequently added if nifekalant failed to control ventricular tachyarrhythmias.
Results: Nifekalant completely suppressed recurrences of ventricular arrhythmias in 28 patients (64%), including 6 patients in whom oral amiodarone failed to control arrhythmias. In 9 of 16 patients in whom nifekalant was partially effective but failed to suppress ventricular arrhythmias, mexiletine was added. The addition of mexiletine prevented recurrences of ventricular tachyarrhythmias in 5 of these 9 patients (56%). There was no death associated with electrical storm. In total, the stepwise treatment with nifekalant and mexiletine was effective in preventing ventricular tachyarrhythmias in 33 of 44 patients (75%). There was no difference in cycle length of the ventricular tachycardia, QRS interval, QT interval, or left ventricular ejection fraction between patients who responded to antiarrhythmic drugs and those who did not. During follow-up, 8 patients had repetitive ventricular tachyarrhythmia recurrences, and the stepwise treatment was effective in 6 of these 8 patients (75%).
Conclusions: The stepwise treatment with nifekalant and mexiletine was highly effective in the suppression of electrical storm. (C) 2016 Published by Elsevier Inc.

DOI： 10.1016/j.jelectrocard.2016.09.005

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Background: Idiopathic ventricular fibrillation (VF) and/or polymorphic VT are occasionally initiated by VT or premature ventricular contraction (PVC) originating from the RVOT. Methods: Among 56 patients without structural heart disease in whom EPS was conducted for idiopathic VT arising from the RVOT, we examined the clinical characteristics in 5 patients with VF or polymorphic VT initiated by PVC originating from RVOT. Results: Episodes of VF were documented in 1 patient and polymorphic VT in 4 patients including one with a family history of aborted sudden death. In holter recording, there was no PVC/VT with short coupling interval in any patients. In Treadmill test, there were no patient with VT/VF inducted by exercise. 2 patients had J waves. The morphologies of PVC triggering polymorphic VT or VF were various:QS pattern was seen in the lead? in 3 patients, RS pattern was seen in the remaining. Conclusion: In this study, we found that the lack of inducibility by exercise and the absence of family history of cardiac disease were not always benign factor in the RVOT-VT/PVC. There were not any special feature in the form of PVC triggering VT/VF. Our findings may be useful to treat the patients with history of syncope and episodes of RVOT VT/VPC. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.PJ2_085

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DOI： 10.1016/j.ijcard.2016.08.042

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

A 73-year-old woman first visited our emergency room with multiple syncopal attacks. Before admission, she had received an antibiotic (Garenoxacin) for 3 days from a local clinic. First electrocardiogram (ECG) showed no ST-segment deviation but mild QT interval prolongation with a positive U wave. Second ECG recording 3 h later showed slightly slower heart rate and revealed marked QTU interval prolongation suggesting the cause of her syncopal attacks. After cessation of Garenoxacin, the QTU interval prolongation shortened. However, both epinephrine infusion and treadmill exercise test reproduced similar QTU interval prolongation and T wave deformities. Later, genetic analysis demonstrated that this patient had a mutation in KCNH2 gene, and she was diagnosed as a type-2 long-QT syndrome which was accentuated by use of garenoxacin. At the emergency out-patient clinic, repetitive ECG recordings can be useful and should be considered in order to identify the cause of syncopal attacks in patients who were prescribed antibiotics and had mild QT interval abnormalities.

DOI： 10.1007/s00380-015-0693-x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Background: The proportion of patients with atrial fibrillation (AF) treated with anticoagulation varies from country to country. In Japan, little is known about regional differences in frequency of warfarin use or prognosis among patients with non-valvular AF (NVAF).
Methods and Results: In J-RHYTHM Registry, the number of patients recruited from each of 10 geographic regions of Japan was based on region population density. A total of 7,406 NVAF patients were followed up prospectively for 2 years. At baseline, significant differences in various clinical characteristics including age, sex, type of AF, comorbidity, and CHADS(2) score, were detected among the regions. The highest mean CHADS(2) score was recorded in Shikoku. Frequency of warfarin use differed between the regions (P&lt;0.001), with lower frequencies observed in Hokkaido and Shikoku. Baseline prothrombin time international normalized ratio differed slightly but significantly between the regions (P&lt;0.05). On univariate analysis, frequency of thromboembolic events differed among the regions (P&lt;0.001), with the highest rate seen in Shikoku. An inverse correlation was detected between frequency of thromboembolic and of major hemorrhagic events (P=0.062). On multivariate analysis, region emerged as an independent risk for thromboembolism.
Conclusions: Thromboembolic risk, frequency of warfarin use, and intensity and quality of warfarin treatment differed significantly between geographic regions of Japan. Region was found to be an independent predictor of thromboembolic events.

DOI： 10.1253/circj.CJ-16-0300

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Language：Japanese   Publisher：公益財団法人 日本心臓財団  

腎動脈アブレーションでは両側腎動脈に高周波通電が行われているが, その根拠は明らかにされていない. 高周波通電が両側腎動脈に行われる理由を検証するため動物実験を行った. ビーグル犬を用いて血圧調整における左右腎交感神経興奮の効果を, 腎動脈高周波アブレーション前後の神経電気刺激の昇圧反応から検討した. 腎動脈にイリゲーションカテーテルを挿入して高周波通電を片側腎動脈に行い, 先端電極からの神経電気刺激をアブレーション前後で施行した. アブレーション前の神経電気刺激で昇圧速脈反応が左右腎動脈で同程度に誘発され, 心拍変動解析の交感神経指標と血中カテコラミン値も上昇した. アブレーションを施行した腎動脈では神経電気刺激による昇圧速脈反応は観察されなくなったが, アブレーションをしなかった腎動脈の神経電気刺激では, アブレーション前と同等の昇圧速脈反応が再度誘発された. 腎交感神経刺激による全身交感神経緊張は左右腎動脈で同等に生じ, 一側腎動脈アブレーションは, 対側腎動脈刺激の昇圧速脈誘発に影響を与えなかった. 腎動脈アブレーションで成果を得るには, 両側腎動脈通電が望まれることを支持する所見と思われる.&lt;/p&gt;

DOI： 10.11281/shinzo.48.608

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Language：Japanese   Publisher：Japanese Heart Rhythm Society  

DOI： 10.5105/jse.36.31

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Other Link： http://search.jamas.or.jp/link/ui/2016172097

Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

Introduction: Recently, direct-acting oral anticoagulants (DOACs) have been introduced, with increasing use in patientswith non-valvular atrial fibrillation (NVAF). However, warfarin continues to be widely used and the benefits and risks of warfarin in NVAF patients warrant closer inspection.
Materials and Methods: Thromboembolism, major hemorrhage, and total and cardiovascular mortalities were analyzed in 7,406 NVAF patients in the J-RHYTHM Registry from January to July 2009, prior to DOAC introduction. Propensity score matching analysis was performed to reduce the differences in clinical characteristics between non-anticoagulant (n = 1002) and warfarin (n = 6404) cohorts to reassess warfarin outcomes over 2 years.
Results: The incidence of thromboembolism was significantly greater in the non-anticoagulant cohort (3.0%) than in the warfarin cohort (1.5%, P &lt; 0.001) with less frequent major hemorrhage in the non-anticoagulant cohort (0.8%) than in the warfarin cohort (2.1%, P = 0.009). Using propensity score matching, new subsets (n = 896 each) were obtained, with matching of the clinical characteristics between warfarin and non-anticoagulant subsets. The warfarin subset had lower risk factors compared with the total warfarin cohort. The incidence of thromboembolism was higher in the non-anticoagulant subset (2.9%) than in the warfarin subset (0.7%, P &lt; 0.001). However, major hemorrhage was not significantly different between the two subsets.
Conclusions: Although warfarin was associated with a significantly higher incidence of hemorrhage in the unmatched cohorts, propensity score matching revealed that warfarin reduced thromboembolism without a significant increase in hemorrhage in the matched subsets with lower risks. Propensity score matching reduced selection bias and provided rational comparisons although it had indwelling limitations. (C) 2015 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.thromres.2015.06.009

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Language：English   Publisher：OXFORD UNIV PRESS  

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Objective The dominant frequency (DF) in frequency analyses is considered to represent the objective cycle length and complexity of activation under conditions of ventricular fibrillation (VF). However, knowledge regarding the mechanisms determining the DF in human VF is limited. We studied the characteristics of the DF of human VF and relationship between DF and the defibrillation threshold.
Methods Seventy-two implantable cardioverter-defibrillator patients and 211 VF were studied. Using defibrillation tests, we performed a frequency analysis with fast Fourier transformation. The correlations between DF and clinical characteristics, including the defibrillation threshold, were assessed.
Results The mean DF of all induced VFs was 5.2 +/- 0.8 Hz. The patients were divided into two groups according to DF: the low-DF (DF &lt;5.2 Hz, n=32) and high-DF (DF &gt;= 5.2 Hz, n=40) groups. The frequency of structural heart disease was significantly higher in the low-DF group. In addition, the QRS duration, QT interval and effective refractory period of the right ventricle (RV-ERP) were significantly longer in the low-DF group. A multivariate analysis showed RV-ERP to be the only independent predictor of DF. Excluding patients receiving group III anti-arrhythmic drugs, which are known to have potent defibrillation threshold effects, the defibrillation threshold was significantly lower in the low-DF group (p=0.026).
Conclusion We found that the DF of human VF is associated with underlying heart disease, the cardiac function, cardiac conduction, ventricular refractoriness and defibrillation threshold. Our findings may be useful for identifying and managing patients with a high defibrillation threshold.

DOI： 10.2169/internalmedicine.54.3113

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BACKGROUND The circadian pattern of ventricular fibrillation (VF) episodes in patients with idiopathic ventricular fibrillation (IVF) is poorly understood. OBJECTIVE The purpose of this study was to assess the circadian pattern of VF occurrence in patients with IVF.
METHODS Excluding Brugada syndrome and other primary electrical diseases, the circadian pattern of VF occurrence was determined in 64 patients with IVF. The clinical and electrocardiographic characteristics were compared among patients with nocturnal (midnight to 6:00 AM) VF and nonnocturnal VF in relation to 3 waves. A 3 wave was defined as either notching or a slur at the QRS terminal &gt;0.1 mV above the isoelectric line in contiguous leads.
RESULTS The overall distribution pattern of VF occurrence showed 2 peaks at approximately 6:00 AM and around 8:00 PM, Nocturnal VF was observed in 20 patients (31.3%), and J waves were present in 14 of these 20 individuals (70.0%), whereas 3 waves were less frequent in the 44 nonnocturnal patients with VF: 16 (36.4%) (P = .0117). Among patients with J waves, nocturnal VF was observed in 46.7% with a peak at approximately 4:00 AM. Nocturnal VF was Less common in patients without 3 waves, occurring in only 17.6% (P = .0124). Both the type and Location of J waves and the pattern of the ST segment were similar between the nocturnal and nonnocturnal VF groups. 3 waves were associated with a VF storm and Long-term arrhythmia recurrence.
CONCLUSION In IVF, the presence of J waves may characterize a higher nocturnal incidence of VF and a higher acute and chronic risk of recurrence.

DOI： 10.1016/j.hrthm.2014.08.022

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Language：Japanese   Publisher：(一社)新潟県臨床検査技師会  

トレッドミル運動負荷試験中のQT間隔の変動がBazett補正式で適正に補正されるか検討した。対象は健常者226名とし、運動によるQT/QTc間隔のダイナミクスを回帰曲線式で分析した。結果、安静臥位から立位への体位変化または運動中の心拍数増加に伴ってBazett補正によるQTc間隔が適正範囲を逸脱した者が23%存在した。

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DOI： 10.1016/j.ijcard.2014.01.036

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DOI： 10.1016/j.ijcard.2013.12.121

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC  

Treatment guidelines for atrial fibrillation (AF) used in Western countries describe female gender as a risk factor for thromboembolic events in patients with nonvalvular AF (NVAF). The present study aimed to determine the impact of gender on prognosis of Japanese patients with NVAF. A subanalysis of 7,406 patients with NVAF (mean age 70 years) who were followed-up prospectively for 2 years was performed using data from the J-RHYTHM registry. The primary end points were thromboembolic events, major hemorrhaging, total mortality, and cardiovascular mortality. Compared with male subjects (n = 5,241), female subjects (n = 2,165) were older and displayed greater prevalences of paroxysmal AF, heart failure, and hypertension but less prevalences of diabetes, previous cerebral infarction, and coronary artery disease. Male and female patients had mean CHADS(2) (Congestive heart failure, Hypertension, Age of 75 years or more, Diabetes mellitus and prior Stroke or transient ischetnic attack) scores of 1.6 and 1.8, respectively (p &lt;0.001); Warfarin was given to 87% of male patients and 86% of female patients (p = 0.760), and the 2 genders displayed similar mean international normalized ratio of prothrombin time values at baseline (1.91 vs 1.90, respectively, p = 0.756). Multivariate logistic regression analysis indicated that male gender was an independent risk factor for major hemorrhaging (odds ratio 1.59,95% confidence interval 1.05 to 2.40, p = 0.027) and all-cause mortality (odds ratio 1.78, 95% confidence interval 1.25 to 2.55, p &lt;0.002) but not for thromboembolic events (odds ratio 1.24, 95% confidence interval 0.83 to 1.86, p = 0.297) or cardiovascular mortality (odds ratio 0.96,95% confidence interval 0.56 to 1.66, p = 0.893). In conclusion, female gender is not a risk factor for thromboembolic events among Japanese patients with NVAF who were treated mostly with warfarin. However, male gender is a risk factor for major hemorrhaging and all-cause mortality. (c) 2014 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.amjcard.2013.11.057

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Objectives This study sought to characterize patients with idiopathic ventricular fibrillation (IVF) who develop electrical storms. Background Some IVF patients develop ventricular fibrillation (VF) storms, but the characteristics of these patients are poorly known. Methods Ninety-one IVF patients (86% male) were selected after the exclusion of structural heart diseases, primary electrical diseases, and coronary spasm. Electrocardiogram features were compared between the patients with and without electrical storms. A VF storm was defined as VF occurring ≥3 times in 24 h and J waves &gt
0.1 mV above the isoelectric line in contiguous leads. Results Fourteen (15.4%) patients had VF storms occurring out-of-hospital at night or in the early morning. J waves were more closely associated with VF storms compared to patients without VF storms: 92.9% versus 36.4% (p &lt
0.0001). VF storms were controlled by intravenous isoproterenol, which attenuated the J-wave amplitude. After the subsidence of VF storms, the J waves decreased to the nondiagnostic level during the entire follow-up period. Implantable cardioverter-defibrillator therapy was administered to all patients during follow-up. Quinidine therapy was limited, but the patients on disopyramide (n = 3), bepridil (n = 1), or isoprenaline (n = 1) were free from VF recurrence, while VF recurred in 5 of the 9 patients who were not given antiarrhythmic drugs. Conclusions The VF storms in the IVF patients were highly associated with J waves that showed augmentation prior to the VF onset. Isoproterenol was effective in controlling VF and attenuated the J waves, which diminished to below the diagnostic level during follow-up. VF recurred in patients followed up without antiarrhythmic agents. © 2013 by the American College of Cardiology Foundation Published by Elsevier Inc.

DOI： 10.1016/j.jacc.2013.05.030

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BACKGROUND A substantial number of patients with idiopathic ventricular fibrillation (IVF) present with no specific electrocardiographic (ECG) findings.
OBJECTIVE To evaluate complete right bundle branch block (RBBB) in patients with IVF.
METHODS Patients with IVF showing complete RBBB were included in the present study. Structural and primary electrical diseases were excluded, and provocation tests were performed to exclude the presence of spastic angina or Brugada syndrome (BrS). The prevalence of complete RBBB and the clinical and ECG parameters were compared either in patients with IVF who did not show RBBB or in the general population and age and sex comparable controls with RBBB.
RESULTS Of 96 patients with IVF, 9 patients were excluded for the presence of BrS. Of 87 patients studied, 10 (11.5%) patients showed complete RBBB. None had structural heart diseases, BrS, or coronary spasms. The mean age was 44 +/- 15 years, and 8 of 10 patients were men. Among the ECG parameters, only the QRS duration was different from that of the other patients with IVF who did not show complete RBBB. Ventricular fibrillation recurred in 3:2 in the form of storms, which were well suppressed by isoproterenol. Complete RBBB was found less often in control subjects (1.37%; P &lt;.0001), and the QRS duration was more prolonged in patients with IVF: 139 +/- 10 ms vs 150 +/- 14 ms (P = .0061).
CONCLUSIONS Complete RBBB exists more often in patients with IVF than in controls. A prolonged (IRS complex suggests a conduction abnormality. Our findings warrant further investigation of the role of RBBB in the development of arrhythmias in patients with IVF.

DOI： 10.1016/j.hrthm.2013.03.013

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DOI： 10.1016/j.hrthm.2013.01.020

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Language：English   Publisher：WILEY-BLACKWELL  

A 65-year-old recipient of an implantable cardioverter defibrillator suffering from ventricular noncompaction developed storms of ventricular tachycardia (VT). Epicardial voltage mapping revealed the presence of a large low-voltage area in the left ventricular apical and inferoposterior wall, and isolated delayed potential was recorded over 1.5 cm in the posterior border between low and normal myocardial voltage. Pacemapping at the delayed potential recording site produced two different QRS depending on pacing output strength, and these two QRS morphologies were similar to clinically documented VTs. During one of the VTs, a mid-diastolic potential was recorded from the site with the delayed potential, and rapid pacing produced concealed entrainment. After epicardial radiofrequency ablation of the isolated delayed potential, VTs were noninducible and the VT storm was suppressed. (PACE 2013; 36:e115-e119)

DOI： 10.1111/j.1540-8159.2010.02999.x

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DOI： 10.1253/circj.CJ-66-0055

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DOI： 10.1016/j.hrthm.2012.09.013

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DOI： 10.1253/circj.CJ-13-0878

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BACKGROUND: Target anticoagulation levels for warfarin in Japanese patients with non-valvular atrial fibrillation (NVAF) are unclear. METHODS AND RESULTS: Of 7,527 patients with NVAF, 1,002 did not receive warfarin (non-warfarin group), and the remaining patients receiving warfarin were divided into 5 groups based on their baseline international normalized ratio (INR) of prothrombin time (≤1.59, 1.6-1.99, 2.0-2.59, 2.6-2.99, and ≥3.0). Patients were followed-up prospectively for 2 years. Primary endpoints were thromboembolic events (cerebral infarction, transient ischemic attack, and systemic embolism), and major hemorrhage requiring hospital admission. During the follow-up period, thromboembolic events occurred in 3.0% of non-warfarin group, but at lower frequencies in the warfarin groups (2.0, 1.3, 1.5, 0.6, and 1.8%/2 years for INR values of ≤1.59, 1.6-1.99, 2.0-2.59, 2.6-2.99, and ≥3.0, respectively; P=0.0059). Major hemorrhage occurred more frequently in warfarin groups (1.5, 1.8, 2.4, 3.3, and 4.1% for INR values ≤1.59, 1.6-1.99, 2.0-2.59, 2.6-2.99, and ≥3.0, respectively; P=0.0041) than in non-warfarin group (0.8%/2 years). These trends were maintained when the analyses were confined to patients aged ≥70 years. CONCLUSIONS: An INR of 1.6-2.6 is safe and effective at preventing thromboembolic events in patients with NVAF, particularly patients aged ≥70 years. An INR of 2.6-2.99 is also effective, but associated with a slightly increased risk in major hemorrhage. (UMIN Clinical Trials Registry UMIN000001569)

DOI： 10.1253/circj.CJ-13-0290

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In two patients treated with cardiac resynchronization therapy (CRT), left ventricular (LV) pacing failure occurred due to ring conductor fractures of the bipolar LV lead (co-radial model). CRT was resumed by pacing between the tip conductor of the LV lead and the coil conductor of the right ventricular lead. However, shortly thereafter, subsequent fracture of the tip conductor developed, and implantation of a new LV lead was required. When one of the bipolar conductors of a co-radial designed LV lead fractures, reimplantation of a new LV lead is a better therapeutic option (than changing the LV pacing mode) in order to reliably continue CRT treatment. © 2013 The Japanese Society of Internal Medicine.

DOI： 10.2169/internalmedicine.52.8988

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DOI： 10.1016/j.jccase.2012.09.001

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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DOI： 10.1016/j.ijcard.2012.05.091

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

Transmural ARI Dispersion in SQTS. A 38-year-old woman with type 1 short-QT syndrome (SQTS) was referred to our hospital. Her ECG showed short QT/QTc interval and peaked T wave. Activationrecovery intervals (ARIs) were calculated from the intracardiac endocardial and epicardial electrode catheters placed in the left ventricle (LV). Intravenous administration of nifekalant prolonged effective refractory period at multiple ventricular sites as well as the QT/QTc interval (from 260/300 to 364/419 ms) on the surface ECG. Nifekalant also enlarged the transmural ARI dispersion of the ventricular repolarization, which was measured by the difference between the longest endocardial ARI and the shortest epicardial ARI during atrial pacing at 90 bpm, from 73 to 103105 ms. These values corresponded to the intervals between the peak and end of the T wave on the surface ECG. Nifekalant-induced QT interval prolongation on the surface ECG may not indicate attenuation of the arrhythmogenic potential in the heart of SQTS patients. (J Cardiovasc Electrophysiol, Vol. 23, pp. 877-880, August 2012)

DOI： 10.1111/j.1540-8167.2012.02292.x

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We report two cases of intermittent Wolff-Parkinson-White (WPW) syndrome. In one patient, early repolarization (ER) was masked during preexcitation whereas in the other, J wave-like notches were observed in the right precordial leads only during preexcitation. The clinical significance of ER is not apparent in WPW syndrome but some possible mechanisms are discussed. (PACE 2012; 35:e231e233)

DOI： 10.1111/j.1540-8159.2012.03360.x

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An asymptomatic 15-year-old boy, who had a family history of sudden cardiac death, was referred for screening for cardiac disease. The 12-lead electrocardiogram at rest showed a short QT/QTc(Bazett)/QTc(Fredericia) interval of 320/388/364 ms, but the intervals were further shortened to 200/339/284 ms after the treadmill test concomitant with appearance of a peaked T wave. Other conventional cardiac examinations were normal, but effective refractory period was less than 180 ms in both ventricles, and double ventricular extrastimulation reproducibly induced nonsustained polymorphic ventricular tachycardia. Intravenous administration of epinephrine also induced a short QT interval and a peaked T wave, and a hump was manifested on the T wave of the first postpacing beat with a longer preceding RR interval. Furthermore, a couple of premature ventricular complexes originated from a similar timing as the hump. Genetic analysis did not show the mutation in KCNQ1, KCNH2, KCNE1, KCNE2, KCNJ2, SCN5A genes but revealed single nucleotide polymorphism (C5457T) in SCN5A gene. (PACE 2012; 35:e239e242)

DOI： 10.1111/j.1540-8159.2012.03363.x

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A storm of J wave-associated idiopathic ventricular fibrillation (VF) was observed in a 49-year-old man. Multiform premature ventricular complexes initiated the episodes of VF. Intravenous isoproterenol attenuated the J wave and suppressed the VF storm. After the implantation of a cardioverter defibrillator, VF was induced by programmed electrical stimulation at baseline, and it was terminated by a 25-J shock after an unsuccessful 15-J shock. During oral treatment with quinidine sulfate, 600 mg daily, the J wave was attenuated and VF became noninducible by programmed electrical stimulation. VF induced by a shock delivered on the T wave was terminated by a single 10-J shock. Mean F-F interval and dominant frequency of the VF were 162 ms and 6.8 Hz at baseline, and 210 ms and 5.0 Hz during the quinidine sulfate treatment. (PACE 2012; 35:e226e230)

DOI： 10.1111/j.1540-8159.2011.03066.x

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DOI： 10.1016/j.jccase.2012.03.008

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Language：English   Publisher：OXFORD UNIV PRESS  

A 34-year-old woman presented with idiopathic premature ventricular complex (PVC) and ventricular tachycardia (VT) originating from the area called the left ventricular summit. Radiofrequency (RF) application both through the coronary sinus and to the epicardial surface transiently suppressed the VT/PVC. Radiofrequency with sufficient energy was only applicable from the endocardial site, and the VT/PVC was successfully eliminated.

DOI： 10.1093/europace/eur382

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Language：Japanese   Publisher：(NPO)日本小児循環器学会  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE INC  

Objectives This study evaluated the pause-dependency of the J-wave to characterize this phenomenon in idiopathic ventricular fibrillation (VF).
Background The J-wave can be found in apparently healthy subjects and in patients at risk for sudden cardiac death, and risk stratification is therefore needed.
Methods Forty patients with J-wave-associated idiopathic VF were studied for J waves with special reference concerning pause-dependent augmentation. J waves were defined as those &gt;= 0.1 mV above the isoelectric line and were compared with 76 non-VF patients of comparable age and sex.
Results The J-wave was larger in patients with idiopathic VF than in the controls: 0.360 +/- 0.181 mV versus 0.192 +/- 0.064 mV (p = 0.0011). J waves were augmented during storms of VF (n +/- 9 [22.5%]), which was controlled by isoproterenol; they disappeared within weeks in 5 patients. In addition, sudden prolongation of the R-R interval was observed in 27 patients induced by benign arrhythmia, and 15 patients (55.6%) demonstrated pausedependent augmentation (from 0.391 +/- 0.126 mV to 0.549 +/- 0.220 mV; p +/- 0.0001). In the other 12 experimental subjects and in the 76 control subjects, J waves remained unchanged. Pause-dependent augmentation of J waves was detected in 55.6% (sensitivity) but was specific (100%) in the patients with idiopathic VF with high positive (100%) and negative (86.4%) predictive values.
Conclusions Pause-dependent augmentation of J waves was confirmed in about one-half of the patients with idiopathic VF after sudden R-R prolongation. Such dynamicity of J waves was specific to idiopathic VF and may be used for risk stratification. (J Am Coll Cardiol 2012; 59: 1948-53) c 2012 by the American College of Cardiology Foundation

DOI： 10.1016/j.jacc.2012.02.028

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The aim of this study was to investigate the relationship between J-wave dynamics and arrhythmias during myocardial ischaemia in patients with vasospastic angina (VSA).
Sixty-seven consecutive patients diagnosed with VSA by a provocation test for coronary spasm were grouped according to whether they had a J wave in the baseline electrocardiograms or not (VSA-JW group, n 14; VSA-non-JW group: n 53). We retrospectively studied the associations between J-wave and ST-segment dynamics and induced ventricular fibrillations (VFs) during coronary spasm. In the VSA-JW group, 7 of the 14 patients showed changes in J-wave morphology and/or gains in J-wave voltage, followed by VF in 4 patients. Compared with patients without VF, the four patients with VF showed similar maximal voltage in the baseline J waves but a higher voltage during induced coronary spasms (0.57 0.49 vs. 0.30 0.11 mV; P 0.011). In three patients with VF, J waves progressively increased and were accompanied by the characteristic coved-type or lambda-shaped ST-segment elevations. In the VSA-non-JW group, only four patients showed new appearances of J waves during coronary spasms and another patient without a distinct J wave developed VF. Ventricular fibrillations were induced more frequently in the VSA-JW group than in the VSA-non-JW group [4/14 (29) vs. 1/53 (2); P 0.012].
J-wave augmentations were caused by myocardial ischaemia during coronary spasms. The presence and augmentation of J waves, especially prominent J waves with the characteristic ST-elevation patterns, were associated with VF.

DOI： 10.1093/europace/eur323

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

Background and Purpose: Some de- and re-polarization patterns can reflect an increased risk of ventricular tachyarrhythmias. We studied whether some electrocardiographic (ECG) patterns are able to predict the development of ventricular fibrillation (VF) during acute myocardial infarction (MI).
Methods: We compared the patterns of ST-T segment of 78 patients who developed VF during acute MI (patient with VF) vs 170 comparable patients with acute MI but with no VF complications.
Results: Of the VF group, 47 developed out-of-hospital VF and 31 developed VF after their admission to the hospital. A steep downsloping ST segment toward a negative T wave with or without a short, flat, or rising portion at the initial portion was observed in 69.2% of the 78 patients: 61.3% in patients with pre-VF and 74.5% in patients with post-VF, vs 9.4% of patients who did not develop VF (P &lt; .0001). In 90.6% of the latter, a typical upward-concave or convex "ischemic" pattern of the ST segment was observed. Thus, the characteristic ST-T patterns were highly associated with VF with a specificity greater than 90%.
Conclusions: A steep downsloping ST segment may characterize the ECGs of patients who develop VF during acute MI. (c) 2012 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2011.11.007

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A 35-year-old man, who had an episode of aborted sudden cardiac death due to ventricular fibrillation, suffered from multiple storms of ventricular tachycardia (VT). Conventional cardiac examinations did not reveal any structural heart diseases, and he had been treated by an implantable cardioverter defibrillator since 2007. At the latest admission, epicardial but not endocardial voltage mapping revealed a small area of low voltage at the left ventricular (LV) postero-lateral wall where a delayed potential was recorded during sinus rhythm. Excellent pacemapping with a prolonged stimulus to QRS interval was obtained from the area, and a mid-diastolic potential was recorded during the VT. Radiofrequency application terminated the VT and any VT became noninducible after the ablation. In some patients diagnosed as LV-VT with no apparent heart disease, arrhythmogenic substrate may exist on the epicardial surface of the ventricle. (PACE 2012; 35:e136e139)

DOI： 10.1111/j.1540-8159.2011.03142.x

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Background: The purpose of this study was to investigate whether heart rate variability parameters can be useful for evaluating cardiac autonomic dysfunction in multiple system atrophy patients. Methods: Both the time and frequency domains of heart rate variability were investigated among 17 multiple system atrophy patients and 27 normal control subjects. Results: All time-and frequency-domain measures, except the low-to high-frequency ratio, were significantly lower in multiple system atrophy patients than in controls. In multiple system atrophy patients, there were significant inverse correlations between heart rate variability parameters and disease duration, as well as disease severity, but heart rate variability parameters were not affected by other autonomic dysfunctions. Conclusions: The cardiac autonomic state of multiple system atrophy was characterized by decreases in both sympathetic and parasympathetic tones. Because heart rate variability parameters were not affected by other autonomic dysfunctions, this may be a useful method for evaluating cardiac autonomic dysfunction in multiple system atrophy. (C) 2012 Movement Disorder Society

DOI： 10.1002/mds.24929

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

DOI： 10.1161/CIRCEP.112.971507

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

Objective To assess the electrophysiological characteristics of the breakout site of ventricular activation using electroanatomical voltage mapping (EVM) and its relation to the optimal ablation site in idiopathic ventricular tachyarrhythmias originating from the outflow tract of the (RVOT) septum.
Methods Twenty-eight patients with symptomatic drug-refractory premature ventricular complexes (PVCs) and/or ventricular tachycardia (VT) originating from the RVOT septum and 5 control subjects with WPW syndrome were included. Low-voltage areas (LVAs) were defined as signal amplitudes between 0.1 and 1.5 mV. The borderline between the normal area and the LVA was defined as "border," and the distance from the LVA to the border (length of LVA) was measured.
Results In all 28 patients and control subjects, there was an LVA below the pulmonary valve. There was no significant difference in length of LVA between patients with idiopathic ventricular arrhythmias and control subjects (2.0+/-0.6 vs. 1.9+/-0.1 cm). In 19 of the 28 patients, the optimal ablation site was identical to the border area. In all 11 patients who had pre-potentials at the successful ablation site, there were two cases with polymorphic VT and/or ventricular fibrillation associated with PVCs. In these two cases, length of LVA was longer than in other patients (4.0 and 3.9 cm vs. 1.8+/-0.5 cm (n=26)), and the optimal ablation site was located at the border area.
Conclusion The border area, including the LVA, tends to be the breakout site and/or origin of ventricular arrhythmias in idiopathic ventricular tachyarrhythmia originating from the RVOT septum.

DOI： 10.1007/s10840-011-9623-8

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Language：English   Publisher：JAPANESE CIRCULATION SOC  

DOI： 10.1253/circj.CJ-88-0022

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS  

DOI： 10.1093/europace/eur279

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

We determined the prevalence of J waves in the electrocardiograms (ECG) of 120 patients with Wolff-Parkinson-White syndrome in comparison with J-wave prevalence in a control group of 1936 men and women with comparable demographic and ECG characteristics and with normal atrioventricular conduction. J waves were present only during manifest preexcitation in 22 of 120 patients (18.3%), disappearing after catheter ablation and suggesting that J waves were associated with the presence of preexcitation. J waves were present in 19 (15.8%) of 120 patients only after ablation, apparently having been masked by early depolarization of the preexcited myocardial region, and in 22 patients (18.3%), J waves were not altered significantly by preexcitation. Thus, the overall J-wave prevalence was 52.5% (63/120) and, excluding those apparently due to preexcitation, 34.8% (41/120), both substantially higher than the prevalence (11.5%) in the control group (P &lt; .001 for both). The patients with J waves appearing only during preexcitation were younger, predominantly females. The presence of J waves after ablation was associated with a history of atrial fibrillation and shorter ventricular effective refractory period. It is concluded that the prevalence of J waves is high in patients with Wolff-Parkinson-White syndrome and is influenced by manifest preexcitation. (C) 2012 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2011.04.006

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A 57-year-old woman showed frequent premature ventricular complexes (PVCs) originating from the right ventricular outflow tract (RVOT), and some of the PVCs triggered polymorphic ventricular tachycardia (PVT). Structural heart diseases were ruled out by conventional cardiac examinations. Radiofrequency catheter ablation was successful in eliminating the PVCs and subsequent PVT. However, epinephrine infusion unmasked her prolonged QT interval, and a genetic analysis revealed a KCNH2 mutation (R694H) as the cause of latent type-2 long QT syndrome (LQTS). This case suggests that latent LQTS may work as an arrhythmogenic substrate of PVT triggered by a benign form of RVOT-PVCs in patients with a structurally normal heart.

DOI： 10.2169/internalmedicine.51.8565

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DOI： 10.2169/internalmedicine.51.7100

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Background The structures composing implantable cardioverter-defibrillator (ICD) leads have become more complicated and thinner with technological advances. Silicon insulation defects with and without clinically manifested electrical abnormalities have been reported in Riata leads (St. Jude Medical).
Objective The aim of this study was to assess the incidence and clinical implications of insulation defects in Riata leads implanted at our hospital.
Methods The subjects included 10 consecutive patients who received 8-French Riata ICD leads with dual-coil conductors (model 1580 or 1581) between 2006 and 2010 at our hospital. Operative records, chest X-rays and interrogation data were reviewed.
Results In all cases, Atlas+ (St. Jude Medical) was used as an ICD generator and the Riata leads were implanted transvenously and fixed to the right ventricular apex. During a mean follow-up period of 52 +/- 9 (36-70) months, chest X-rays revealed insulation defects in Riata leads and conductor wires projecting from the bodies of the Riata leads in two of 10 (20%) patients. One of the patients received inappropriate ICD therapies due to T-wave oversensing based on attenuation of R waves and augmentation of T waves 41 months after implantation. In the other patient, an insulation defect without any clinically manifested electrical troubles was detected 50 months after implantation.
Conclusion Riata leads have a high incidence of insulation defects, which may be occasionally accompanied by inappropriate ICD discharges. For patients with Riata leads, careful observation of any changes in the lead-electrical measurements and a routine chest X-ray follow-up are necessary.

DOI： 10.2169/internalmedicine.51.7805

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An 8-year-old boy suffered from an unconsciousness attack and torsade de pointes arrhythmia during sleep or at rest. His electrocardiogram showed prolonged QT intervals, but the T wave morphology was atypical for type 1, 2 or 3 congenital long-QT syndrome (LQTS). Intravenous epinephrine slightly prolonged the QT interval whereas mexiletine infusion shortened the QT interval. Although these clinical characteristics might suggest type 3 LQTS, a genetic analysis identified the G604S-KCNH2 mutation (type 2 LQTS). Because mismatches between the genotype and phenotype of LQTS are possible, genetic analysis of LQTS is important to identify the most appropriate therapeutic option and risk stratification.

DOI： 10.2169/internalmedicine.51.7494

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Language：Japanese   Publisher：Japan Heart Foundation  

DOI： 10.11281/shinzo.44.S2_87

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Background-Recently, we and others reported that early repolarization (J wave) is associated with idiopathic ventricular fibrillation. However, its clinical and genetic characteristics are unclear.
Methods and Results-This study included 50 patients (44 men; age, 45 +/- 17 years) with idiopathic ventricular fibrillation associated with early repolarization, and 250 age-and sex-matched healthy controls. All of the patients had experienced arrhythmia events, and 8 (16%) had a family history of sudden death. Ventricular fibrillation was inducible by programmed electric stimulation in 15 of 29 patients (52%). The heart rate was slower and the PR interval and QRS duration were longer in patients with idiopathic ventricular fibrillation than in controls. We identified nonsynonymous variants in SCN5A (resulting in A226D, L846R, and R367H) in 3 unrelated patients. These variants occur at residues that are highly conserved across mammals. His-ventricular interval was prolonged in all of the patients carrying an SCN5A mutation. Sodium channel blocker challenge resulted in an augmentation of early repolarization or development of ventricular fibrillation in all of 3 patients, but none was diagnosed with Brugada syndrome. In heterologous expression studies, all of the mutant channels failed to generate any currents. Immunostaining revealed a trafficking defect in A226D channels and normal trafficking in R367H and L846R channels.
Conclusions-We found reductions in heart rate and cardiac conduction and loss-of-function mutations in SCN5A in patients with idiopathic ventricular fibrillation associated with early repolarization. These findings support the hypothesis that decreased sodium current enhances ventricular fibrillation susceptibility. (Circ Arrhythm Electrophysiol. 2011;4:874-881.)

DOI： 10.1161/CIRCEP.111.963983

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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DOI： 10.1111/j.1540-8167.2011.02046.x

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DOI： 10.1111/j.1540-8167.2010.01974.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：NATURE PUBLISHING GROUP  

Hypertension is well known to increase atrial fibrillation (AF) and the development of AF is associated with atrial chamber remodeling. Although mineralocorticoid receptor (MR) inhibition provides cardiovascular protection, the role of MR on atrial structural remodeling and inducibility of AF in hypertension remains unclear. Here, we investigated roles of the MR on atrial structural remodeling and inducibility of AF in hypertensive rats by using MR antagonist eplerenone (EPL). Dahl salt-sensitive (DS) rats were fed a normal-salt or a high-salt (HS) diet from 7 weeks, and a non-antihypertensive dose of EPL or vehicle was administrated from 13 weeks, at which time myocytes hypertrophy, interstitial fibrosis in the atrium and AF inducibility had increased, until 20 weeks. There was no significant difference in systolic blood pressure between DS+HS (186 +/- 4mmHg) and DS+HS+EPL (184 +/- 5mmHg) at 20 weeks. Burst atrial pacing demonstrated decreased AF inducibility in DS+HS+EPL (0 of 10) compared with DS+HS (7 of 10). Fibrosis and myocytes hypertrophy in the atrium were decreased in DS+HS+EPL with the reduction of atrial inflammatory cytokines. These beneficial effects of EPL were associated with less atrial oxidative stress, as assessed by 4-hydroxy-2-nonenal staining, and reduced activation of the Rho GTPase Rac1 in the atrium. Thus, MR has important roles in atrial structural remodeling and AF inducibility in Dahl rats. The effects of MR are associated, at least in part, with activation of Rac1-oxidative stress/inflammatory axis. Hypertension Research (2011) 34, 584-591; doi:10.1038/hr.2010.277; published online 20 January 2011

DOI： 10.1038/hr.2010.277

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

It is not known if J waves of early repolarization can be affected by depolarization or not. We report 2 cases in whom J waves were unmasked by preexcitation. A 59-year-old woman with Wolff-Parkinson-White syndrome who had frequent episodes of tachycardia underwent radiofrequency catheter ablation. The 12-lead electrocardiogram on admission showed delta waves and a notch in leads II, III, and a VF (J waves), which disappeared after the elimination of preexcitation. A 56-year-old man with Wolff-Parkinson-White syndrome was admitted for catheter ablation for supraventricular tachycardia. His electrocardiogram showed delta waves in I, II, aVL, V(2) to V(6), and J waves in the inferior leads and V(3) through V(6) with ST elevation and ST elevation in V(2). After ablation, J waves disappeared and were replaced by S waves. However, ST elevation remained in the precordial leads. The 2 cases suggest that J waves may be affected by the depolarization process: preexcitation. (c) 2011 Published by Elsevier Inc.

DOI： 10.1016/j.jelectrocard.2010.09.004

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Ablation of Bidirectional VT. A 64-year-old recipient of implantable cardioverter defibrillator presenting with a 4.7 x 3.3 cm nonischemic, biventricular aneurysm developed multiple electrical storms due to ventricular tachycardia (VT) with 2 distinct QRS morphologies. Endocardial electroanatomical mapping revealed the presence of a low-voltage area corresponding to the aneurysm, where multiple delayed potentials were recorded. Activation mapping and entrainment pacing of both VT revealed the, respectively, forward and reverse propagation of the wavefront across a single reentrant circuit inside the ventricular aneurysm. Delivery of 3 applications of radiofrequency energy to a critical segment of the reentrant pathway eliminated both VT and the electrical storms. (J Cardiovasc Electrophysiol, Vol. 22, pp. 467-467).

DOI： 10.1111/j.1540-8167.2010.01888.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Congestive heart failure (CHF) and atrial fibrillation (AF) often coexist, and each increase the morbidity and mortality associated with the other. Until now, many studies have reported that a strategy of rate control, in combination with anticoagulation in patients at risk of thromboembolic events, appears to be at least equivalent to a strategy of maintaining sinus rhythm with currently available pharmacological therapeutic options. As compared to rhythm control therapy, rate control treatment is simple and relatively easy. Therefore, pharmacological rate control should be considered initially in patients with AF associated with CHF. However, cardiac symptoms associated with AF may continue after achieving reasonable ventricular rate control. Either pharmacological or non-pharmacological rhythm control needs to be considered at that time. Amiodarone is the only recommended antiarrhythmic drug in the recent therapeutic guidelines for CHF, and can be used for both rhythm and rate control of AF. However, there is no question that some patients require early non-pharmacological rhythm control instead of long-lasting rate control. Catheter ablation (CA) can be applicable even in AF associated with CHF, but the results of CA are closely associated with the clinical and electrophysiological characteristics in each patient, as well as with the experience with this procedure in each institution. Indications for and the appropriate period of CA need to be carefully examined in each individual. (Circ J 2011; 75: 970-978)

DOI： 10.1253/circj.CJ-11-0080

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Premature ventricular complexes (PVC) falling after the end of the T wave triggered ventricular fibrillation (VF) at night and monomorphic ventricular tachycardia (MVT) during daytime, in a recipient of implantable cardioverter defibrillator with Brugada syndrome. Treatment with bepridil (1) decreased the height of ST segment elevation in leads V1-V3, (2) completely eliminated VF, and (3) markedly decreased the incidence of PVC and MVT. Albeit rare, VF can be triggered by late-coupled PVC, due to a mechanism other than phase 2 reentry in some patients with Brugada syndrome. (PACE 2011; e1-e5).

DOI： 10.1111/j.1540-8159.2010.02735.x

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A 60-year-old man with arrhythmogenic right ventricular cardiomyopathy was readmitted for the battery exchange of his implantable cardioverter-defibrillator (ICD). Since (i) he had been treated with a dual-coil shock lead (Sprint Fidelis, Medtronic) and (ii) pre-operative venography showed mild collateral flow to the left subclavian vein, a single-coil lead was additionally implanted. However, the single-coil defibrillation system was unable to terminate the induced ventricular fibrillation (VF), thus dual defibrillation shock pathways were created using the connection to the superior vena cava coil of the Fidelis lead. The combined connections of the two shock leads provided an appropriate margin of the defibrillation threshold.

DOI： 10.2169/internalmedicine.50.5792

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We injected acetylcholine (Ach) into the coronary artery to ascertain whether coronary vasospasm contributed to the syncopal events or chest oppression suffered by 3 patients with long QT syndrome (LQTS). During the test, a quadripolar electrode catheter was placed in the right ventricle and the activation-recovery interval was reanalyzed from the stored data. Intracoronary Ach transiently prolonged the QT intervals in all 3 patients without inducing coronary vasospasm. The Ach-induced QT prolongation was associated with enhanced spatial and temporal dispersion of intra-ventricular repolarization. The electrophysiological abnormalities were consistent with the putative arrhythmogenic mechanisms identified in experimental studies of LQTS.

DOI： 10.2169/internalmedicine.50.5114

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Inappropriate inhibition of atrial pacing due to T-wave oversensing (TWOS) was observed in a patient presenting with congenital long QT syndrome, treated with an implantable cardioverter defibrillator (ICD) and beta-adrenergic blocker. Development of TWOS was associated with further QT interval prolongation in the absence of amplitude changes in the intracardiac T and R waves. Replacement of the ICD generator with a sensing filter designed to attenuate the intracardiac T wave suppressed TWOS and normalized the pacing functions.

DOI： 10.2169/internalmedicine.50.4837

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Objective: The aim of the present study was to assess characteristics of ventricular tachycardia (VT) of electrical storm (ES) in ICD patients with structural heart disease. Methods: We included 156 consecutive patients who implanted ICD due to secondary prevention. ES was defined as the occurrence of at least 3 episodes of VT/VF within 24-hours. Basic treatment for ES was as follows
sedation, β-blockers, and class I and/or III antiarrhythmic drugs. We defined that elimination of ES for 2 weeks after basic treatment was drug effective (DE), if not, drug refractory (DR). Results: During a mean follow-up period of 54 ± 37 months, ES occurred in 42 patients (OMI in 12, DCM in 15, HCM in 6, ARVC in 5, cardiac sarcoidosis in 4). Patients with DE and DR were 30 and 12 patients, respectively. There were no significant differences in age, sex, and LVEF. However, cycle length of VT (VTCL) was significantly longer in patients with DR than with DE (384 ± 16 vs. 305 ± 10 ms, p&lt
0.05). All 12 patients with DE required for Catheter ablation. Conclusion: Longer VTCL in ES was related to drug refractoriness, which might be caused by stability of reentry circuit in spite of antiarrhythmic therapy. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.OP06_3

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Method: We investigated the outcomes of 136 patients with Sprint-Fidelis in 5 centers in Niigata Prefecture. Results. Incidence: Lead troubles occurred in 9 patients (6.6%). The mean period before the trouble was 31 months (16-57 months). Implantation: Among these 9 patients, the lead was implanted using a cut-down technique in 4, an extra-thoracic approach in 4 and a subclavian approach in 1. Discovery: The lead troubles in 5 were discovered at regular clinics. The other 4 patients emergently visited because of the lead integrity alert (LIA) or inappropriate ICD discharges. In the 9 patients, the average sensing integrity counter was 338/day and mean F-F interval, of which was recognized as NST, was less than 200ms. The LIA: The LIA had been programmed in 7, and 5 of the patients visited before inappropriate ICD discharges. However, the other 2 elderly patients couldn't notice the alert sound. Extraction: Lead extraction was attempted in 6 and 5 leads were removable without any complications. Conclusions: The incidence of troubles with Sprint-Fidelis is high, and it occurs in the relatively late phase. The LIA is useful to detect the lead problems but its efficacy may be limited in elderly patients. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.OP53_2

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Background: J-waves are considered to reflect early repolarization. We have previously reported the disappearance of J waves after catheter ablation of an accessory pathway in patients with Wolff-Parkinson-White syndrome. Here, we further studied the association of an accessory pathway on J-waves with Wolff-Parkinson-White syndrome. Methods: We included 124 patients with Wolff-Parkinson-White syndrome who underwent catheter ablation, and 1936 controls without structural heart disease or ECG abnormalities. Results: The prevalence of J-waves was higher in patients with Wolff-Parkinson-White syndrome (n=69, 56%) than the controls (n=222, 11.5%). After successful ablation of the Wolff-Parkinson-White patients, J-waves disappeared in 22 patients, while J-waves were still apparent or after ablation in 21 patients. The prevalence of atrial fibrillation was higher in patients with J-waves (n=31, 45%) after ablation than those without (n=15, 33%). The ventricular and atrial refractory period tended to be shorter in patients with J-waves, after ablation than those without such waves. Conclusion: J-waves were frequently observed and were affected by ablation of an accessory pathway in patients with Wolff-Parkinson-White syndrome although the exact nature of this association is still undetermined. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.OP52_3

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Acute physical and psychological stress caused by earthquake can provoke cardiovascular events. We retrospectively investigated the incidence of acute cardiovascular events from September 25, 2004, to November 19, 2004, in 8 hospitals that treated most patients with such disorders in the area affected by the mid-Niigata prefecture earthquake. The number of cardiovascular events markedly increased in the week following the earthquake, with a daily median (range) of 6 (0-21) compared with 2 (0 4) in the prior 4 weeks. The number of cases of sudden death increased in the week after the earthquake, with a daily median of 3 (0-6) compared with 1 (0-3) in the prior 4 weeks. Of the 14 cases of acute coronary syndrome presenting during the week after the earthquake, 4 of the 14 cases occurred on the day of the earthquake. Pulmonary embolism increased to 9 cases in the 4 weeks after the earthquake, compared to only 1 case reported in the 4 weeks before the earthquake. Takotsubo cardiomyopathy increased in the 4 weeks after the earthquake to 25 cases compared with only 1 case reported in the 4 weeks before the earthquake. Although 10 patients (40%) with Takotsubo cardiomyopathy developed life-threatening heart failure, all recovered within several weeks following the improvement of apical dysfunction. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.AHJS_5

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Methods: A total of 24 consecutive patients suffered sustained ventricular tachycardia (VT) (group A: n=13), ventricular fibrillation (VF) (group B: n=7) or repeated non-sustained ventricular tachycardia (NSVT) (group C: n=4). ventriucular arrhythmia (VA) was complicated with ischemic heart disease (IHD) in 11 patients (group I) and with other diseases in another 13 patients (group non-I). Nifekalant hyddrochloride (NIF) was administrated during cardiopulmonary resuscitation (CPR) in 13 patients. Results: NIF administration was effective in terminating VA in 19 of 24 patients (79.2%). NIF administration directly terminated VT in 6 patients, and VT was successfully cardioverted using additional direct-current (DC) shock after NIF administration in another 4 patients in group A with DC shock-resistant VT. Refractory VF was also successfully cardioverted by additional DC shock after NIF administration in 4 patients in group B. Repeated NSVT was not undertaken after NIF administration in all patients in group C. NIF was effective in terminating VA in all patients in group I as well as in 8 patients in group non-I. In 11 of 17 patients, continuous intravenous NIF infusion prevented the recurrence of VA. VA was successfully controlled by continuous intravenous infusion of NIF in 6 of 10 patients in group I. Conclusion: Nifekalant was effective in terminating refractory ventricular arrhythmia. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.OP02_2

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Effects of magnesium administration (0.2ml/kg, iv) on the QT interval and transmural ventricular repolarization were compared among the 4 models of QT interval prolongation: (20 experiments) bepridil (BEP), amiodarone (AMD), E-4031 (E) or anthopleurin-A (AP-A). Using plunge needle electrodes, transmural electrograms were obtained from the left ventricle, and the activation-recovery interval (ARI) and transmural ARI-dispersion were analyzed. Results: (1) After administration of each drug, ARIs at all LV layers were prolonged, and transmural ARI-dispersions were enlarged in the AP-A and E models. BEP (4 mg/kg) homogeneously prolonged ARIs, and it produced a relatively small transmural ARI-dispersion (32±10 ms) similar to the AMD model (1.5 mg/kg/hr) (32±7 ms). (2) Magnesium injection (0.2 mEq/kg, iv) shortened ARIs and suppressed Torsades de Pointes in the AP-A model. (3) Magnesium did not shorten nor homogenize ARI distribution in the other 3 models. Magnesium slightly prolonged the ARIs in the E model. Conclusions: Magnesium did not reduce the transmural dispersion of repolarization except in AP-A model. Inhibition of the triggered premature beats seems to be another therapeutic effect of magnesium treatment for QT interval prolongation. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.PJ2_043

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Background: Significance of an ST-T abnormality in subjects with no apparent heart diseases is to be determined. Subjects and methods: The study involved 44,990 adults (16,368 males and 28,622 females) aged 40-85 years who underwent an annual health examination. Cardiovascular risks (CVRs) were considered positive if 1) body mass index was ≥25 Kg/m2, 2) systolic blood pressure (BP) ≥ 130 mmHg and/or diastolic BP ≥ 85 mmHg, 3) triglyceride ≥ 150 mg/dl, 4) HDL-C level ≤40 mg/dl for men and ≤50 mg/dl for women, or 5) fasting blood glucose ≥110 mg/dl. The relation between CVRs and ST-T abnormalities were evaluated. Results: ST-T abnormalities were found in 6.49% in males, and more frequently in females: 8.45%. Each CVR and the number of combined CVRs were risk factors for ST-T abnormalities on ECG (P &lt
0.0001 for a trend). On the other hand, ECG-based LVH was found in 5.7% but showed no relation with CVRs or their combinations. ST-T abnormalities may represent preclinical cardiac involvement of CVRs more sensitively than LVH on ECG and ECG findings may be used in mass examinations. Conclusions: ST-T abnormalities without apparent heart diseas may be considered to be nonspecific but this cross-sectional study showed that they are related to CVRs and may be used as an early marker of preclinical cardiac damage by CVRs. © 2011, Japanese Heart Rhythm Society. All rights reserved.

DOI： 10.4020/jhrs.27.202

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A 60-year-old man with arrhythmogenic right ventricular cardiomyopathy was readmitted to exchange the battery of his implantable cardioverter-defibrillator (ICD). When a dual-chamber ICD was implanted 6 years ago, induced ventricular fibrillation (VF) was terminated successfully by a 20-joule shock. Since (1) he had been treated with a dual-coil shock lead (Sprint Fidelis) and (2) preoperative venography showed mild collateral flow to the left subclavian vein, a single-coil lead (Sprint Quattro) was also implanted. However, the single-coil defibrillation system was unable to terminate the induced VF with a 25-joule shock, and a maximum shock of 35 joules was required to resume sinus rhythm. Therefore, dual defibrillation shock pathways were created using the additional connection of the superior vena cava coil of the Fidelis lead to the ICD. As a result, induced VF was terminated successfully by 15∼25 joules, and the shock impedance was decreased from 63 to 39 ohms. Using a combined connection between two implanted leads and an ICD generator is uncommon, but it can help some patients, as in our case.

DOI： 10.4020/jhrs.27.PJ2_070

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Language：Japanese   Publisher：Japan Heart Foundation  

DOI： 10.11281/shinzo.43.1297

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Other Link： http://search.jamas.or.jp/link/ui/2012011517

Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

2:1 AV Block in KCNQ1. The case of a 32-year-old pregnant woman, who had had several syncopal episodes during swimming and running at 9 and 10 years of age and whose fetus had 2:1 AV block, is presented. The mother and baby had the same heterozygous single nucleotide substitution in KCNQ1 at T587M. After 27 weeks of gestation, the fetal 2:1 AV block disappeared, and 1:1 AV conduction resumed, with a fetal heart rate of 110-120 beats/min. The maternal electrocardiogram revealed a normal QTc interval (433 ms) without ST-T abnormalities at gestational week 23, but the QTc was 490 and 531 ms at 1 and 2 months postpartum, with biphasic T waves in leads V2 and V3. This case is the first report of fetal 2:1 AV block with KCNQ1 mutation (T587M) and unmasked maternal QT prolongation in the postpartum period. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1170-1173).

DOI： 10.1111/j.1540-8167.2010.01758.x

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Introduction: There is increasing evidence to support a link between inflammation and atrial fibrillation (AF). However, the role of inflammation on new-onset AF is still to be elucidated. Methods: Rats underwent induction of experimental autoimmune myocarditis (EAM). Atrial structural change was evaluated by echocardiography and histological analysis. Electrophysiological data and the in vivo atrial response to burst atrial pacing were evaluated in the acute (2 weeks after EAM induction) and chronic phases (8 weeks after induction). In addition, atrial pacing after 2, 4, and 6 h after lipopolysaccharide (LPS) infusion, when the expression of gap junctions was modified, were challenged with young healthy rats. Results: AF was induced in 11 of 15 chronic phase EAM rats but not in either acute phase EAM rats or LPS infusion rats (P&lt
.01). Echocardiography showed dilatation of both atrium and ventricle and a decrease in the ejection fraction in the chronic phase. Histology revealed severe inflammatory lesions only in the acute phase. Interstitial atrial fibrosis as well as the area of atrial myocyte increased in the chronic phase but not in the acute phase. Conclusions: AF could be induced in the chronic phase of myocarditis rats, but not in the acute phase of myocarditis rats or in rats with LPS infusion. Acute inflammation per se did not increase the occurrence of AF induction. Atrial structural remodeling caused by inflammation and hemodynamic effects is necessary to induce AF. © 2010 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.carpath.2009.07.002

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Patients: The study consisted of 66 consecutive patients with HCM who were admitted to Niigata University Hospital between 1992 and 2005. Their clinical characteristics and ECG morphology were investigated according to the type of HCM.
Results: The type of HCM was asymmetric hypertrophy (ASH) in 34 patients (51%), obstructive HCM (HOCM) in 9 (14%), apical HCM (ApHCM) in 14 (21%), and midventricular obstruction (MVO) in 9 (14%). The cause of admission was ventricular tachyarrhythmia in 25 patients (38%), unexplained syncope in 11 (17%), and heart failure in 30 (45%). Sustained monomorphic ventricular tachycardia (SMVT) occurred in 19 patients and ventricular fibrillation in 6. In the 19 patients with SMVT, 12 had MVO and 3 of these had previous apHCM. Six of the 19 patients with SMVT had ASH, and 3 had abnormal apical wall motion. In 14 patients, the SMVT appeared to originate from the apical aneurysm based on the morphology of the tachycardia. Ventricular tachyarrhythmia recurred in 14 of the 25 patients (56%), and 4 of the 18 patients with an ICD had electrical storm. ASH with abnormal wall motion of the LV apex or MVO was recognized in the 4 patients with electrical storm; they commonly had abnormal Q waves and ST elevation in leads V4-V6.
Conclusion: Ventricular tachyarrhythmia was responsible for 38% of hospitalizations in HCM, and SMVT occurred in patients with MVO and/or with abnormal wall motion of the LV apex. Electrical storm was more common in patients with ST elevation in precordial leads V4-V6. (J Cardiovasc Electrophysiol, Vol. 21, pp. 991-999, September 2010).

DOI： 10.1111/j.1540-8167.2010.01769.x

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Methods: We used plunge needle electrode to record transmural left ventricular (LV) repolarization and activation-recovery interval (ARI) to estimate local repolarization. The correlation between paced cycle length and ARI was separately examined in the LV endocardium, mid-myocardium (Mid), and epicardium. Attempts to induce VTA were made during bradycardia and sympathetic stimulation.
Results: Bepridil and E-4031 prolonged QT interval and ARI in all LV layers, though the magnitude of prolongation was greatest in Mid, increasing the transmural ARI dispersion, particularly during bradycardia. Compared with E-4031, bepridil caused mild, reverse use-dependent changes in ventricular repolarization, and less ARI dispersion than E-4031 during slow ventricular pacing. Both drugs increased ARI(max) and cycle length at 50% of ARI(max), though the changes were smaller after bepridil than after E-4031 administration. Bradycardia after the administration of each drug induced no VTA; however, sympathetic stimulation induced sustained polymorphic VTA in two of five dogs treated with E-4031 versus no dog treated with bepridil.
Conclusions: Unlike the pure I(kr) blocker, E-4031, bepridil exhibited weak properties of reverse use-dependency and protected against sympathetic stimulation-induced VTA. It may be an effective supplemental treatment for recipients of implantable cardioverter defibrillator. (PACE 2010; 950-959).

DOI： 10.1111/j.1540-8159.2010.02768.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Background: The efficacy of antiarrhythmic drugs in terminating sustained monomorphic ventricular tachycardia (SMVT) was assessed in a retrospective manner to provide a basis for recommending their use.
Methods and Results: The 90 patients were included in this study to evaluate the efficacy to terminate SMVT using procainamide or lidocaine. All patients were alert and responsive. The mean systolic blood pressure was 91 +/- 25 mmHg (range, 40-150 mmHg). SMVT was diagnosed from ECG recordings and later in an electrophysiologic study. VTs with a cycle length of 329 +/- 55 and 324 +/- 61 ms were treated with the mean doses of 358 +/- 50 mg and 81 +/- 30 mg of procainamide and lidocaine and were terminated in 53/70 (75.7%) and in 7/20 (35.0%) respectively. The drugs were discontinued if there was no rise in blood pressure after slowing of the tachycardia rate or if there were signs of impending deterioration in consciousness. Though procainamide was effective, blood pressure was often low and DC shock should be available at all times during administration of the drug.
Conclusions: Procainamide, the relatively older drug, was more effective than lidocaine in terminating SMVT associated with structural heart diseases. This is a retrospective analysis but can form the basis for formulating guidelines for initial management of SMVT. (Circ J 2010; 74: 864-869)

DOI： 10.1253/circj.CJ-09-0932

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Background: Because bepridil blocks multiple myocardial ionic channels, including the muscarinic acetylcholine receptor-operated potassium current (I(KAch)), bepridil is expected to suppress atrial fibrillation (AF) mediated by vagal nerve stimulation (VNS).
Methods and Results: The therapeutic effects of bepridil were studied with a special focus on heart rate variability (HRV) in a canine model of AF. During VNS, AF was induced in 9 of 9 experiments before, vs 3 of 9 experiments after administration of bepridil (P&lt;0.01). During 350 ms atrial pacing, VNS shortened the right and left atrial monophasic action potentials at 90% repolarization (MAP90) by -31 +/- 8% and -22 +/- 12%, respectively, vs -10 +/- 13% and -6 +/- 8%, respectively, after bepridil (P&lt;0.01, N=9). Bepridil prolonged the sinus cycle length, although it had no significant effect on the conduction time measured at 300 ms pacing. Statistically insignificant change was observed in the VNS-induced slowing of the sinus cycle length and in the VNS-induced increase in high frequency amplitude of HRV before (1.2 +/- 0.7 to 5.3 +/- 4.0 ms) vs after (1.7 +/- 0.8 to 5.4 +/- 2.3 ms) bepridil administration.
Conclusions: Bepridil prevented the VNS-induced shortening of atrial MAP90 and suppressed the inducibility of AF during VNS in two-thirds of the experiments. As far as this study shows, it may be possible that inhibition of I(KAch) played a part in this antifibrillatory effect. (Circ J 2010; 74: 895-902)

DOI： 10.1253/circj.CJ-09-0716

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Background: The efficacy of antiarrhythmic drugs in terminating sustained monomorphic ventricular tachycardia (SMVT) was assessed in a retrospective manner to provide a basis for recommending their use.
Methods and Results: The 90 patients were included in this study to evaluate the efficacy to terminate SMVT using procainamide or lidocaine. All patients were alert and responsive. The mean systolic blood pressure was 91 +/- 25 mmHg (range, 40-150 mmHg). SMVT was diagnosed from ECG recordings and later in an electrophysiologic study. VTs with a cycle length of 329 +/- 55 and 324 +/- 61 ms were treated with the mean doses of 358 +/- 50 mg and 81 +/- 30 mg of procainamide and lidocaine and were terminated in 53/70 (75.7%) and in 7/20 (35.0%) respectively. The drugs were discontinued if there was no rise in blood pressure after slowing of the tachycardia rate or if there were signs of impending deterioration in consciousness. Though procainamide was effective, blood pressure was often low and DC shock should be available at all times during administration of the drug.
Conclusions: Procainamide, the relatively older drug, was more effective than lidocaine in terminating SMVT associated with structural heart diseases. This is a retrospective analysis but can form the basis for formulating guidelines for initial management of SMVT. (Circ J 2010; 74: 864-869)

DOI： 10.1253/circj.CJ-09-0932

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A delayed pericardial effusion developed in a recipient of a cardioverter defibrillator (ICD). After an uneventful implant procedure and postoperative recovery, the patient suffered loss of appetite and fatigue, and was re-admitted to the hospital 48 days later. Her vital signs were stable and cardiac silhouette on chest roentgenogram was normal. However, blood cell counts and chemistry revealed the presence of anemia and liver dysfunction, an echocardiogram showed a diffuse pericardial effusion, and computed tomography suggested that the ICD lead, screwed in the right ventricular outflow tract, had perforated the wall. In order to make a prompt diagnosis and initiate timely corrective treatment, the physician in charge of long-term follow-up should remember that a pericardial effusion can be delayed and accumulate in the absence of typical signs of cardiac tamponade after ICD lead implantation.

DOI： 10.2169/internalmedicine.49.2936

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A 75-year-old man was admitted to our hospital in January 2010 for evaluation of syncope and abnormal ECG. ECG showed type 1 ST elevation in lead V-1 and he was diagnosed as Brugada syndrome. During cardiac catheterization, baseline coronary angiography was normal, but intracoronary ergonovine maleate induced spasms of the right and left coronary arteries concomitant with chest pain and ST elevation on ECG. J waves were accentuated or newly developed. Soon after an intracoronary injection of nitroglycerin, chest pain was relieved and ischemia-induced J wave disappeared and the ST segment returned to the same morphology as baseline. Extrastimuli induced ventricular fibrillation. He received an implantable cardioverter-defibrillator. He was also treated with Ca antagonist and isosorbide dinitrate and has had an uneventful course for 5 months.

DOI： 10.2169/internalmedicine.49.3933

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Ventricular fibrillation associated with coronary vasospasm developed 8 h after successful radiofrequency (RF) ablation of the right accessory pathway in an 81-year-old male. A segment of the coronary vasospasm was located close to the accessory pathway, where seven RF ablations had been applied. Although rare, physicians should carefully consider the risk of such events when an RF current is applied near a coronary artery.

DOI： 10.1093/europace/eup219

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Background: The relationship between the activation delay during programmed stimulation and the inducibility of ventricular fibrillation (VF) and filtered QRS duration on signal-averaged ECG (SAECG) were assessed in patients with Brugada syndrome (BS).
Methods and Results: The activation delay was assessed using the interval between the stimulus and the QRS complex during programmed stimulation in 25 patients with BS and 10 with idiopathic ventricular tachycardia (controls). The mean increase of delay (MID) was used to characterize the conduction curves. The filtered QRS duration (fQRSd) in leads V(2) (RfQRSd) and V(5) (LfQRSd) were also evaluated using SAECG. Both MIDs at the right ventricular outflow tract (RVOT) were significantly greater in symptomatic and asymptomatic BS patients than in the control group (symptomatic, 7.1 +/- 2.7 ms vs control, 2.5 +/- 1.2 ms, P&lt;0.001, asymptomatic, 7.3 +/- 3.3 ms vs control, P&lt;0.001, respectively). The MID correlated with the His-ventricular interval; however, there were no significant correlations between the MID and RfQRSd or RfQRSd-LfQRSd.
Conclusions: The MID, which indicates an increase of the St-QRS during premature stimulation, was much greater in patients with BS (regardless of clinical symptoms) than in the control group, especially in the RVOT, which might be related to the easy inducibility of VF from the RVOT. (Circ J 2009; 73: 1408-1415)

DOI： 10.1253/circj.CJ-08-1111

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

Purpose: This Study examined the effects of verapamil (5-10 mg intravenous) on the cardiac electrical activity of 10 Brugada syndrome (BS) patients having vasospastic angina, atrial fibrillation, and/or hypertension.
Results: Verapamil showed no significant change ill the ST-segment elevation. Likewise, there was no significant change in the lengths of QRS complex, HV and corrected QT intervals, or effective refractory period at the right ventricle, The conduction time between right ventricular apex and Outflow tract, measured at 400-millisecond pacing, was mildly prolonged by verapamil. At baseline, induced ventricular fibrillation (VF) was terminated by a 200-J shock in all patients. After verapamil, VF was reinduced in 7, was noninducible in 2, and self-terminated in 1 patient. Mean F-F interval was shorter after than before verapamil, and a 360-J shock was required in 2 of the 7 patients.
Conclusion: In some BS patients, calcium channel blockade may modify the electrical characteristics of VF. (c) 2009 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2009.03.009

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL PUBLISHING, INC  

In two patients with variant forms of Brugada electrocardiographic abnormalities, ST segment elevation, and reciprocal ST segment depression developed during intravenous administration of pilsicainide. In one patient, pilsicainide accentuated the ST segment elevation in leads I, aV(L), and V(1)-V(3) and caused ST segment depression in leads II, III, and aV(F). Coronary angiograms at the time of ST segment elevation were normal. In the other patient, pilsicainide accentuated the coved-type ST segment elevation in leads II, III, and aV(F) and caused ST segment depression in leads I, aV(L), and V(2)-V(5). Frequent premature ventricular complexes (PVCs) with two different left bundle branch block patterns developed during ST segment elevation. Intravenous isoproterenol returned the ST segment to baseline in both patients and suppressed the PVCs in the second patient. We hypothesize that a wide area of epicardial myocardium with large I(to) current might explain the reciprocal ST segment depression observed at the time of accentuated ST segment elevation.
(PACE 2009; 32:811-815).

DOI： 10.1111/j.1540-8159.2009.02371.x

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A 44-year-old female presented with incessant, drug-refractory atrial tachycardia (AT). An electrophysiological study suggested focal abnormal automaticity, and localized the AT origin to the apex of the right atrial appendage (RAA). Repeated radiofrequency catheter ablation to the site of the earliest endocardial activation during AT failed. At surgery, right atrial appendectomy terminated the AT. On macroscopic findings, the cavity of the RAA became a dead-end before the apex. In patients with drug and radiofrequency catheter ablation, refractory focal AT arising from the RAA, especially the apex of the RAA, in our opinion surgical treatment could be considered in the lack of efficacy of ablation.

DOI： 10.1093/europace/eup046

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Language：English   Publisher：JAPANESE CIRCULATION SOC  

DOI： 10.1253/circj.CJ-08-1134

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL PUBLISHING, INC  

We observed a case of idiopathic ventricular arrhythmias originating from the right ventricular outflow tract (RVOT). The origin of target premature ventricular contraction (PVC) and nonsustained ventricular tachycardia (VT) was within a wide low-voltage area around the RVOT. During radiofrequency (RF) application to the site of arrhythmia origin, polymorphic VT and ventricular fibrillation were repeatedly triggered by new PVC that had developed near the site of ablation. This electrical storm persisted &gt; 30 minutes after cessation of RF current delivery, and was suppressed by additional RF applications to the site of origin of the new PVC.
(PACE 2009; 32:406-409).

DOI： 10.1111/j.1540-8159.2008.02253.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

The effect of the electrical charge or the size of tile amino acid residue at the pore center of a slowly activation component of the delayed rectifier potassium channel: KCNQ1 was studied. K+ currents were measured after transfection of one of four KCNQ1 mutants: substituting Isoleucine with Lysine, Glutamate, Valine or Glycine and then transfected in COS-7 cells. Both the negatively- and positive charged residue 1313 K and 1313 E showed a loss of function when expressed alone and a dominant negative suppression when co-expressed with wild type KCNQ1. When the Site Was Substituted with the smallest neutral amino acid residue: 1313G, there was a small reduction of current when transfected alone and a gain of function when co-transfected with the wild type. 1313V showed no difference from the wild type. Changes of amino acid residue at the pore center of KCNQ1 may alter the channel function but this depends on tile electrical charge or the size of amino acid residue. (C) 2008 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2008.11.076

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A 39-year-old man received implantable cardioverter defibrillator (ICD) shocks during sinus rhythm, triggered by an increase in amplitude and oversensing of intracardiac T waves, caused by hyperkalemia. After treatment of hyperkalemia, the T wave morphology normalized, and oversensing and inappropriate ICD shocks were eliminated. Alteration of the intracardiac electrogram was well correlated to the surface electrocardiogram (ECG) changes. Intracardiac T waves can be altered by hyperkalemia and it seems that this alteration can be estimated by surface ECG analysis.

DOI： 10.2169/internalmedicine.48.2139

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Macro-reentrant ventricular tachycardia (VT) developed in a 20-year-old man, 17 years after surgical repair of tetralogy of Fallot. Activation mapping of the VT revealed its counterclockwise propagation around the right ventricle, and through a critical pathway between a transannular patch and the tricuspid annulus. This critical pathway was 6 cm long and contained myocardium with a normal amplitude, while the area of low voltage was limited adjacent to the transannular patch. A linear lesion was created by radiofrequency energy delivered only to the low voltage area. After ablation, the activation wavefront through the low voltage area was blocked, and VT became non-inducible.

DOI： 10.2169/internalmedicine.48.2048

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：KARGER  

The differential effects between olmesartan (OM), an angiotensin 2 type 1 receptor blocker (ARB), and azelnidipine (AZ), a calcium channel blocker (CCB), on atrial structural remodeling were studied in spontaneously hypertensive rats (SHR). Eight weeks after treatment, both OM and AZ decreased systolic blood pressure to similar levels. Histological analysis revealed that both OM and AZ had decreased the size of the atrial myocytes and interstitial fibrosis in the atrium, and that the effects of OM were greater than those of AZ. These beneficial effects of OM were associated with less atrial oxidative stress, as assessed by 3-nitrotyrosine staining, and less activation of Rac1, a regulatory component in NADPH oxidase. These results suggest that the ARB was more effective than the CCB in ameliorating atrial structural remodeling due to the suppression of oxidative stress. Copyright (C) 2009 S. Karger AG, Basel

DOI： 10.1159/000218103

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Background Cardiac resynchronization therapy (CRT) has recently been introduced as a new option for patients with severe heart failure, but its effect on renal function remains unclear.
Methods and Results Twenty-three patients receiving CRT were studied. Responders were those who showed &gt; 0% increase in left ventricular ejection fraction after CRT by echocardiography. Clinical parameters, echocardiographic measurement, renal function, and prescriptions were examined before and 3 months after CRT, and the relationship between the response to CRT and renal function was examined. The responders had a better prognosis than the non-responders (p &lt; 0.05). There was a significant difference in the change in the estimated glomerular filtration rate between the responders and non-responders (p &lt; 0.05), even in patients with renal dysfunction before CRT (p &lt; 0.01). Prescriptions of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers (ACEI/ARB) were 100% in the CRT responders and 60% in the non-responders (p &lt; 0.05). Up-titration of blockers could be significantly achieved in the CRT responders compared with the non-responders (p &lt; 0.05).
Conclusions Preservation of renal function was observed in the responders to CRT, even in patients with renal dysfunction. Prescription of ACEI/ARB and up-titration of beta-blockers increased in the CRT responders. These results may contribute to the beneficial effects of CRT. (Circ J 2008; 72: 1794-1799)

DOI： 10.1253/circj.CJ-08-0424

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS  

DOI： 10.1093/europace/eun166

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS  

DOI： 10.1093/europace/eun095

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

Mutation in the Selectivity Filter of the KCNQ1.
Introduction: Slowly activating delayed-rectifier potassium currents in the heart are produced by a complex protein with alpha and beta subunits composed of the potassium voltage-gated channel KQT-like subfamily, member 1 (KCNQ1) and the potassium voltage-gated channel Isk-related family, member 1 (KCNE1), respectively. Mutations in KCNQ1 underlie the most common type of hereditary long QT syndrome (LQTS). Like other potassium channels, KCNQ1 has six transmembrane domains and a highly conserved potassium selectivity filter in the pore helix called "the signature sequence." We aimed to investigate the functional consequences of a newly identified mutation within the signature sequence.
Methods and Results: Potassium channel genomic DNA from a family with clinical evidence of LQTS was amplified by polymerase chain reaction (PCR), and the resulting products were then sequenced. Three family members had a double-point mutation in KCNQ1 at nucleotides 938 (T-to-A) and 939 (C-to-A), resulting in an isoleucine-to-lysine change at amino acid position 313. These patients displayed prolonged QTc intervals (629, 508, and 500 ms(1/2,) respectively) and repetitive episodes of syncope, but no deafness. Three-dimensional structure modeling of KCNQ1 revealed that this mutation is located at the center of the channel pore. COS-7 cells displayed a lack of current when transfected with a plasmid expressing the mutant. In addition, the mutant displayed a dominant negative effect on current but appeared normal with respect to plasma membrane integration.
Conclusion: An I313K mutation within the selectivity filter of KCNQ1 results in a dominant-negative loss of channel function, leading to a long QT interval and subsequent syncope.

DOI： 10.1111/j.1540-8167.2007.01076.x

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DOI： 10.1016/j.jacc.2008.01.031

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Language：English   Publisher：(一社)日本循環器学会  

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Aims The effects of adrenergic activity and beta-blockade were studied in a canine experimental model of type-3 tong QT syndrome (LQT3) induced by application of anthopleurin-A.
Methods and results Boluses of epinephrine at 0.5 and/or 1.0 mu g/kg were administered before and after propranolol, 0.3 mg/kg, and the distribution of the ventricular repolarization and the development of polymorphic ventricular tachyarrhythmia (VA) were assessed. Using needle electrodes, transmural unipolar electrograms were recorded across the left ventricle (W) and right ventricle (RV). Activation-recovery interval (ARI) was measured in each electrogram to estimate local repolarization during RV pacing at the cycle length of 750 ms after the creation of complete atrioventricular block. Before propranolol, epinephrine, 0.5 mu g/kg, did not induce VA in any experiment. However, a dose of 1.0 mu g/kg induced polymorphic VA following multiple premature ventricular complex (PVC) in four of six experiments. Epinephrine, 0.5 mu g/kg, shortened ARI at all sites and lessened LV transmural ARI dispersion. Neither ARI nor its dispersion could be determined after 1.0 mu g/kg of epinephrine because of the induction of PVC, polymorphic VA, or both. Propranolol (i) prevented epinephrine-induced PVC and polymorphic VA in all experiments, (ii) slightly prolonged ARI at all sites, along with a decrease in IV transmural. ARI dispersion, and (iii) reversed the epinephrine-induced shortening of ARI.
Conclusion In this LQT3 model, an increase in adrenergic activity by epinephrine had dose-dependent, opposite effects on ventricular electrical stability. Since beta-adrenergic blockade suppressed epinephrine-induced PVC and polymorphic VA, it might be considered for supplemental therapy to suppress VA in patients presenting with LQT3.

DOI： 10.1093/europace/eun002

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

Tachycardia-induced cardiomyopathy is characterized by ventricular systolic dysfunction and congestive heart failure resulting from persistent or highly frequent tachyarrhythmias with uncontrolled heart rate. While reversible and often considered benign, few studies have examined the outcome of the disorder.
The clinical characteristics, treatment, and long-term outcomes of 12 consecutive patients with tachycardia-induced cardiomyopathy (9 men, age, 51.9 +/- 17.6 years) were studied. The mean period between the occurrence of tachyarrbythmias and the development of congestive heart failure was 26.0 +/- 34.3 days. The mean heart rate on admission was 156.3 +/- 28.7 beats/min. All patients had severe heart failure with a NYHA functional class of 2.3 +/- 0.5, left ventricular ejection fraction of 0.32 +/- 0.10, and brain natriuretic peptide level of 505.7 +/- 449.1 pg/mL. In all patients, cardiac dysfunction recovered after 53.5 +/- 61.3 days. During the follow-up of 53 +/- 24 months, 2 patients had a recurrence of heart failure with uncontrolled tachyarrhythmia and 1 patient died suddenly.
In tachycardia-induced cardiomyopathy, recurrent heart failure with uncontrollable tachyarrhythmia and sudden death were observed after recovery from cardiac dysfunction. A substrate for heart failure and/or life-threatening arrhythmia might persist, and careful, long-term follow-up seems required.

DOI： 10.1536/ihj.49.39

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Background In both Brugada syndrome (BS) and arrhythmogenic right ventricular cardiomyopathy (ARVC), electrical abnormalities in the right ventricular outflow tract (RVOT) are important for arrhythmogenesis.
Objectives The aim of this study was to compare conduction delay in the right ventricular in BS with that in ARVC using the signal-averaged electrocardiogram.
Methods Twenty patients with BS (18 men and 2 women; 55 +/- 12 years old; 9 symptomatic and 11 asymptomatic) and eight patients with ARVC (six men and two women; 53 +/- 16 years old) were included. We assessed the presence of late potentials (LPs) and the filtered QRS duration (fQRSd) in V-2 and V-5 using a high-pass filter of 40 Hz (fQRSd:40) and 100 Hz (fQRSd:100).
Results In ARVC, there was no significant difference in fQRSd:40 between V2 and V5 (158 +/- 19 vs. 145 +/- 17 ms, respectively): however, in BS, fQRSd:40 in V2 was significantly longer than fQRSd:40 in V5 (147 +/- 15 vs. 125 +/- 10 ms, P &lt; 0.001). In ARVC, there was no significant difference between fQRSdA0 and fQRSd:100 in V-2 and V-5 (158 +/- 19 vs. 142 +/- 23 ms and 145 +/- 17 vs. 132 +/- 9 ms, respectively). In contrast, in BS, fQRSd:100 was significantly shorter than fQRSd:40 in V2 (110 +/- 8 ms vs. 147 +/- 15, P &lt; 0.001). The relative decrease in fQRSd: 100 compared with fQRSd:40 in V2 was significantly greater in BS than in ARVC.
Conclusion The dominant prolongation of the fQRSd in the right precordial. lead in BS was different from the characteristics of ARVC, which may be caused by the conduction delay due to fibro-fatty replacement in RV.

DOI： 10.1093/europace/eum128

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL PUBLISHING  

Background: Cardioembolic strokes are extensive and have a poor prognosis. To identify the cardiovascular risk factors of cardioembolic stroke, we evaluated the cardiovascular status with special reference to persistent atrial fibrillation (AF) and paroxysmal atrial fibrillation (PAF) combined with the type of acute ischemic stroke.
Methods: We divided 315 consecutive patients admitted to our Department of Neurosurgery with an acute ischemic stroke into four types of brain infarction using clinical history, onset pattern of stroke, and brain imaging: cardioembolic (group E, n = 105), lacunar (group L, n = 92), atherothrombotic (group T, n = 111), and unclassified (n = 7). All patients underwent standard electrocardiography (ECG), a 24-hour ECG recording (Holter ECG) and transthoracic echocardiography (UCG).
Results: Persistent AF or PAF was detected in 97 patients (31.5%) using Holter ECG: more frequently in group E (67.6%) than in groups L (15.2%) or T (9.2%). Persistent AF or PAF was first diagnosed on admission using a standard ECG in 16 patients (5.2%) with no previous history and 14 of these patients belonged to group E (13.3%). PAF was newly detected on Holter ECG in another 26 patients (8.4%) and 13 of these patients (12.4%) belonged to group E. Concerning UCG, left atrial enlargement and mitral regurgitation were more frequent in group E than in group L or T.
Conclusion: Holter ECG in addition to ECG on admission is important for detecting persistent AF or PAF in patients with ischemic stroke, especially with cardioembolism as diagnosed by neuroimaging.

DOI： 10.1111/j.1540-8159.2007.00823.x

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Objective: We compared the effectiveness of sotalol on mortality and the recurrence of ventricular tachyarrhythmia (VTA) between idiopathic dilated cardiomyopathy (IDCM) and coronary artery disease (CAD).
Patients: Forty patients with spontaneous VTA and induced VTA associated with CAD (n = 23) and IDCM (n = 17) were studied. In all patients, sotalol was prescribed and an electrophysiologic study (EPS) was performed to evaluate its effect on the induction of VTA. There were no significant differences in left ventricular ejection fraction (LVEF) between CAD and IDCM (35% +/- 10% vs. 35% +/- 12%).
Results: After sotalol, there were no significant differences in the QTc interval on electrocardiogram (ECG) or in the effective refractory period in the apex of the right ventricle between the two groups, but sotalol was more effective in preventing the induction of VTA in CAD than in IDCM (65% vs. 29%; P &lt; 0.05). During a mean follow-up period of 47 +/- 27 months, the overall VTA recurrence rate was significantly lower in CAD than in IDCM (P &lt; 0.01). The all-cause mortality rate tended to be lower in CAD than in IDCM, but the difference was not significant (P = 0.07). Electrical storm (ES) occurred more frequently in IDCM than in CAD, (41% vs. 13%; P &lt; 0.05), and all patients with ES (n = 10) failed to respond to sotalol as assessed by EPS.
Conclusion: Sotalol reduced the overall VTA recurrence rate and all-cause mortality more in CAD than in IDCM.

DOI： 10.1111/j.1540-8159.2007.00825.x

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Background: In patients with Brugada syndrome, class I antiarrhythmic drugs can trigger ventricular arrhythmias (VA). The incidence and initial characteristics of VA that developed after pilsicainide was examined in 28 patients with Brugada-type electrocardiographic (ECG) abnormalities and with a positive response in the pilsicainide test. The clinical outcome was also compared between patients with and without pilsicainide-induced VA.
Methods and Results: In all patients, pilsicainide increased ST segment elevation and accentuated type 1 ECG changes. Ventricular tachycardia (VT) developed in 3 patients and premature ventricular complexes (PVC) in 2 other patients. These 5 patients (group I) had higher ST segment elevation in lead V2 on the ECG at baseline and after pilsicainide and showed a longer QTc interval after pilsicainide than the other 23 patients (group II). However, there was no difference between the 2 groups regarding incidence of prior cardiac events, results of signal-averaged ECG, HV interval, inducibility of ventricular fibrillation by programmed electrical stimulation, or QRS duration. In 1 patient, PVC originated from 3 sites, 2 of which triggered polymorphic VT. The right ventricular (RV) outflow tract was the origin of 2 types of PVC, and other RV sites of 5 other types. During a 45 +/- 37 months follow-up, polymorphic VT recurred in 2 patients in group II.
Conclusions: Pilsicainide induced VA in some patients with Brugada syndrome, but this result may not be used as a parameter of the risk stratification of Brugada syndrome. Multiple PVC induced by pilsicainide and triggering polymorphic VT originated from several RV sites is an important factor when considering patients for treatment with catheter ablation.

DOI： 10.1111/j.1540-8159.2007.00728.x

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Language：English   Publisher：ELSEVIER IRELAND LTD  

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by adrenergic induced bidirectional or polymorphic ventricular tachycardias. Some of CPVT families were reported to be associated with cardiac ryanodine receptor gene (RyR2) mutations. However, association between RyR2 and other arrhythmogenic disorders is not clarified. In this study, we analyzed 83 Japanese patients including patients with long-QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation, arrhythmogenic right ventricular caridiomyopalby and CPVT. Genetic screening of RyR2 revealed 3 distinct mutations among 4 families with CPVT (75% of incidence). However, no mutation was found in other groups. This is the first report to demonstrate prevalence of RyR2 mutations in various arrhythmogenic disorders in Japan. RyR2 mutations were detected frequently in CPVT but not in other diseases. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.ijcard.2006.02.024

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Language：Japanese   Publisher：The Japanese Society of Electrocardiology  

DOI： 10.5105/jse.27.53

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Other Link： http://search.jamas.or.jp/link/ui/2007161755

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Ventricular tachyarrhythmias (VTA), a major cause of sudden cardiac death, require meticulous management in order to prevent recurrent episodes. Recently, non-pharmacological interventions, including radiofrequency catheter ablation and implantable cardioverter defibrillators (ICD), have become important treatments of VTA. Catheter ablation is curative in a relatively high percentage of patients presenting with idiopathic monomorphic ventricular tachycardia (VT). For VT associated with structural heart disease, however, the efficacy of catheter ablation remains limited, and ICD is the first-line therapy. In a subset of patients presenting with recurrent episodes of ventricular fibrillation (VF), catheter ablation is a therapeutic option when the VF is triggered by specific premature ventricular complexes. In Japan, unlike in the United States and Europe, ICD have not yet been accepted as first-line prevention of sudden cardiac death caused by VTA. The efficacy of ICD is occasionally limited by intolerable complications, such as electrical storm, inappropriate shock delivery and infection. Catheter ablation and ICD therapy might need to be combined for problematic cases.

DOI： 10.1253/circj.71.A97

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Aims To avoid frequent discharges of implantable cardioverter defibrillators, antiarrhythmic drugs may be needed in some patients with ventricular tachyarrhythmias. For ventricular tachyarrhythmias refractory to conventional antiarrhythmic drugs, we evaluated the efficacy of bepridil, a multiple ion-channel blocker.
Methods and results Sixteen patients with structural heart disease and ventricular tachyarrhythmias refractory to multiple antiarrhythmic drugs (4.1 +/- 1.6 drugs including class III drugs) were enrolled. Bepridil was prescribed at a mean dose of 156 +/- 40 mg/day. Bepridil prolonged the QT/QTc interval without affecting heart rate or the QRS duration. During a mean follow-up of 52 +/- 44 months, bepridil completely suppressed ventricular tachyarrhythmias in 6 of the 16 patients (38%) and the drug decreased the frequency of ventricular tachyarrhythmia recurrences by&gt; 75% in 3 of the other 10 patients. The markers of complete suppression of ventricular tachyarrhythmias during bepridil treatment included a smaller number of VT morphologies, a better NYHA functional class, and a greater drug-induced prolongation of the QT/QTc interval. The result of electrophysiologic study-guided evaluation of bepridil was closely associated with the clinical efficacy of bepridil in 7 of 8 patients.
Conclusion Bepridil appears to be useful to suppress drug-refractory ventricular tachyarrhythmia recurrence.

DOI： 10.2169/internalmedicine.46.6024

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A 17-year-old man was referred to our hospital for treatment of common paroxysmal atrial flutter. His electrocardiogram at rest showed subtle ST-segment elevation in leads II, III, and aV(F). Intravenous pilsicainide caused further ST-segment elevation in the inferior leads, new ST-segment depression in leads V2-V6, two distinct forms of premature ventricular complexes (PVCs) triggering short runs of polymorphic ventricular tachycardia (VT). An infusion of isoproterenol suppressed these arrhythmias and normalized the ST-segment. Pilsicainide may induce PVCs and polymorphic VT in atypical Brugada syndrome.

DOI： 10.1111/j.1540-8159.2006.00562.x

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Language：English   Publisher：ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

DOI： 10.1016/j.yjmcc.2006.08.057

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

This study was performed to examine the role played by the autonomic nervous system in the antiarrhythmic effects of magnesium sulfate (Mg++) in a canine model of polymorphic ventricular tachyarrhythmia facilitated by anthopleurin-A and a slower heart rate induced QT interval prolongation. In 6 experiments, complete atrioventricular block was created to control the heart rate and bradycardia at 800- to 1500-ms cycle lengths was applied for 60 see before and after drug-induced autonomic block. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and activation-recovery intervals (ARI) were measured. Before drug-induced autonomic block, polymorphic ventricular tachyarrhythmia developed in all 6 experiments during bradycardia before but not after the administration of Mg++ (0.2 ml/kg intravenous bolus). During drug-induced autonomic block, triggered premature activity decreased without significant changes in underlying dispersion of repolarization and polymorphic ventricular tachyarrhythmia developed during bradycardia in I experiment. Administration of Mg++ during drug-induced autonomic block eliminated premature activity and polymorphic ventricular tachyarrhythmia during bradycardia. The distribution of left ventricular (IV) and right ventricular repolarization and dispersion of transmural repolarization were analyzed before and 60 see after Mg+ administration during ventricular pacing at 80 bpm. Mg++ caused a modest shortening of ARI at all sites before and after drug-induced autonomic block. Since ARI shortening was greater at the mid-myocardial sites than at other IV sites, Mg++ decreased transmural ARI dispersion from 77 +/- 16 to 46 +/- 21 ms before drug-induced autonomic block and from 79 +/- 7 to 51 +/- 16 ms after drug-induced autonomic block. The antiarrhythmic effects of Mg++ in this model of long QT syndrome were attributable to its direct pharmacological properties and not to changes in ambient autonomic nervous activity. The blockade of sympathetic activity decreased the incidence of premature events and partially suppressed polymorphic ventricular tachyarrhythmia in this model.

DOI： 10.1097/01.fjc.0000246262.29397.7a

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Background Whether amiodarone can improve the patient's clinical outcome by reducing implantable cardioverter-defibrillator (ICD) therapy deliveries for ventricular tachycardia or fibrillation (VT/VF) has not been clearly evaluated.
Methods and Results A total of 507 patients with VT/VF due to organic heart disease who had ICDs implanted were enrolled in this study. The patients were divided into 3 groups: Arniodarone (n=247), Class I antiarrhythmic drug (n=103) and Control (n=157) groups, and the total cause mortality and arrhythmic event free survival rates were evaluated between the groups. The mean follow-up period was 38 +/- 27 months. The left ventricular ejection fraction was significantly decreased in the Arniodarone group (Amiodarone: 37 +/- 15%; Class I: 39 +/- 16%; Control: 44 +/- 17%). The mortality and arrhythmic events were significantly higher in the Class I group than the Amiodarone group (p &lt; 0.05), but there was no significant difference between the Arniodarone and Control groups (arrhythmic event free rate at 5 years: Amiodarone: 53%; Class I: 35%; Control: 48%; 5 year survival: 86%, 74% and 77%, respectively). Side effects from amiodarone were found in 12% of the patients, but no fatal events were observed.
Conclusions The present study could not demonstrate the benefit of amiodarone in ICD patients, probably due to a significant clinical bias exerted in selecting this drug.

DOI： 10.1253/circj.70.977

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

A 43-year-old man presented with electrocardiographic findings consistent with Brugada syndrome. Though the baseline coronary angiogram was normal, intracoronary infusion of ergonovine maleate caused complete occlusion of the left anterior descending and a 99% occlusion of the proximal right coronary artery, each relieved by intracoronary isosorbide dinitrate. Double extrastimuli delivered at the right ventricular outflow tract induced ventricular fibrillation terminated by a 200-J shock. Verapamil, 10 mg IV, increased ST-segment elevation and programmed stimulation repeated after the drug induced ventricular fibrillation with shorter F-F intervals and lower amplitude signals, which was not terminated by 200 J and required an additional 360-J shock. Ca2+ antagonism may have been adverse in this patient with Brugada syndrome because the drug has the potential to increase the voltage gradient through the right ventricle and to slow intraventricular conduction at very fast heart rates. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2005.10.002

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Background: Genetically abnormal action potential duration (APD) can be a cause of arrhythmias that include long and short QT interval syndrome.
Purpose: The aim of this study was to evaluate the arrhythmogenic effect of short QT syndrome induced by the over-expression of Kv1.5 in rat.
Methods: From Sprague-Dawley rats on fetal days 18-19, cardiomyocytes were excised and cultured with and without transfection with the Kv-1.5 gene using an adenovirus vector. The expression of Kv1.5 was proven by immunohistochemistry and Western blot analysis. In the culture dish and in the whole cells, the electrical activities were recorded using the whole-cell patch-clamp technique and the effects of 4-AP and verapamil were tested.,
Results: After transfection with Kvl.5 for 12 h, immunohistochemical staining and Western blot analysis were positive for Kvl.5 while they were negative in the control transfected with only Lac-Z. In the culture dish, the myocytes showed spontaneous beating at 115 beats/min (bpm) just prior to the transfection with Kvl.5 and increased to 367 bpm at 24 h. The control myocytes showed stable beating rates during culturing. 4-AP at 200 mu M slowed down the rate and verapamil abolished the beating. In the whole cells, the maximal resting membrane potential was slightly depolarized and APD was extremely abbreviated both at 50% and 90% of repolarization compared with those of the control. Rapid spontaneous activities were found in a single myocyte with Kv1.5 transfection and 4-AP slowed down the frequency of the activities with a reversal of the shortened APD.
Conclusion: The over-expression of Kv1.5 induced short APD and triggered activities in rat cardiomyocytes. This model can be used to study the arrhythmogenic substrate of short QT syndrome. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2006.05.030

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：INTERNATIONAL HEART JOURNAL ASSOCIATION  

Intracardiac electrograms are important for discrimination of tachyarrhythmia by implantable cardioverter defibrillators (ICD). A low R-wave can cause not only undersensing of ventricular tachyarrhythmia but also inappropriate discharges due to oversensing of unexpected signals because of its characteristic sensing algorithm. Therefore, this study aimed to investigate adverse events associated with R-wave amplitude. We included 115 consecutive patients followed-up over one year after implantation of a transvenous ICD system. The status of the ICD was checked every 3 months and intracardiac ventricular electrograms were analyzed. The decrease in R-wave amplitude was high in arrhythmogenic hypertrophy cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and sarcoidosis. Low R-waves (&lt; 5.0 mV) were observed in 13 patients at a follow-up of 15 +/- 16 months after implantation, and the mean R-wave was 3.0 +/- 0.8 mV. The frequency of low R-waves was high in ARVC (38%), sarcoidosis (33%), and dilated cardiomyopathy (17%). All of the dilated cardiomyopathy patients with low R-waves had severe left ventricular dysfunction. Inappropriate ICD therapy resulting from T-wave oversensing occurred in 7 patients and the R-wave was &lt; 5.0 mV in 6 of the patients. The frequency of inappropriate therapy was high in patients with sarcoidosis. In 3 patients, inappropriate therapy caused ventricular tachyarrhythmia. In conclusion, decreases in R-wave amplitude occurred in some progressive cardiac disorders and caused inappropriate ICD discharges having arrhythmogenicity. Physicians should attempt to obtain a high R-wave amplitude during ICD implantation and careful follow-up is required, especially in patients with ARVC or sarcoidosis.

DOI： 10.1536/ihj.47.363

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Although catecholaminergic polymorphic ventricular tachycardia (CPVT) is associated with fatal ventricular arrhythmias and sudden death, the ECG findings are not fully understood. In this paper, we report on alterations in the U-wave.
Seven patients from 6 families with CPVT in which bidirectional tachycardia and polymorphic VT were induced by exercise or isoproterenol infusion visited our hospitals. VT was not inducible by programmed electrical stimulation. A novel gene mutation of the ryanodine receptor 2 (RyR2) was confirmed in 2 families.
In one of these patients, U-wave alternans was observed following ventricular pacing at 160 beats/min. In the other patient, U-wave alternans was observed during the recovery phase after the exercise stress test, which was terminated because of polymorphic VT. In both cases, leads V-3-V-5 were the leads showing alternans most clearly. In the third patient, a negative U-wave became positive following a pause from sinus arrest and a change in T-wave was also noted.
Since such findings were not found in the other subjects who underwent electrophysiologic study, isoproterenot infusion or exercise stress testing, the phenomenon seems to be relevant to the underlying pathogenesis of CPVT. The genesis and significance of U-wave alteration need to be determined.

DOI： 10.1536/ihj.47.381

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Background Suppression of implantable defibrillator discharges associated with ventricular tachyarrhythmia (VTA) has been reported for sotalol. This study aimed to investigate the efficacy of intravenous nifekalant hydrochloride in predicting the effects of oral sotalol.
Methods and Results The present study included 14 patients who had sustained VTA associated with structural heart disease. All patients also had inducible VTA. To compare the effects of nifekalant and sotalol, programmed electrical stimulation was performed, in the basal state, after nifekalant administration, and after sotalol administration. Nifekalant and sotalol similarly prolonged the corrected QT interval and ventricular effective refractory periods, but the heart rate was slowed by sotalol only. In 4 of 5 patients whose VTA became non-inducible by nifekalant, subsequent treatment with sotalol also suppressed the inducible VTA. In all of the 9 patients non-responding to nifekalant, VTA remained inducible during sotalol treatment. Nifekalant accurately predicted the response to sotalol during electrophysiologic study in 13 of 14 patients. Of 11 patients who remained on sotalol, VTA recurred in 3 non-responders during a follow-up of 46 +/- 11 months.
Conclusions Nifekalant and sotalol had similar effects on inducible VTA. The response of inducible VTA to nifekalant may predict the clinical efficacy of sotalol.

DOI： 10.1253/circj.70.583

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Tumor necrosis factor-alpha (TNF-alpha) affects contractility and ionic currents in the heart. However, the electrophysiological effects, especially on delayed rectifier K currents (IK), have not yet been fully elucidated. We examined the effects of TNF-alpha on IK. Using a voltage-clamp method, IK was measured in guinea pig ventricular myocytes in the basal state and after pharmacological intervention. To specify the site of the action of TNF-alpha, the myocytes were incubated with pertLISSiS toxin or Al-olcoylethanolarnine, it cerarnidase inhibitor, and IK was measured. TNF-alpha suppressed IK when it was enhanced by isoproterenol, histamine or forskolin but not in the basal state or when IK was augmented by an internal application of cyclic AMP. Both pre-itICUbation with pertUSSiS toxin and N-olcoylethanolamine abolished the inhibitory action of TNF-alpha on isoproterenol-augmented IK. TNF-alpha inhibits IK, mainly IKs, when it is augmented by PKA as a result of the generation of sphingosine. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2006.03.115

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

Objective: This study investigated the treatment of ventricular tachycardia (VT) after repair of tetralogy of Fallot or double outlet of the right ventricle.
Background: The ideal antiarrhythmic therapy for VT in patients after repair of congenital heart disease, especially without left ventricular dysfunction, has not yet been established.
Methods: Seven consecutive patients (2 women and 5 men) with stable monomorphic sustained VT were investigated. The mean age was 25 +/- 7 years (range, 16-35 years). Four patients had undergone surgical repair of tetralogy of Fallot, and 3 had surgical correction of double outlet of the right ventricle at the mean age of 18 +/- 7 years (range, 9-27 years) before documentation of the arrhythinia.
Results: The mean ejection fraction of the left ventricle was 60% +/- 8% (range, 50-72). Fourteen sustained monomorphic VTs were induced in 7 patients using programed electrical stimulation. The mean cycle length of tachycardia was 346 +/- 77 milliseconds (range, 260-480 seconds). The site of the surgical correction of the right ventricle was associated with the origin of VT in all patients. Radiofrequency catheter ablation was attempted in 8 VTs in 7 patients: 7 clinical and 1 nonclinical VTs. In 6 patients, class III antarrhythinic agents were added because VT remained inducible after ablation. During a follow-up of 61 +/- 29 months (range, 15-110 months), there were no recurrences of VT.
Conclusion: In patients with drug-refractory VT originating from the right ventricle late after congenital heart disease, and when their left ventricular function do not deteriorate, combined therapy for radiofrequency catheter ablation with class III antiarrhythmic agents might effective and should be considered as a therapeutic option. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2005.08.005

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Background Implantable cardioverter-defibrillators (ICDs) are the most effective therapy in reducing the mortality of patients with life-threatening ventricular tachyarrhythmias. However, the ICD cannot prevent the recurrence of tachycarida attacks and that limits the clinical usefulness of them. The Nippon ICD Plus Pharmachologic Option Necessity (NIPPON) trial was designed as the first prospective randomized study to test the hypothesis whether amiodarone could improve the patient's clinical outcome by reducing the amount of ICD therapy in the Japanese patient Population.
Methods and Results Approximately 400 patients with organic heart disease and spontaneous episode(s) of sustained ventricular tachycardia/fibrillation (VT/VF) will be randomly assigned to one of 2 groups; the amiodarone group and non-amiodarone group. Both groups of patients will be followed at least for 24 months. The end-point committee will adjudicate events in a blinded fashion. The primary end-points of this Study are determination of the appropriate therapy from the ICD and alteration of the assigned treatment because of its harmful effects and/or frequent ICD therapies.
Conclusion The NIPPON study is expected to confirm our understanding of the prognostic and therapeutic usefulness of adjuvant amiodarone therapy for patients with an ICD and with a history of sustained VT/VF.

DOI： 10.1253/circj.70.316

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Background Implantable cardioverter-defibrillators (ICDs) are the most effective therapy in reducing the mortality of patients with life-threatening ventricular tachyarrhythmias. However, the ICD cannot prevent the recurrence of tachycarida attacks and that limits the clinical usefulness of them. The Nippon ICD Plus Pharmachologic Option Necessity (NIPPON) trial was designed as the first prospective randomized study to test the hypothesis whether amiodarone could improve the patient's clinical outcome by reducing the amount of ICD therapy in the Japanese patient Population.
Methods and Results Approximately 400 patients with organic heart disease and spontaneous episode(s) of sustained ventricular tachycardia/fibrillation (VT/VF) will be randomly assigned to one of 2 groups; the amiodarone group and non-amiodarone group. Both groups of patients will be followed at least for 24 months. The end-point committee will adjudicate events in a blinded fashion. The primary end-points of this Study are determination of the appropriate therapy from the ICD and alteration of the assigned treatment because of its harmful effects and/or frequent ICD therapies.
Conclusion The NIPPON study is expected to confirm our understanding of the prognostic and therapeutic usefulness of adjuvant amiodarone therapy for patients with an ICD and with a history of sustained VT/VF.

DOI： 10.1253/circj.70.316

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The beneficial effects of quinidine on ST-segment elevation, inducible ventricular tachyarrhythmias, and episodes of ventricular tachyarrhythmia have been reported in Brugada syndrome. This is the first report describing quinidine-induced elimination of the late potential, which is considered one of the parameters for an arrhythmic event, in a patient with Brugada syndrome. (c) 2006 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2005.07.009

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SAECG and EPS in Brugada Syndrome. Background: Electrical abnormalities in the RVOT may be involved in Brugada syndrome.
Objectives: We investigated the relationship between the signal-averaged ECG (SAECG) and electrophysiologic study (EPS), especially focusing on conduction delay in the outflow tract of the right ventricle (RVOT) and its contribution to clinical characteristics.
Methods: Twenty-four patients with Brugada syndrome (23 men and 1 woman; 61 +/- 16 years old) were studied. We assessed the presence of late potential (LP) in SAECG and the filtered QRS duration in the right precordial leads (V-1 or V-2; RfQRS) and in the left precordial leads (V-5 or V-6; LfQRS) and the difference between them. In 18 patients, SAECG was evaluated for an LP on three separate occasions.
Results: SAECG was positive for LP in 15 patients at least once; and in 7 patients, SAECG was positive for an LP on multiple occasions, and 6 of 7 patients (86%) had a history of cardiac arrest. The difference between RfQRS and LfQRS was significantly greater in patients with cardiac arrest than in patients with syncope or in asymptomatic patients; 29 +/- 10, 14 +/- 11 (P &lt; 0.01), and 7 +/- 5 msec (P &lt; 0.001), respectively. All patients were alive and one patient with cardiac arrest had an appropriate VF therapy delivered by the ICD.
Conclusions: The dominant prolongation of the filtered QRS duration in the right precordial leads may be related to the risk of arrhythmic event in Brugada syndrome.

DOI： 10.1111/j.1540-8167.2005.00262.x

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Background Some patients with an implantable cardioverter-defibrillator (ICD) suffer from burst of inappropriate multiple discharges (severe electrical storm), and because the current therapeutic options are limited, the effect of nifekalant hydrochloride, a new class III drug, on severe electrical storm was investigated in the present study.
Methods and Results Ninety-one consecutive patients treated with ICD were included in the study (M 70; mean age 58 years; left ventricular ejection fraction 45 +/- 15%). Severe electrical storm was defined as more than 10 ICD discharges within 1 h. During a mean follow-up period of 30 +/- 13 months, 41/91 (45%) patients had appropriate ICD therapy for arrhythmias and severe electrical storm occurred in 11 of them (12%) at 20 +/- 18 months after ICD implantation. The mean number of ICD discharges/h during severe electrical storm was 18 +/- 12. In 4 of 10 patients, severe electrical storm was successfully suppressed by a combination of deep sedation and beta-blocking agent; 6 other patients were refractory to this treatment, but severe electrical storm was successfully suppressed by intravenous administration of nifekalant hydrochloride with no adverse effects.
Conclusions Nifekalant hydrochloride is an effective and safe treatment for severe electrical storm.

DOI： 10.1253/circj.69.1508

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Background: Disopyramide is thought to have an advantageous effect for atria] fibrillation (AF) associated with vagal activity because of its anticholinergic effect.
Method: We used a canine vagal nerve stimulation (VNS) model. The monophosic action potential (MAP) duration at 90% repolarization (MAP(90)). the intraatrial conduction time. the induciblity of AF by electrical stimulation, and the amplitude of high-frequency component (HF-amp) of the heart rate variability (HRV) were evaluated before and after the administration of disopyramide (I mg/kg) (group D, n = 8) or pilsicainide (1 mg/kg) (group P n = 5).
Results: In group D, HF-amp decreased in the baseline condition from 1.1 +/- 0.6 to 0.6 +/- 0.4 ins and the degree of VNS-induced augmentation of HF-amp was attenuated from +492% to +127%. VNS-induced shortening of MAP(90) was also attenuated in the right atrium (from -30 +/- 15% to -10 +/- 6%) and in the left atrium (from -15 +/- 9% to -6 +/- 6%). In group P, little (effect was shown in these parameters, The vagotonic AF became noninducible in all eight experiments in group D, while in only one of five in group R
Conclusion: The beneficial effect of disopyramide for vagotonic AF is based on the decrease of basal vagal tone and attenuation of the effect of vagal stimulation in the atrial myocardium. 111711 is a useful parameter for evaluation of the effect of antiarrhythmic drugs on the autonomic nerve system, and the evaluation of variability maybe useful for testing drug efficacy for arrhythimas.

DOI： 10.1111/j.1540-8159.2005.40071.x

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

DOI： 10.1161/CIRCULATIONAHA.104.530568

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Vasospastic angina (VSA) and Brugada syndrome (BS) are classified into different categories of cardiac disease, but both can be causes of sudden cardiac death from ventricular fibrillation (VF). The coexistence of VSA and BS in the same patient is possible, and this raises several questions: (1) what is the incidence of the coexistence of BS and VSA in the same patient? (2) is susceptibility to VF enhanced by the coexistence of the 2 diseases? and (3) is there any possibility of Ca-antagonists being used for the treatment of VSA-aggravated BS? In our institution, VSA coexisted in 5 of the 3 8 patients with BS (13.1%). Anginal episodes were confirmed clinically in 4 of the 5 patients, and syncope attack occurred after the symptom of chest pain in 2 patients. However, VF did not develop during the coronary vasospasm in any of the patients. Treatment with Ca-antagonist was effective for VSA, and neither aggravation of Brugada-type electrocardiographic abnormality nor an increase in the incidence of syncope attack was observed. Although the coexistence of BS and VSA in the same patient is not rare, neither enhanced susceptibility to VF nor the proarrhythmic effect of Ca-antagonist has been confirmed in our experience. However, careful attention is required in such patients because the influence of myocardial ischemia and/or the effect of Ca-antagonist may be different in each patient with BS. (c) 2005 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jelectrocard.2005.06.004

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We describe here the case of a 58-year-old female patient who experienced inappropriate shocks from her implantable cardioverter-defibrillator (ICD). Stored electrograms from her ICD showed hi.-h frequency noise preceding the shock. Although the pacing threshold was normal and lead fracture was not found in chest X-rays, pacing lead impedance decreased to 480 Omega. Moreover, such high frequency noise was observed by electrogram telemetry, but not by routine evaluation every 3 months. ICD lead dysfunction was Suspected, so we elected to replace the ICD lead system. At the time of the operation. lead impedance was 410 Omega and pacing threshold was the same as it was at the time of the ICD implantation, and no lead insulation disturbances were observed in the generator pocket. However. manipulation of the lead system produced high frequency noise reproducibly. Since some of the ICD lead dysfunction initially was clinically silent at rest. dysfunction was difficult to detect before serious problems occurred. Therefore, more careful evaluation of the ICD lead system is needed during long-term follow-up of ICD implants.

DOI： 10.1536/ihj.46.909

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Background: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg++) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA).
Methods: In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg++ was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg++ administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured.
Results: Mg++ rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg++ caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg++ injection. However, this effect was transient, and, at 120 seconds after Mg++ administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg++ in this model.
Conclusion: Since these effects were transient, a continuous intravenous infusion of Mg++ is preferred to prevent recurrences of VTA.

DOI： 10.1111/j.1540-8159.2005.00178.x

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DOI： 10.1001/jama.294.3.305

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Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST-segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST-elevation at the I-point (STJ), and the ST-segment configuration in leads V1-V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated STJ by &gt;= 0.1 mV Of these 3 patients, ST-segment elevation was normalized in 2 patients, while the ST-segment configuration was unchanged in another. In another 3 patients, quinidine augmented STJ by &gt;= 0.1 mV without any change of ST-segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST-segment in the remaining 2 patients. The favorable effects of quinidine on the ST-segment tended to be more pronounced in patients with prominent ST-elevution at baseline. In 1 patient, quinidine was effective in eliminating both ST-segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST-segment elevation were variable. Quinidine may potentially augment the ST-segment elevation in some patients with Brugada syndrome.

DOI： 10.1111/j.1540-8159.2005.09494.x

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The aim of this study was to investigate the long-term efficacy and safety of electrophysiologic study (EPS)-guided sotalol administration combined with implantable cardioverter defibrillators (ICD) for ventricular tachyarrhythmias (VTA). This study enrolled 92 patients with both structural heart disease and sustained VTA. Sotalol was administered to 57 patients, and its efficacy was assessed by EPS. Long-term treatment was continued in combination with ICD in 31 patients (57%) whose VTA was no longer inducible (responder group) and in 16 patients whose VTA remained inducible (non-responder group). The long-term outcomes were compared among the responder group, the nonresponder group, and 35 ICD recipients untreated with antiarrhythmic drugs (ICD-only group). During a mean follow-up of 44 +/- 33 months, the recurrence of VTA was not significantly different between all patients treated with sotalol (30%) and patients in the ICD-only group (46%). However, the recurrence of VTA was significantly lower in the responder (13%) than in the nonresponder (63%) or the ICD-only groups (46%). There was no significant difference in VTA recurrence between the nonresponder and the ICD-only groups. One patient each in the responder and the ICD-only groups died suddenly, and all-cause mortality was similar in the three groups. The incidence of inappropriate ICD discharges was less in the sotalol than in the ICD-only groups. No patient had to discontinue long-term sotalol treatment because of the adverse effects. In conclusion, sotalol reduced VTA recurrence in the responding patients and inappropriate ICD discharge. EPS may predict the efficacy of sotalol for VTA recurrence.

DOI： 10.1111/j.1540-8159.2005.09413.x

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Introduction: In patients with Brugada syndrome, implantable cardioverter defibrillator (ICD) is the only reliable treatment to prevent sudden death though, in some cases, internal defibrillation may be unsuccessful. The aim of this study was to examine the determinants of defibrillation failure, with a focus on electrophysiologic characteristics.
Methods: The study included 51 patients treated with ICD: 22 with Brugada syndrome and 29 with structural heart disease (SHD). The prevalence of defibrillation energy requirement precluding the programming of a 10-J safety margin, the mean right ventricular effective refractory period (ERP), and mean induced ventricular fibrillation cycle length (VFCL) from the stored ICD electrograms, were compared between the two patient groups.
Results: High defibrillation requirements were observed in 18% of patients with Brugada syndrome versus 0% of patients with SHD. However, the patients with SHD had larger heart size than those with Brugada syndrome. Mean VFCL and mean ERP were both significantly shorter in patients with Brugada syndrome than in patients with SHD, and ERP and VFCL were significantly correlated.
Conclusion: Patients with Brugada syndrome have a high prevalence of high defibrillation energy requirement, and short ventricular ERP and VFCL.

DOI： 10.1046/j.1540-8167.2005.40579.x

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Language：English   Publisher：ELSEVIER SCI IRELAND LTD  

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an autosomal dominant inherited disorder characterized by adrenergic induced polymorphic ventricular tachycardias and associated with sudden cardiac death. The human cardiac ryanodine receptor gene (RyR2) was linked to CPVT. A 20-year-old male was referred to our hospital because of recurrent syncope after physical and emotional stress. Routine cardiac examinations including catheterization revealed no structural abnormality. Exercise on treadmill induced premature ventricular contraction in bigeminy and bidirectional ventricular tachycardia was induced during isoproterenol infusion. beta-Blocking drug was effective in suppressing the arrhythmias. We performed genetic screening by PCR-SSCP method followed by DNA sequencing, and a novel missense mutation R2401H in RyR2 located in FKBP12.6 binding region was identified. This mutation was not detected in 190 healthy controls. Since FKBP12.6 plays a critical role in Ca channel gating, the R2401H mutation can be expected to alter Ca-induced Ca release and E-C coupling resulting in CPVT. This is the first report of RyR2 mutation in CPVT patient from Asia including Japan. (c) 2004 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.ijcard.2003.11.050

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：TAYLOR & FRANCIS INC  

Hyperthyroidism is associated with low exercise tolerance despite high cardiac output and sometimes with the development of heart failure. L-type calcium channels may play a role in the mechanism, but this has not been fully understood. We examined the effects of thyroid hormone on gene expression and function of L-type calcium channels in rat ventricles by the ribonuclease protection assay and whole-cell patch-clamp technique, respectively. The effects of bisoprolol, betablocking agent, on the regulation of calcium channel by thyroid hormone was also studied. In hyperthyroid animals, the mRNA of the calcium channel alpha I c subunit was reduced on day 4, compared with that in euthyroid animals, and remained low on day 8. Bisoprolol did not affect the thyroid hormone mediated decrease in alpha] c subunit mRNA. While L-type calcium current was greater in hyperthyroid than euthyroid myocytes on day 4, it was smaller, on day 8. In addition, the isoproterenol-induced increase in calcium current in euthyroid rats was attenuated in hyperthyroid rats. Acetylcholine decreased calcium current in hyperthyroid myocytes, but not in euthyroid myocytes. In conclusion, L-type calcium current was increased by thyroid hormone in rat ventricular myocytes by the activation of the adenylate cyclase cascade, despite a decreased calcium channel gene expression. These genomic and non-genomic modifications may play an important role in the association of high cardiac output with low exercise tolerance, and in the development of heart failure in hyperthyroidism.

DOI： 10.1080/07435800500229227

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Background The purpose of this study was to assess the candidates suitable for cardiac resynchronization therapy (CRT) and to examine the significance of the QRS duration in Japanese patients with idiopathic dilated cardiomyopathy (DCM).
Methods and Results The study population consisted of 357 patients. The selection criteria for candidates suitable for CRT were QRS duration = 130 ms, left ventricular ejection fraction (LVEF) = 35% and New York Heart Association (NYHA) functional class III or IV by ACC/AHA/NASPE 2002 guidelines. We divided the study population into 2 groups: group A with a QRS duration &lt; 130 ms, and group B with a QRS duration = 130 ms. In 25 of the 375 patients (7.0%), all the criteria were fulfilled. Group B had a significantly larger left ventricular diameter end-diastole and end-systole than group A (P &lt; 0.0001). Group B had a lower LVEF (P &lt; 0.0001). There was a fair inverse correlation (r = -0.58, P &lt; 0.0001) between the length of the QRS duration and LVEF.
Conclusion Approximately 7% of the Japanese patients with DCM are CRT candidates. In the present study, we found that prolonged QRS duration was associated with poor systolic function.

DOI： 10.1253/circj.68.1104

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A 74-year-old man with a history of partial gastrectomy presented with an electrocardiogram consistent with Brugada syndrome and marked meal related fluctuations in the ST segment. ST-segment elevation was prominently attenuated at 30 minutes and increased at 120 minutes after meals. Analysis of heart rate variability revealed a relationship between postprandial heightened parasympathetic activity and increase in Brugada-type ECG abnormality. A rapid postprandial increase in blood glucose may initially stimulate sympathetic nervous activity and secondarily increase parasympathetic tone. Food intake can be associated with fluctuations in ST-segment elevation in patients with the Brugada syndrome.

DOI： 10.1111/j.1540-8159.2004.00676.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

A 30-year-old man was admitted for treatment of tachycardia-induced cardiomyopathy caused by incessant atrioventricular nodal reentrant tachycardia (AVNRT). An echocardiogram revealed dilatation of all cardiac chambers with severe globally depressed biventricular systolic function. During an electrophysiologic study, HV interval was prolonged to 118 ms by atrial extrastimulus and 2:1 HV block was documented during AVNRT. Four weeks after catheter ablation for AVNRT, an echocardiogram demonstrated regression of the wall motion abnormality of both ventricles and of their dimensions. in the electrophysiologic study, the HV conduction disturbance disappeared. So far, this is the first case in which tachycardia-induced cardiomyopathy was accompanied by transient His-Purkinje conduction abnormality.

DOI： 10.1016/j.jelectrocard.2004.07.009

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Language：English   Publisher：JAPAN SOC INTERNAL MEDICINE  

Since the first clinical use of implantable defibrillator in human, the technology and the function of implantable cardioverter-defibrillator (ICD) have been much improved and now, ICD can be implanted within the chest wall. ICD is the most reliable therapy to prevent sudden cardiac death (SCD) in patients with documented VT/NF and the efficacy is most clear in patients with depressed heart function. It is now extended as a tool of the primary prevention of SCD in high risk patients after myocardial infarction. However, such beneficial effect is not applicable to DCM though patients might have depressed heart function. ICD is not free from procedure- or device-related problems which need to be resolved. From unknown causes, VTNF might recur in an incessant form and an emergency admission is needed. Therefore, even during ICD therapy, patients often require antiarrhythmic drugs or catheter ablation.

DOI： 10.2169/internalmedicine.43.360

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Background: Cardiac sarcoidosis is increasingly recognized and is associated with poor prognosis. Ventricular tachycardia (VT) associated with cardiac sarcoidosis is the most likely cause of sudden death in most patients, but the mechanism has not been well established.
Hypothesis: This study investigated the mechanisms and outcome of VT associated with cardiac sarcoidosis.
Methods: The study included eight consecutive patients (five men, three women, aged 54 19 years) who had sustained monomorphic VT associated with cardiac sarcoidosis in our hospital.
Results: The average ejection fraction was 43 +/- 11%. Twenty-two VTs were observed in these patients, and mean heart rate during VT was 192 +/- 29 beats/min (range 144-259). The phenomenon of transient entrainment was documented in 10 of 22 (45%) VTs by ventricular pacing (eight in the active phase). Another five (23%) VTs could not be entrained, but could be initiated by programmed stimulation and terminated by rapid pacing, reproducibly. In 3 of the 22 (14%) VTs, cardioversion was required urgently because of the fast rate, while the remaining 4 (18%) could be induced during electrophysiologic study.
Conclusions: In this study, there was a high possibility that the mechanism of 15 (68%) VTs was reentry. Reentrant substrate is formed not only in association with the healing of cardiac granulomas in the inactive phase of cardiac sarcoidosis but also in the active phase. Ventricular tachycardia with cardiac sarcoidosis, even if this mechanism is reentry, has different inducibility between the active and inactive phases in an electrophysiologic study. This makes the therapy for cardiac sarcoidosis (e.g., coil icosteroids, antiarrhythinic agents, and catheter ablation) difficult. The implantable cardioverter-defibrillator is an effective treatment for ventricular tachyarrythmia with cardiac sarcoidosis.

DOI： 10.1002/clc.4960270409

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DOI： 10.1161/01.CIR.0000109525.74497.6F

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

Atrial fibrillation is one of the common arrhythmias associated with hyperthyroidism. This study examined the effects of thyroid hormone (T3) on mRNA expression and currents of major ionic channels determining the action potential duration (APD) in the rat atrium using the RNase protection assay and the whole-cell patch-clamp technique, respectively. T3 increased the Kv1.5 mRNA expression and decreased the L-type calcium channel mRNA expression, while the Kv4.2 mRNA expression did not change. APD was shorter in hyperthyroid than in euthyroid myocytes. The ultrarapid delayed rectifier potassium currents were remarkably increased in hyperthyroid than in euthyroid myocytes, whereas the transient outward potassium currents were unchanged. L-type calcium currents were decreased in hyperthyroid than in euthyroid myocytes. T3 shifted the current-voltage relationship for calcium currents negatively. In conclusion, T3 increased the outward currents and decreased the inward currents. The resultant changes of ionic currents shortened APD, providing a substrate for atrial fibrillation. (C) 2003 Elsevier Inc. All rights reserved.

DOI： 10.1016/S0006-291X(03)01420-7

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL FUTURA PUBLISHING, INC  

Introduction: Compared to concordant T wave alternans (CA), discordant T wave alternans (DA) may be associated with an increased dispersion of repolarization (DR) and a greater propensity to develop reentrant ventricular tachyarrhythmias. The electrophysiologic mechanisms of DA in the in vivo heart are not well understood.
Methods and Results: The mechanisms of DA were investigated in the canine anthopleurin-A surrogate model of long QT3 syndrome using tridimensional analysis of activation and repolarization patterns from 256 to 384 unipolar electrograms. Cardiac repolarization was evaluated as the activation-recovery interval (ARI) of local electrograms. Two mechanisms for the development of DA were observed. (1) Stepwise shortening of cycle length (CL) superimposed on preexisting DR resulted in different diastolic intervals (DI) at midmyocardial sites compared to epicardial and endocardial sites. The dispersion of DI coupled with different restitution kinetics at those sites induced DA. (2) The dependence of conduction velocity on DI as the CL is abruptly shortened could result in differential conduction delays at mid sites. This enhanced the dispersion of DI between sites and, coupled with the different restitution kinetics, induced DA. The critical step for the development of DA in both mechanisms was the occurrence of short ARI in two consecutive beats either at epicardial sites in the first mechanism or at mid sites in the second mechanism. Sites with DA had significantly more DR compared to sites with concordant T wave alternans, and ventricular tachyarrhythmias developed mainly in the presence of DA.
Conclusion: In the in vivo heart, DA developed due to critical interaction between dispersion of DI and differences in restitution kinetics at different myocardial sites. The dispersion of DI could result from preexisting DR or differential conduction delay at a critical short CL. DA is critically linked to the development of malignant tachyarrhythmias.

DOI： 10.1046/j.1540-8167.2003.03028.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

Andersen's syndrome (AS) (which is characterized by periodic paralysis, cardiac arrhythmias and dysmorphic features), a hereditary disease, and missense mutations of KCNJ2 (which encodes an inward rectifying potassium channel) have been reported recently. We performed clinical and molecular analyses of a patient with AS, and found a novel mutation (G215D) of KCNJ2. Twelve-lead electrocardiography revealed a long QT interval and frequent premature ventricular contractions, and polymorphic ventricular tachycardia was induced by programmed electrical stimulation. Use of a conventional whole-cell patch-clamp system with COS7 cells demonstrated that the G215D mutant was non-functional, and that co-expression of wild type (WT)- and mutant-KCNJ2 shows a dominant negative effect on both inward and outward currents. We performed confocal laser scanning microscopy to assess the cellular trafficking of WT- and mutant-KCNJ2 subunits tagged with yellow fluorescent protein (YFP) and cyan fluorescent protein (CFP), respectively. Tagging with the YFP did not affect the channel function of WT-KCNJ2 and both proteins showed similar plasma membrane fluorescence patterns. Furthermore, the result of fluorescence resonance energy transfer (FRET) studies at the plasma membrane region suggested that both YFP-tagged WT- and CFP-tagged mutant-KCNJ2 combine to construct a hetero-multimer of the potassium channel. In conclusion, the G215D mutant of KCNJ2 is distributed normally in the plasma membrane, but exhibits a dominant-negative effect and reduces the Kir2.1 current, presumably due to hetero-multimer construction. (C) 2003 Elsevier Science Ltd. All rights reserved.

DOI： 10.1016/S0022-2828(03)00046-4

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

A 71-year-old woman had undergone valvular heart surgery in 1981, and implantation of a permanent ventricular pacemaker for ventricular pauses during atria] fibrillation in 2001. One year after pacemaker implantation, she complained of faintness. When pacing at 100 beats/min the pacemaker functioned properly. However, pacing and sensing failure was detected at a pacing rate of 60 beats/min. At rapid pacing rates, the lead tip was in closer contact with the endocardium, and its microdislodgment was undetectable. The symptoms have resolved since the lead was repositioned.

DOI： 10.1046/j.1460-9592.2003.00138.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL PUBLISHING ASIA  

The ventricular tachyarrhythmias associated with the LQT3 syndrome are typically bradycardia-dependent. However, some episodes can be associated with exercise or emotional stress, suggesting a different arrhythmogenic mechanism when sympathetic activity predominates. This study examined the potential arrhythmogenic mechanisms during periods of autonomically mediated transient heart rate acceleration in a canine anthopleurin-A model of LQT3 syndrome. Using plunge needle electrodes, transmural unipolar electrograms of the left ventricle were recorded from endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) sites. The activation-recovery interval (ARI) was measured to estimate local refractoriness. The cardiac cycle length was gradually shortened by cessation of vagal stimulation (vagal stimulation protocol (VSP)), and intramural electrograms and onset mode of ventricular tachyarrhythmias were analyzed in 7 experiments. The VSP was performed 8 times before and 5 times after administration of mexiletine in each experiment. Before mexiletine, vagal stimulation slowed the heart rate and created large transmural ARI dispersion because of a greater ARI prolongation at Mid rather than Epi/Endo sites. After cessation of vagal stimulation, unipolar electrograms started to show ARI alternans and ventricular premature beats developed sporadically. Sustained ventricular tachyarrhythmias were induced in 12 of the 56 trials of the VSP. Initiation of ventricular tachyarrhythmias was,associated with delayed conduction at Mid/Endo sites. Mexiletine attenuated transmural ARI dispersion, and neither ARI alternans nor ventricular tachyarrhythmias was observed during all 35 trials of the VSP after mexiletine administration. Heart rate acceleration induced by an abrupt shift to a state of predominant sympathetic activity enhances arrhythmias in this LQT3 model. Mexiletine homogenizes ventricular repolarization, suppresses premature complexes and was antiarrhythmic during ventricular tachyarrhythmias induced by the VSP.

DOI： 10.1253/circj.67.263

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

This study presents a patient with idiopathic dilated cardiomyopathy who had suffered from multiple ICD shocks. Amiodarone and a,B-blocker failed to suppress ventricular tachycardia. His ECG showed a very wide QRS complex with an intraventricular conduction delay, so biventricular (BV) pacing was attempted. The BV pacing successfully prevented the multiple ICD shocks accompanied with an improvement in left ventricular systolic function and physical activity.

DOI： 10.1046/j.1460-9592.2003.00156.x

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

This patient was a 50-year-old man. Oral pilsicainide unmasked a Brugada-type ECG abnormality and self-terminating polymorphic VT was repetitively induced. The polymorphic VT always developed following a specific ventricular premature complex showing a left bundle branch block pattern suggesting a limited origin in the right ventricle.

DOI： 10.1046/j.1460-9592.2002.01649.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC  

Activation recovery interval (ARI) calculated from intracardiac electrograms in patients with long QT syndrome (LQTS) was correlated with local effective refractory period (ERP). Epinephrine induced ARI prolongation and increased ARI dispersion, whereas mexiletine diminished heterogeneity of ventricular repolarization.

DOI： 10.1016/S0002-9149(02)02506-7

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

Introduction: T wave alternans (TWA) is characterized by cycle-to-cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin-A model of long QT syndrome.
Methods and Results: The cardiac cycle length was gradually shortened by interruption of vagal stimulation, and TWA was induced in six canine hearts. Transmural unipolar electrograms were recorded with plunge needle electrodes from endocardial (Endo), mid-myocardial (Mid), and epicardial (Epi) sites, along with the surface ECG and BP. The activation-recovery interval (ARI) was measured to estimate local refractoriness. During TWA, ARI alternans was greater at the Mid than the Epi/Endo sites, and it was associated with the development of marked spatial dispersion of ventricular repolarization. As TWA increased, ventricular activation of the cycles associated with shorter QT intervals displayed delayed conduction at the Mid sites as a result of a critically longer ARI of the preceding cycle and longer QT interval, while normal conduction was preserved at the Epi site. Delayed conduction at the Mid sites manifested as surface ECG QRS and BP waveform alternans, and spontaneous ventricular tachyarrhythmias developed in absence of ventricular prematurity. In other instances, in absence of delayed conduction during TWA, ventricular premature complexes infringed on a prominent spatial dispersion of ventricular repolarization of cycles with long QT intervals and initiated ventricular tachyarrhythmia. \ Conclusion: TWA accompanied by QRS alternans may signal a greater ventricular electrical instability, since it is associated with intramural delayed conduction, which can initiate ventricular tachyarrhythmia without ventricular premature complexes.

DOI： 10.1046/j.1540-8167.2002.00599.x

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Language：English   Publisher：BLACKWELL PUBLISHING ASIA  

DOI： 10.1253/circj.66.308

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V-1 to V-3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V-1 to V-3, and T wave alternans became visible in leads V-2 and V-3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V-3 to V-6 concomitant with visible QT/T alternans in leads V-4 and V., and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricalar tachyarrhythmias in such patients.

DOI： 10.1046/j.1540-8167.2002.00191.x

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Language：Japanese   Publisher：Elsevier B.V.  

DOI： 10.1016/j.jconrel.2014.02.001

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL SCIENCE ASIA  

The study prospectively investigated the incidence, cause and efficient management of inappropriate discharge by the fourth generation implantable cardioverter-defibrillator (ICD) system in 45 patients (mean age, 57 +/- 16 years). During the follow-up period of 27 +/- 17 months, 18 patients (40%) experienced one or more inappropriate therapies: sinus and supraventricular tachycardia (15 patients) and T wave oversensing (3 patients). In the 15 patients, re-programming of the tachycardia detection interval and/or additional treatment with beta -blocking agents were effective. In the 3 patients with T wave oversensing, the arrythmia was associated with an increase in T wave amplitude, change in T wave morphology and decreased R wave amplitude, and re-programming of the sensitivity of the local electrogram or changing the number of intervals to detect ventricular tachycardia decreased the number of inappropriate discharges in all 3 patients. In conclusion, inappropriate therapies are common problems in patients treated with the fourth generation ICD system, but most of them can be resolved using the dual-chamber ICD system. However, in patients with T-wave oversensing, it is difficult to avoid inappropriate discharge completely, even if the dual-chamber ICD system is implanted.

DOI： 10.1253/jcj.65.927

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Futura  

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Intracoronary acetylcholine administration, which was performed to exclude vasospasms, unmasked an abnormal QT interval prolongation and initiated torsades de pointes in a patient with normal QT interval at rest.

DOI： 10.1046/j.1460-9592.2001.01561.x

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

Rapid discharges from the myocardium extending from the left atrium onto the pulmonary vein (PV) have been shown to initiate AF, and AF may be eradicated by the catheter ablation within the PV. However, if there is any difference in the distribution patterns of the myocardial sleeve onto the PV between the subjects with and without AF is to be determined. Twenty-one autopsied hearts were examined. Eleven patients previously had AF before death and another 10 patients had normal sinus rhythm as confirmed from the medical records including ECGs before death. After exposing the heart, the distance to the peripheral end of the myocardium was measured from the PV-atrial junction in each PV. Then, the PVs were sectioned and stained and the distal end of myocardium and the distribution pattern were studied. The anteroposterior diameter of the left atrium was also measured. In 74 of 84 PVs, the myocardium extended beyond the PV-atrial junction. The myocardium was localized surrounding the vascular smooth muscle layer forming a myocardial sleeve. The peripheral end of the myocardial sleeve was irregular and the maximal and minimal distances were measured in each PV, The myocardium extended most distally in the superior PVs compared to the inferior ones and the maximal distance to the peripheral end was similar between the AF and non-AF subjects (8.4 +/- 2.8 vs 8.7 +/- 4.4 mm for the left superior and 6.5 +/- 3.5 vs 5.1 +/- 3.9 mm for the right superior PV, respectively). A significant difference was found in the maximal distance in the inferior PVs: 7.3 +/- 4.6 vs 3.3 +/- 2.8 mm for the left (P &lt; 0.05) and 5.7 +/- 2.4 vs 1.7 +/- 1.9 mm for the right inferior PV (P &lt; 0.001) in the subjects with and without AF, respectively. The diameter of left atrium was slightly dilated in AF patients but insignificantly (4.1 +/- 0.1 vs 3.6 +/- 0.1 cm, P &gt; 0.07). The myocytes on the PV were less uniform and surrounded by more fibrosis in patients with AF compared to those without AF. In conclusion, the myocardium extended beyond the atrium-vein junction onto the PVs. The distribution patterns of the myocardium was almost similar between subjects with and without AF, but the histology suggested variable myocytes in size and fibrosis in patients with AF.

DOI： 10.1046/j.1460-9592.2001.01459.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL SCIENCE ASIA  

In experimental studies and/or human body surface mapping, the activation -recovery interval (ARI) is used as a parameter to estimate local repolarization. However, it has not been clarified whether the ARI calculated from the intracardiac unipolar electrogram of humans reasonably represents the local effective refractory period (ERP). Measurement of ARIs at multiple ventricular sites can be helpful in assessing the dispersion of ventricular refractoriness of humans, so we examined the relationship between ERP and ARI in the control state and under treatment with dl-sotalol during clinical electrophysiologic studies (EPS). Of 19 patients, an EPS was performed in the control state in 12 and during treatment with dl-sotalol in the other 7. Quadripolar electrode catheters with an interelectrode distance of 5 mm were placed at the right atrium and in the right ventricle. Using atrial pacing, the heart rate was increased incrementally by 10 beats/min, and ERP and ARI were measured for each pacing rate. The ER-P at the right ventricle was measured by single extrastimulation between the first and third distal electrodes of the catheter in the right ventricle, and the ARI was calculated from the second distal unipolar electrode of the same catheter as the interval between the minimum derivative of the intrinsic deflection and the maximum derivative of the T wave. In all patients, the unipolar electrogram was stable during the entire EPS, and 83 data points in the control group and 50 in the dl-sotalol group were analyzed. At each pacing rate, the beat-to-beat difference of ARI was less than 10 ms. As the atrial pacing rate increased, the ERP and ARI were progressively shortened, and linear regression analysis revealed an excellent correlation between ERP and ARI. At the same pacing rate, the ERP and ARI in the dl-sotalol group were longer than those in the control group, but no difference was observed in the slope (close to 1.0) and in the intercept of the regression lines between ERP and ARI. In the human ventricle, the ARI calculated from the intracardiac unipolar electrogram represents the local ERP both in the control state and under treatment with dl-sotalol. The ARI can be used as a parameter of local refractoriness and used to study the distribution of refractoriness in the human ventricle.

DOI： 10.1253/jcj.65.702

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN SOC INTERNAL MEDICINE  

Monomorphic ventricular tachycardia (VT) developed in two patients with cardiac sarcoidosis. Before treatment with prednisolone, technetium or gallium scintigram revealed abnormal accumulation in the heart and bilateral hilar lymph nodes, but programmed electrical stimulation failed to induce VT in either case. Prednisolone was administered and the abnormal accumulation of the scintigra ms disappeared. However, VT became reproducibly inducible, and in one of the patients, transient entrainment was demonstrated in clinical VT morphology. Defibrillators were implanted in both patients. Some VTs associated with cardiac sarcoidosis are due to reentry, and inducibility of VT is not associated with the activity of cardiac sarcoidosis. Even though steroid therapy suppresses the activity of cardiac sarcoidosis, defibrillator implantation is necessary to prevent a possible arrhythmic event during the followup.

DOI： 10.2169/internalmedicine.40.731

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

Previous tridimensional activation mapping showed that the development of functional conduction block at the onset of torsades de pointes was regionally heterogeneous; conduction block was frequently observed in the LV and the interventricular septum (IVS) but not in the RV, in the canine anthopleurin-A (AP-A) model of long QT syndrome (LQTS). This may be related to the distribution of myocytes with M celllike electrophysiological characteristics. To better understand the regional difference of arrhythmogenicity in LQTS, the authors investigated cycle length related modulation of ventricular repolarization among three different layers: the endocardium (End), mid-myocardium (Mid), and epicardium (Epi) of the LV and RV and at two different areas: the Epi and septum (Sep) in the IVS. The LQT3 model was produced by AP-A in dogs. Using constant pacing and single premature stimulation (S1S2), the ventricular repolarization pattern was analyzed from 256 unipolar electrograms. Activation-recovery intervals (ARIs) were used to estimate local repolarization. In seven experiments, AP-A increased regional ARI dispersion to 88.1 +/- 36.0 ms in the LV, to 72.9 +/- 35.7 ms in the IVS, and to 23.0 +/-8.7 ms in the RV at the pacing cycle length (CL) of 1,000 ms. Development of the large ARI dispersion was due to greater ARI prolongation at the Mid site in the LV and at Sep site in the IVS. As the S1S2 interval was shortened, regional ARI dispersion decreased gradually, and finally, ARI dispersion showed a reversal gradient of repolarization between the Mid and Epi sites in the LV and between the Sep and Epi sites in the IVS. Two factors contributed to create the reversal gradient of repolarization: (1) a difference in restitution kinetics at the Mid site in the LV and at the Sep site in the IVS, characterized by a larger Delta ARI and slower time constant (tau), and (2) a difference in diastolic intervals at each site resulting in different input to restitution at the same CL. However, the RV showed small alteration in the transmural dispersion of repolarization in the S1S2 protocol. S-2 created heterogeneous functional conduction block in the LV and IVS but not in the RV. In the LQT3 model, the arrhythmogenicity of torsades de pointes is primarily due to dispersion of repolarization in the LV and IVS because of prominent distribution of M cells. The RV seems to participate passively in reentrant excitation during torsades de pointes.

DOI： 10.1046/j.1460-9592.2001.01247.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL SCIENCE ASIA  

This report describes the clinical management of 2 patients with ventricular fibrillation (VF) who received inappropriate shocks from an implantable cardioverter defibrillator (ICD) due to T-wave oversensing. Cardiac sarcoidosis was confirmed as the underlying heart disease in 1 patient and idiopathic dilated cardiomyopathy in the other. Within 2 months after ICD implantation, both patients received several inappropriate shocks during sinus rhythm. Stored electrograms showed decreased R-wave amplitudes and increased T-wave amplitudes. The ICD sensed both R- and T-waves as ventricular activation, which met the rate criteria for VF treatment. Reprogramming the sensing threshold in association with administration of a drug to slow the heart rate decreased the incidence of the inappropriate shocks in both patients, but these palliative measures did not completely suppress the inappropriate shocks. To avoid T-wave oversensing, the repositioning or adding of a sensing lead is required. The potential risk of T-wave oversensing in ICD patients who have small R-wave amplitudes should be recognized.

DOI： 10.1253/jcj.65.685

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL SCIENCE ASIA  

Beta-blockade is widely reported to reduce the incidence of syncope in 75-80% of patients with congenital long QT syndrome (LQTS). However, despite full-dose beta -blockade, 20-25% of patients continue to have syncopal episodes and remain at high risk for sudden cardiac death. In some patients refractory to beta -blockade, the recurrence of arrhythmias is successfully prevented by left stellate ganglionectomy, and also by labetalol, a nonselective beta -blockade with alpha1-blocking action. These observations suggest that not only beta -adrenoceptors, but also alpha1-adrenoceptors, play an important pathogenic role, especially under sympathetic stimulation, in LQTS. The clinical effects of alpha1-blockade in congenital LQTS were investigated in 8 patients with familial or sporadic LQTS. Two measurements of the QT interval were taken, from the QRS onset to the T wave offset (QT) and from the QRS onset to the peak of the T wave (QTp). Using the Bruce protocol, an exercise test was performed after administration of beta -blockade alone and again after administration of alpha1-blockade. The following were compared: (1) Bazzet-corrected QT (QTc) and QTp (QTpc) intervals in the supine and standing position before exercise and in the early recovery phase after exercise; and (2) the slopes (reflecting the dynamic change in the QT interval during exercise) of the QT interval to heart rate were obtained from the linear regression during the exercise test. In the supine position before exercise, there was no change in the QTc before or after the addition of alpha1-blockade (498 +/- 23 vs 486 +/- 23 ms [NS]). However, in the upright position before exercise and in the early recovery phase after exercise, QTc was significantly shortened from 523 +/- 21 to 483 +/- 22 ms (p&lt;0.01), and from 521&lt;plus/minus&gt;30 to 490 +/- 39 ms (p&lt;0.01), respectively, by &lt;alpha&gt;1-blockade. The QTpc was unchanged in any situation. Consequently, QTc-QTpc was significantly shortened by alpha1-blockade in the upright position before exercise and in the early recovery phase after exercise (131 +/- 36 to 105 +/- 37 ms (p&lt;0.05), and 132&lt;plus/minus&gt;29 to 102 +/- 31 ms (p&lt;0.01), respectively). The slopes of the QT interval-heart rate relation by linear regression became significantly steeper from -2.23&lt;plus/minus&gt;0.38 to -2.93 +/-0.76 (p&lt;0.01) with the addition of &lt;alpha&gt;1-blockade. The findings suggest that the addition of alpha1-blockade attenuated the exercise-induced prolongation of the QT interval and that the rate adaptation of the QT interval to heart rate during exercise was improved. This indicates that additional treatment with alpha1-blockade may be beneficial to prevent cardiac events in LQTS patients in whom ventricular arrhythmia is resistant to beta -blockade.

DOI： 10.1253/jcj.65.654

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Language：Japanese   Publisher：The Japanese Society of Electrocardiology  

DOI： 10.5105/jse.21.336

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

A 71-year-old man who experienced aborted sudden death was referred to our hospital, Coronary artery disease and cerebral accident were ruled out by conventional tests. The 12-lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V-1 to V-3, Double ventricular extrastimuli at coupling intervals &gt;180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V-1 to V-3, and visible T wave alternans was induced in leads V-2 and V-3 at a dose of 450 mg, Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V-2 and V-3, Class I antiarrhythmic drug-related T wave alternans has been reported rarely in Brugada syndrome, but it may represent enhanced arrhythmogenicity of VF, We need to monitor closely and study the clinical implications of T wave alternans in Brugada syndrome.

DOI： 10.1046/j.1540-8167.2001.00493.x

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Language：English   Publisher：ELSEVIER SCIENCE INC  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

Sustained monomorphic ventricular tachycardia (VT) can be frequently entrained and interrupted with rapid pacing and the mechanism of the pacing-induced interruption is considered to be due to orthodromic block.
This study focused on the incidence of VT which was interrupted at a critical cycle length and was characterized by an abrupt loss of constant fusion in the surface electrocardiogram (ECG), and the role of orthodromic block as the cause of such characteristic change and interruption of VT M as analyzed.
Among 45 consecutive patients with symptomatic VT, rapid pacing was performed in 43 VTs of 39 patients. The exit was mapped as the earliest site of the activation during VT and an electrode catheter was located at the site. Rapid pacing was performed at progressively shorter cycle lengths in steps of 10 msec until VT was interrupted and the timing of the orthodromic and direct capture was compared at the exit.
Abrupt loss of constant fusion was observed in 25 of 39 patients (64.1%). and the loss was invariably associated with interruption of VT. When the timings of the activation of the exit were compared, which were measured from the preceding (n-1) stimulus as the time reference, the direct capture was relatively delayed compared to that of the orthodromic capture. This finding suggests that orthodromic
In the remaining 13 patients (35.9%), the surface ECG showed a gradual transition into the fully paced QRS morphology. The direct capture M as confirmed in the non-fused beats, but it was not necessarily associated with interruption of VT. The interval from the stimulus to the entrained electrogram at the exit showed a gradual prolongation until the exit was finally captured directly from the pacing site.
The confirmation of constant fusion followed by abrupt loss in ECG can be a reliable hallmark of orthodromic block as the cause of the interruption of VT during transient entrainment at a critical paced cycle length.

DOI： 10.1536/jhj.42.67

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Brugada Syndrome and Vasospastic Angina. We present two patients with vasospastic angina and Brugada-type ECG abnormalities. The first patient complained of chest pain, and transient ST segment elevation was confirmed on EGG. Coronary angiogram showed no organic stenosis. The second patient had syncopal episodes following anginal chest pain, and the same symptoms were reproduced by intracoronary acetylcholine injection that Induced vasospasm. In both patients, ECG at rest showed ST segment elevation in leads V-1 and V-2 and a right bundle branch block pattern that were accentuated by a Class I antiarrhythmic drug. Ventricular fibrillation also was induced by programmed electrical stimulation. Susceptibility to ventricular fibrillation can be modulated by the interaction of coronary vasospasm with Brugada syndrome or vice versa; therefore, it is important to study the clinical implications of the coexistence of the two diseases in such patients.

DOI： 10.1046/j.1540-8167.2001.00108.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL SCIENCE ASIA  

A 49-year-old man was referred fur further treatment of sustained monomorphic ventricular tachycardia (VT) associated with cardiac sarcoidosis. During an electrophysiologic study (EP), dl-sotalol suppressed the spontaneous VT and prevented induction of VT. However, when predonisolone treatment was started, monomorphic VT recurred frequently. To terminate the VT, a temporal pacing lead was placed at the apex of the right ventricle, and programmed electrical stimulation was attempted from the lead. During the EP study, 2 different monomorphic VTs were repetitively induced and both types were able to be terminated by rapid ventricular pacing; in one of the VT morphologies, constant and progressive fusion was obvious during the ventricular pacing. Some monomorphic VTs associated with cardiac sarcoidosis are due to reentry with an excitable gap, but the clinical efficacy of EP-guided antiarrhythmic drug treatment seems to be less certain during steroid therapy. In the present case, a defibrillator device was implanted to prevent a possible arrhythmic event.

DOI： 10.1253/jcj.64.635

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

To study the role of antitachycardia burst pacing in patients with reentrant pleomorphic ventricular tachycardia (VT) associated with non-coronary artery diseases, the efficacy of antitachycardia pacing and appropriate antitachycardia pacing cycle length were evaluated in each pleomorphic VT morphology of seven patients.
Seven patients were included in this study, Clinically documented pleomorphic VTs were reproduced in an electrophysiologic study. For each VT, rapid ventricular pacing was attempted from the apex of the right ventricle at a cycle length which was 20 ms shorter than that of VT and repeated after a decrement of the cycle length in steps of 10 ms until the VT was terminated or accelerated.
All 16 VTs could be entrained by the rapid pacing, and 13 of the 16 VTs (81 %) were terminated, whereas pacing-induced acceleration was observed in the other 3 VTs of the 3 patients. VT cycle length (VTCL), block cycle length (BCL) which was defined as the longest VT interrupting paced cycle length, %BCL/VTCL and entrainment zone which was defined as VTCL minus BCL, varied in each VT morphology of each patient. In two patients, antitachycardia pacing was effective in all VT morphologies and the maximum difference of the %BCL/VTCL among the pleomorphic VTs was less than 10 %. Thus, antitachycardia pacing seemed to be beneficial for these patients. In the other 5 patients, a difference of more than 10 % in %BCL/VTCL was observed among the pleomorphic VT morphologies and/or at least one VT morphology showed pacing-induced acceleration. Compared to the 13 terminated VTs, three accelerated VTs had a wide entrainment zone [160 +/- 34 vs 90 +/- 48 ms, p &lt; 0.04] and small %BCL/VTCL [61 +/- 6 vs 77 +/- 11 %, p &lt; 0.03].
In pleomorphic VTs associated with non-coronary artery diseases, responses to rapid pacing was not uniform, VT might be terminable or accelerated even in the same patient. We need to pay close attention when programming antitachycardia pacing in patients with pleomorphic VT.

DOI： 10.1536/jhj.41.313

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

In idiopathic left ventricular tachycardia (ILVT), the reentrant circuit is considered to involve the Purkinje system, and the Purkinje potential (P-potential) appears to be a marker for successful ablation. However, the characteristics of the reentrant circuit in ILVT have not yet been defined. In 2 cases of ILVT, we performed detailed mapping along the left ventricular septum during VT and sinus rhythm. ILVTs were successfully ablated at the posteroapical area of the left ventricular septum where the high frequency P-potential was recorded and this portion was considered to be the exit site of the reentrant circuit. A small P-potential was also recorded at the portion proximal to the exit site, and it preceded the P-potential at the exit site. However, the local ventricular electrogram at the exit site preceded that at the proximal site during VT. Moreover, the small P-potential was orthodromically entrained by ventricular pacing from the proximal site. These findings suggest that the reentry circuit of ILVT appeared to have considerable size.

DOI： 10.1016/S0022-0736(00)80076-X

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL SCIENCE ASIA  

An implantable cardioverter defibrillator (ICD) was implanted in 2 patients with ventricular tachyarrhythmia related to old myocardial infarction, and defibrillation tests were attempted at the time of ICD implantation and at 2 or 4 weeks after the operation. Ventricular fibrillation (VF) was induced by T-wave shocks, but the amplitude of the ventricular electrogram was different in each VF. In most of the VFs with large ventricular electrograms, the local activity was appropriately detected. However, many undersensed beats were observed in other VFs that had fine ventricular electrograms and a longer time was needed before delivering the shock. The amplitude of the ventricular electrogram might be small in some cases of VF and this might result in undersensing and/or unsuccessful defibrillation. Close attention must be paid to the amplitude of ventricular activation in each VF to avoid possible difficulty in ICD therapy.

DOI： 10.1253/jcj.63.1007

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC  

The effective refractory period was shorter in patients with than without chronic atrial fibrillation (AF). The effective refractory period was prolonged, and at 12 and 24 hours after cardioversion of AF it was the same as the subjects without AF.

DOI： 10.1016/S0002-9149(99)00544-5

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

A 72-year old male with an old myocardial infarction who had drug-refractory ventricular tachyarrhythmias received an implantable cardioverter-defibrillator (ICD). The patient did not take his prescribed beta-blocking agent for two days, following which he experienced six discrete shocks for spontaneous VT while riding his bicycle. Both 5J and 30J cardioversions were ineffective at terminating the VT and accelerated VT developed following the shocks. After admission, an electrophysiological study was performed while he was taking the P-blocking agent, both low and high energy cardioversions reproducibly terminated the clinical VT without showing any accelerated rhythm. These findings suggest that the increase in sympathetic discharge may enhance the proarrhythmic potential of ICDs.

DOI： 10.1536/jhj.40.665

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

A 33 year-old woman was referred to our hospital for further treatment of ventricular tachycardia (VT). During treatment with amiodarone (200 mg/day), clinical VT at the cycle length of 510 ms was induced. During the VT, rapid ventricular pacing was repeated at progressively shorter cycle lengths after a decrement of 10 ms steps. The VT was entrained by the rapid pacing and reproducibly terminated at a. paced cycle length of 380 ms. Four weeks after reducing the amiodarone to 100 mg/day, programmed stimulation was repeated. The VT with the same morphology but with a slightly shorter cycle length of 480 ms was again induced. However, at this time, rapid pacing from the same site could not terminate VT and transient acceleration developed at a shorter paced cycle length of 260 ms. The QT (QTc) interval, effective refractory period at the pacing site and width of the paced QRS complex were similar before and after changing the amiodarone treatment. The most characteristic change of VT in the second study was a widening of the entrainment zone, which was calculated as the difference between VT cycle length and the longest pacing cycle length which interrupts VT during the entrainment (from 130 to &gt; 220 ms), and it may be explained by the preferential shortening of the action potential duration and/or facilitation of the depressed cell to cell conduction within the reentry circuit. Amiodarone must exert a preferential action in the reentry circuit and modulate the conduction property as well as the effective refractory period. We should pay close attention to the efficacy of antitachycardia pacing during the modification of amiodarone treatment.

DOI： 10.1536/jhj.40.471

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE INC  

OBJECTIVES The purpose of this study was to investigate the electrophysiologic mechanism(s) that underlie the transition of one or more short-long (S-L) cardiac, sequences to ventricular tachyarrhythmias (VTs) in the long QT syndrome.
BACKGROUND One or more S-L cardiac cycles, usually the result of a ventricular bigeminal rhythm, frequently precedes the onset of VT in patients with either normal or prolonged QT interval. Electrophysiologic mechanisms that underlie this relationship have not been fully explained.
METHODS We investigated electrophysiologic changes associated with the transition of a S-L cardiac sequence to VT in the canine anthopleurin-A model, a surrogate of LQT3. Experiments were performed on 12 mongrel puppies after administration of anthopleurin-A. Correlation of tridimensional activation and repolarization patterns was obtained from up to 384 electrograms. Activation-recovery intervals were measured from unipolar electrograms and were considered to represent local repolarization.
RESULTS We analyzed 24 different episodes of a S-L sequence that preceded VT obtained from 12 experiments. The VT followed one S-L sequence (five episodes), two to five S-L sequences (12 episodes) and more than five S-L sequences (seven episodes). The single premature ventricular beats coupled to the basic beats were consistently due to a subendocardial focal activity (SFA). There were two basic mechanisms for the development of VT after one or more S-L sequences: 1) in 10 examples of a S-L sequence due to a stable unifocal bigeminal rhythm, the occurrence of a second SFA, which arose consistently from a different site, infringed on the pattern of dispersion of repolarization (DR) of the first SFA to initiate reentrant excitation; 2) in the remaining 14 episodes of a S-L sequence, a slight lengthening (50 to 150 ms) in one or more preceding cycle lengths (CLs) resulted in alterations of the spatial pattern of DR at key sites to promote reentry. The lengthening of the preceding CL produced differentially a greater degree of prolongation of repolarization at midmyocardial and endocardial sites compared with epicardial sites with consequent increase of DR. The increased DR at key adjacent sites resulted in the development of de novo zones of functional conduction block and/or slowed conduction to create the necessary prerequisites for successful reentry.
CONCLUSIONS The occurrence of VT after one or more S-L cardiac sequences was due to well defined electrophysiologic changes with predictable consequences that promoted reentrant excitation. (C) 1999 by the American College of Cardiology.

DOI： 10.1016/S0735-1097(98)00700-1

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC  

We recently reported a marked QT prolongation and torsade de pointes (TDP) induced by an intracoronary acetylcholine (ACh) administration in patients with long QT syndrome, but the mechanism was not determined. In the present study, the effect of atropine on the ACh-induced QT prolongation and TDP was studied in long QT syndrome. Nine patients with congenital long QT syndrome were studied. ACh at doses of 20, 50, and 100 mu g were injected in a stepwise manner into the left main coronary artery, and the changes in the QT interval were measured. In 4 of the 9 patients, ACh administration at a dose of 100 mu g was repeated after an intravenous atropine administration at a dose of 0.5 mg. The QT intervals were measured using 12-lead electrocardiograms, and the data were compared before and after atropine administration. The coronary angiograms were normal and coronary spasm was not induced by ACh in all patients. The intracoronary administration of ACh at a dose of 100 mu g significantly prolonged the corrected QT interval (QT(c)), from 511 +/- 26 to 629 +/- 40 ms (p &lt;0.05). In 5 of the 9 patients, TDP was induced and was spontaneously terminated within 10 seconds (n = 4) or required direct-current shock (n = 1). After atropine administration, intracoronary ACh at the same dose resulted in no QT prolongation, and the QT(c) interval remained unchanged (525 +/- 29 vs 520 +/- 21 ms before and after atropine), and no TDP was induced. These findings indicate that the muscarinic receptor is involved in ACh-induced QT prolongation and TDP, both of which were prevented by the atropine administration. (C)1999 by Excerpta Medica, Inc.

DOI： 10.1016/S0002-9149(98)00976-X

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

An implantable cardioverter defibrillator (ICD) was implanted in a patient with ventricular fibrillation (VF) related to old myocardial infarction. During VF, amplitude of ventricular activation was small, and the ventricular sensitivity at 1.2 mV failed to detect several small ventricular activations. When the sensitivity was changed to 0.3 mV, both under- and oversensed beats occurred during VF, and at the ventricular sensitivity of 0.15 mV, the undersensed beats disappeared while oversensed beats markedly increased. Defibrillation test was repeated one and four weeks after the implantation, and these inappropriate beats were minimized at the ventricular sensitivity of 0.3 mV. We should pay attention to the amplitude of ventricular activation to avoid possible trouble in ICD therapy.

DOI： 10.1536/jhj.40.87

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

DOI： 10.1016/S0022-0736(99)90076-6

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Tachycardia-dependent QT/T alternans occurs in patients with the congenital or idiopathic form of long-QT syndrome (LQTS) and may presage the onset of polymorphic ventricular tachyarrhythmias. To examine the electrophysiological basis of arrhythmogenicity of QT/T alternans in LQTS, the tridimensional repolarization pattern of QT/T alternans was studied in the anthopleurin-A model of LQTS, a surrogate for LQT3. In 11 anesthetized mongreal puppies, tridimensional repolarization and activation patterns were analyzed from 256 to 384 unipolar electrograms. Cardiac repolarization was evaluated as the activation-recovery interval (ARI) of local electrograms. To induce QT/T alternans, the pacing cycle length (CL) was abruptly shortened in steps of 50 ms from a basic drive of 1000 ms, ARIs were calculated at epicardial (Epi), midmyocardial (Mid), and endocardial (End) sites. ARI restitution at each site was assessed by using a single premature stimulation delivered after the basic drive. ARI alternans occurred at longer CLs at Mid sites compared with End and Epi sites, and the magnitude of alternans at Mid sites was greater. Two factors contributed to the modulation of ART during QT/T alternans: (1) differences in restitution kinetics at Mid sites, characterized by larger Delta ARI and a slower time constant ( tau), and (2) differences in diastolic intervals resulting in different input to restitution at the same constant CL, These 2 factors could explain not only the onset of alternans at Mid sites at longer CLs but also the critical observation that ARI dispersion between Epi and Mid sites during alternans was greater than during the slower basic CL. Marked ARI alternans could be present in local electrograms without manifest alternation of the QT/T segment in the surface EGG. The latter was seen at critically short CLs associated with reversal of the gradient of ARI between Epi and Mid sites, with a consequent reversal of polarity of the intramyocardial QT wave in alternate cycles. The arrhythmogenicity of QT/T alternans was primarily due to the greater degree of spatial dispersion of repolarization during alternans than during slower rates not associated with alternans. This could result in functional conduction block and reentrant ventricular tachyarrhythmias during the fixed drive associated with alternans.

DOI： 10.1161/01.RES.83.6.614

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

In nine patients who had inducible monomorphic sustained ventricular tachycardia (VT), rapid pacing was performed in 11 episodes of morphologically distinct VT at progressively shorter cycle lengths and VT was interrupted at a critical cycle length. The VT interrupting critical cycle length was defined as the block cycle length (BCL) and the effect of Class I antiarrhythmic drugs were examined. Both the VT cycle length (VTCL) and the BCL were prolonged after administration of either drug. The overall mean ratio of the BCL to the VTCL was unchanged after procainamide administration, but increased after the use of mexiletine. The ratio, however, varied in individual VTs and the BCL after treatment with Class I antiarrhythmic drugs could not be predicted from the ratio baseline value, although the ratio was always &gt; 60% and the hazard of VT acceleration might be avoided if the BCL is used.

DOI： 10.1111/j.1540-8159.1998.tb00265.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

Radiofrequency catheter ablation was attempted in a patient with atrioventricular nodal reentrant tachycardia (AVNRT). AVNRT tl as easily inducible but an intermittent loss of the atrial activation was observed during AVNRT suggesting the presence of a proximal common pathway. During sinus rhythm, a relatively delayed activation that was compatible with a slow potential, was recorded anterior to the ostium of coronary sinus, and radiofrequency catheter ablation application (20 watts) to the site induced junction tachycardia. After an additional radiofrequency catheter ablation application to close the site, AVNRT became noninducible without deterioration of atrioventricular conduction through a fast pathway. This is the first case in which radiofrequency catheter ablation application to the slow potential recording site has been successful, even in AVNRT having a proximal common pathway.

DOI： 10.1111/j.1540-8159.1998.tb00195.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

In 23 consecutive patients, radiofrequency (RF) ablation was used as treatment for idiopathic ventricular tachycardia (VT) originating from the outflow tract of the right ventricle. In this study, rye focused on the repetitive ventricular response (&gt; 5 consecutive QRS beats during RF application). The incidence and clinical implications of the repetitive ventricular response were examined through the results of endocardial mapping and RF ablation. VT origin was mapped as the earliest activation site during VT, and it was determined within 0.5 X 0.5 cm (narrow site) in 13 patients and wider than 0.5 x 0.5 cm (wide origin) in the other 10 patients. The repetitive ventricular response was induced during application of RF current in 14 of 23 patients (61%), and it was more frequently observed in VT from a wide origin (100%) than in the VT from a narrow site (31%). The QRS morphology of the repetitive ventricular response was identical to that of clinical VT. As RF application was continued and/or repeated, the RR interval of the repetitive ventricular response was gradually prolonged, the number of consecutive QRS complexes was decreased, and clinical VT was finally eliminated. The overall success rate of RF ablation was 96% (22/23 patients), and no complications were observed. In conclusion, a repetitive ventricular response was frequently/observed in idiopathic right VT. The changing pattern of repetitive ventricular response, slowing, and/or disappearing was consistent with successful RF ablation.

DOI： 10.1111/j.1540-8159.1998.tb00122.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BRITISH MED JOURNAL PUBL GROUP  

A 41 year old man with incomplete right bundle branch block and persistent coved-type ST elevation in the right precordial leads during sinus rhythm had an episode of syncope while driving. He had never had syncope before and there was no family history of sudden cardiac death. Ventricular fibrillation was induced during electrophysiological study (EPS) by double extrastimuli applied to the right ventricle. Disopyramide was effective in preventing ventricular fibrillation during EPS. beta Adrenoceptor stimulation manifested bifid T waves and reduced ST segment elevation in right precordial leads. Simultaneously recorded monophasic action potential (MAP) duration at 90% repolarisation did not change in the right ventricular outflow tract, while it shortened in the left ventricular septum. These findings suggest that right precordial bifid T waves might result from relatively early repolarisation of the left ventricles. Moreover the gradient of action potential duration might explain the mechanism of ST segment abnormalities in a patient with Brugada syndrome.

DOI： 10.1136/hrt.79.3.305

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

Two patients with long QT syndrome, who bad episodes of syncope, underwent recordings of the monophasic action potential (MAP) from the right ventricle. Intracoronary administration of acetylcholine (ACh) induced prolongation of MAP duration and caused Torsade de Pointes (Tdp) in both patients. In one patient, intravenous atropine administration did not induce any change in MAP duration. In the other patient, ACh was administered after atropine. According to the results of the present study, abnormal regulation of the muscarinic receptor-mediated K-channel may be involved in the mechanism causing prolongation of MAP duration caused by ACh administration.

DOI： 10.1536/ihj.39.225

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BRITISH MED JOURNAL PUBL GROUP  

Background-Recent molecular biological investigations have identified abnormal genes in familial forms of long QT syndrome, but in bradycardia dependent acquired long QT syndrome, no such genetic abnormality has yet been identified.
Objective-To investigate the relation between the responses of QT interval to pacing change and to disopyramide.
Methods-This study included 13 patients with bradyarrhythmia who had undergone pacemaker implantation. The patients were divided into two groups: group I (n = 8), patients with QT prolongation (QT interval greater than or equal to 500 ms) during bradycardia; group II (n = 5), patients without QT prolongation (QT interval &lt; 500 ms) during bradycardia. The responses of QT interval caused by the change of pacing rate were determined and compared with the changes of the QT interval after disopyramide administration.
Results-The QT interval in group I was significantly longer than that in group II when the pacing rate was decreased from 110 to 50 beats/min: mean (SD) 451 (16) v 416 (17) ms at 90 beats/min (p = 0.0033), and 490 (19) v 432 (18) ms at 70 beats/min (p = 0.0002), respectively. The QT interval was prolonged significantly by disopyramide in both groups, but the change was more pronounced in group I than in group II: 78 (33) v 35 (10) ms (p &lt; 0.05).
Conclusions-This study suggests that the patients showing bradycardia dependent QT prolongation are also more markedly affected by disopyramide and that abnormal potassium channel may be the underlying mechanism.

DOI： 10.1136/hrt.79.1.56

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

In a patient with nonischemic ventricular tachycardia (VT), VT was entrained and the conduction time from the pacing site to the entrained local electrogram showed a rate dependent shortening and its degree affected by the pacing site, The QRS complex, which was entrained by the last pacing stimulus, was constant and identical to that of VT and no rate dependent facilitated conduction was observed when the heart was paced at similar paced cycle lengths during sinus rhythm. As the mechanism of the-shortening of the conduction time through the reentrant circuit, a shift of-the entrance seems most likely.

DOI： 10.1111/j.1540-8159.1998.tb01071.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Churchill Livingstone Inc.  

Congenital or idiopathic long QT syndrome is characterized by a frequently lethal ventricular arrhythmia called torsades de pointes (TdP) as well as a prolonged QT interval. The long QT interval related to an abnormal gene of the Na+ channel has been shown to be shortened by mexiletine. However, the action of K+ channel openers on the QT interval associated with abnormal genes of the K channel has yet to be studied. Seven patients of five families with long QT syndrome were included in this study, of whom six had syncope and six had documented TdP. Either long QT interval or sudden cardiac death had been observed in family members of all seven patients. At 1 to 3 weeks after admission, when TdP or frequent ventricular arrhythmia had subsided, nicorandil, an ATP-sensitive K channel opener, was administered orally at a dose of 15 mg/day in five patients and at 30 mg/day in the remaining two patients, and the effects were assessed on the third day after drug administration. In four patients, the effective refractory period was measured in the right ventricle before and after administration of K channel opener administration. The QT interval (QTc) prior to administration of the K channel opener was 0.60 ± 0.09 ms (mean ± SD) (0.61 ± 0.10 second(1/2)), which was shortened to 0.54 ± 0.05 ms (0.55 ± 0.06 second(1/2)) on the third day of drug administration (P &lt
.05 for both): 10.4 ± 8.0% (8.6 ± 5.5%). The QT interval at varying preceding R-R intervals on Holter electrocardiograms showed a shift toward the right as a result of the drug administration. The effective refractory period showed a significant prolongation, 256 ± 26 ms versus 280 ± 22 ms before and after drug administration, respectively (P &lt
.05). Intravenous administration of nicorandil resulted in no significant change in heart rate or blood pressure, while QTc showed a tendency to shorten, but nonsignificantly (P = .08). However, a hump on the monophasic action potential was abolished, especially at the long preceding R-R interval induced by premature stimulation of the ventricle. It is concluded that nicorandil shortens the QT interval slightly when administered orally, whereas the effective refractory period shows a slight prolongation. The physiologic and clinical significance of these effects needs to be studied further.

DOI： 10.1016/S0022-0736(98)90042-5

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER HEART ASSOC  

Background The long-QT syndrome (LQTS) is an electrophysiological (EP) entity characterized by prolongation of cardiac repolarization and the occurrence of polymorphic ventricular tachyarrhythmias (VTs), sometimes with a twisting QRS morphology, better known as torsade de pointes (TdP). In the present study, detailed analysis of ventricular tridimensional activation patterns during nonsustained TdP V-T was performed to provide an EP mechanism of the periodic transition in QRS axis.
Methods and Results The studies were conducted with the anthopleurin-A canine model of LQTS. Tridimensional isochronal maps of ventricular activation were constructed from 256 bipolar electrograms obtained from the use of 64 plunge needle electrodes. In 26 episodes of nonsustained TdP VT, detailed activation maps could be accurately constructed during QRS-axis transitions in surface ECGs. The initial bed of all VTs consistently arose as a subendocardial focal activity, whereas subsequent beats were due to reentrant excitation in the form of rotating scrolls. The VT ended when reentrant excitation was terminated. In 22 of 26 episodes, the transition in QRS axis coincided with the transient bifurcation of a predominantly single rotating scroll into two simultaneous scrolls involving both the right ventricle and left ventricle separately. The common mechanism for initiation or termination of bifurcation was the development of functional conduction block between the anterior or posterior right ventricle free wall and the ventricular septum. In 4 of 26 episodes, a fast polymorphic VT, with an apparent shift in QRS axis, was due to a predominantly single localized circuit that varied its location and orientation from beat to beat, with the majority of ventricular myocardium being activated in a centrifugal pattern.
Conclusions The study provides for the first time an EP mechanism for the characteristic periodic transition of the QRS axis during TdP VT in the LQTS.

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BRITISH MED JOURNAL PUBL GROUP  

Objective-To assess the long term outcome of radiofrequency (RF) catheter ablation for idiopathic ventricular tachycardia (VT) originating from the outflow tract of the right ventricle, with special reference to the morphological variation in the VT-QRS complexes.
Patients-13 patients whose ventricular tachycardia was treated with RF ablation were followed up more than 18 months after RF ablation.
Results-Endocardial mapping revealed the various extensions of ventricular tachycardia origin (from 0.5 x 0.5 cm to 2.0 x 2.0 cm) in which the earliest local electrogram was recorded during ventricular tachycardia. In all five tachycardias from a relatively wider origin (more than 0.5 x 0.5 cm) and in four of eight from a narrow origin (&lt;0.5 x 0.5 cm), subtle morphological variation in the VT-QRS complexes was observed. In tachycardias with morphological variation, the local electrogram at the tachycardia origin also showed concomitant variation in morphology and activation sequence. Ventricular tachycardia from a narrow site was eliminated by RF ablation to the confined site, but a larger number of RF applications was required in tachycardias from a wider origin. All 13 tachycardias were successfully ablated by RF current, and during the follow up period of 28.2 (SD 7.2) months, recurrence was observed in only one patient who had a wider origin.
Conclusions-Long term efficacy of RF ablation was excellent in idiopathic ventricular tachycardia originating from the outflow tract of the right ventricle. Subtle morphological variations were frequently observed in this type of ventricular tachycardia, and about half of them represented a relatively wider arrhythmogenic area.

DOI： 10.1136/hrt.78.3.255

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：FUTURA PUBL CO  

Two different monomorphic VTs were observed in two patients after a corrective operation for tetralogy of Fallot. The activation pattern of the wavefronts of the two VTs were different: in a counter-clockwise direction around the anatomical obstacle due to a ventriculotomy of the right ventricle in one VT; and in a clockwise direction around the same obstacle in the other VT. The different revolutions of the wavefronts could be the mechanism for the different morphologies of VT.

DOI： 10.1111/j.1540-8159.1997.tb04250.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

In reentrant ventricular tachycardia CVT), the postpaced return cycle (RC) during transient entrainment at a pacing site far from the central common pathway is longer than the VT cycle length (VTCL), when VT is represented by a figure-eight model. However, the reentrant circuit has not been fully elucidated.
The purpose of this study was to present VT in which the postpaced RC became identical to VTCL during transient entrainment while fusion is evident in the surface electrocardiogram (ECG).
Among 38 patients with inducible reentrant VTs who underwent electrophysiologic study (EPS), 10 VTs of six patients were selected. All patients had underlying heart diseases: dilated cardiomyopathy (n=2), coronary artery disease (n=1), postoperative tetralogy of Fallot (TOF; n=2), and arrhythmogenic right ventricular dysplasia (n=1). Catheter mapping was performed to demonstrate that the site of origin was distant from the pacing site.
The cycle length of induced VT (n=19 VTs) was 380 +/- 41 msec. Five patients (83%) had two morphological VTs; one a left bundle branch block (LBBB) and the other a right bundle branch block (RBBB) pattern. During rapid pacing, constant fusion was observed in all VTs, but the postpaced RC was identical to VTCL. In 2 patients (4 VTs), the revolution of wavefronts around an anatomical obstacle (scar of myotomy in TOF, and infarction) was demonstrated.
The fact that the postpaced RC was identical to VTCL but showed fusion in the surface ECG can be explained by macro-reentry. The pacing site must be located at the preferential route of the macroreentrant circuit.

DOI： 10.1536/ihj.38.369

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：BRITISH MED JOURNAL PUBL GROUP  

A transvenous implantable cardioverter defibrillator (ICD) was implanted into a 58 year old woman with idiopathic dilated cardiomyopathy who had drug refractory monomorphic ventricular tachycardia (VT). Antitachycardia pacing failed to terminate the VT; termination was attempted at 24 J, which was above the defibrillation threshold. When cardioversion at 24 J was delivered, VT with a different morphology and slower rate was reproducibly initiated. At 3 J, however, the original VT was successfully terminated without initiation of the slower VT. A new VT may be induced by high energy cardioversion. This may be a manifestation of the proarrhythmic potential of ICDs.

DOI： 10.1136/hrt.77.4.373

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

An electrophysiologic study was attempted in a patient who experienced cardiac arrest. Programmed electrical stimulation from the right ventricle, without the use of any drugs, induced ventricular fibrillation (VF) twice. Disopyramide prevented the induction of ventricular arrhythmia by rendering VF to a nonsustained polymorphic ventricular tachycardia when administered at 300 mg/day, and noninducible at 400 mg/day. However, ST segment elevation and the rSr' pattern in leads V1-3 characteristic of Brugada syndrome became exaggerated by disopyramide. Disopyramide exerted discrepant action on the electrocardiographic (ECG) abnormalities and induction of VF in this patient, suggesting the efficacy of antiarrhythmic drugs assessed by an electrophysiologic study may be unrelated to ECG abnormalities in cases of Brugada syndrome.

DOI： 10.1016/S0022-0736(97)80021-0

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Language：English   Publisher：CELL PRESS  

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RF catheter ablation was performed in 16 patients with nonreentrant idiopathic VT originating from the RVOT. All documented VT was monomorphic, but subtle morphological variation in the VT-QRS complex was observed in 10 (63%) of 16 patients. Through endocardial mapping, VT Origin was determined within a narrow site (&lt; 0.5 X 0.5 cm) in 4 of the 10 patients with the morphological variation. In the other 6 of 10 patients, the origin extended to an area of &gt; 0.5 X 0.5 cm. In VT with morphological variation, the local electrogram at the site of VT origin also showed variation in morphology and activation sequence. For VT of narrow origin, RF application to the site eliminated the TIT. However, in VT from a wide arrhythmogenic area, RF current had to be delivered to 3-7 distinct sites to cover the possible origin, and specific QRS configuration of VT and/or PVC was ablated at each of the earliest activation site. All but one VT were successfully ablated by RF current. Subtle morphological variation was frequent in this type of VT, and about half were associated with a wide arrhythmogenic area. Precise mapping and analysis of the efficacy of each RF application might be helpful to better understand the relationship between subtle changes of VT-QRS morphology and their origins.

DOI： 10.1111/j.1540-8159.1997.tb06177.x

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE INC  

Objectives. The action of mexiletine on diseased myocardium was assessed in reentrant ventricular tachycardia (VT).
Background. Whether class Ib antiarrhythmic agents exert a preferential action on the central common pathway of reentrant ventricular tachycardia has not yet been studied in humans.
Methods. In 10 consecutive patients (7 with a previous myocardial infarction, 3 with nonischemic disease), VT was induced and entrained with rapid pacing. The orthodromic conduction time was measured from stimulus to the entrained electrogram at the exit from the presumed central common pathway (i.e., the earliest site of activation). Mexiletine at 125 to 250 mg was administered intravenously, and when VI with the same configuration was induced, the study was repeated. The action of mexiletine on the central common pathway was assessed from the changes in VT cycle length and orthodromic conduction time. The effects on QRS complex duration, local conduction time between the exit and the pacing site and duration of the local electrogram were compared between normal and diseased myocardium.
Results. Mexiletine prolonged the VT cycle length in all patients, from (mean +/- SD) 316 +/- 30 to 360 +/- 64 ms (mean change 20 +/- 7%, p &lt; 0.001); during entrainment of VT, the orthodromic conduction time was prolonged, from 306 +/- 58 to 367 +/- 89 ms (mean change 18 +/- 9%, p &lt; 0.001). These changes were highly correlated (r = 0.95, p &lt; 0.001). QRS duration changed little (4 +/- 3%), and local conduction time showed no change. The duration of the fragmented electrogram width was prolonged by mexiletine: from 146 +/- 50 to 176 +/- 56 ms (mean change 23 +/- 8%, during VT, p &lt; 0.001). Only a slight change occurred in the effective refractory period, both at the pacing site and at the exit.
Conclusions. Mexiletine caused little change in conduction time in normal myocardium but prolonged VT cycle length, orthodromic conduction time and duration of the local electrogram at the earliest site of activation of VT. From these findings, a preferential action of mexiletine on diseased myocardium was suggested but seemed to occur only at higher frequencies during tachycardia. (C) 1996 by the American College of Cardiology

DOI： 10.1016/S0735-1097(96)00375-0

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

The most common mechanism of monomorphic sustained ventricular tachycardia (VT) is reentry with an excitable gap, but the electrophysiological properties and response to antiarrhythmic agents in the area of slow conduction are not yet fully known.
The conduction time through the area of slow conduction may show a frequency-dependent delay in some VT but in others, constant conduction time was observed as the paced cycle length was decreased while VT was entrained. VT with a so-called decremental property could be terminated more often with rapid pacing with less risk of acceleration of the VT rate.
When the excitable gap was estimated by the width of the zone of entrainment: defined as the difference between the cycle length of VT and the longest VT-interrupting paced cycle length during transient entrainment, there was no difference in the width of the zone of entrainment between the responders (VT induction was prevented with drugs) and the non-responders (VT remained inducible). The cycle length of VT was not a predictor of drug-efficacy. However, when the drug-effect was assessed at the intermediate doses, VT of those with a significantly narrowed width of the zone of entrainment were subsequently suppressed when the same drug was added.
In conclusion, the electrophysiological properties of the area is diverse and it might affect pacing-induced terminability.
Whether an antiarrhythmic agent is able to prevent VT-induction or not can not be predicted from the basal electrophysiologic parameters, but a significant narrowing of the width of the zone of entrainment, and hence the excitable gap, can be a hallmark for drug-efficacy.

DOI： 10.1536/ihj.37.773

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC  

Intracoronary acetycholine prolonged the QT interval in 5 patients with congenital long QT syndrome but not in subjects with normal QT intervals. Prolongation was not due to bradycardia or adrenergic drive, and atropine was suggested to attenuate the response.

DOI： 10.1016/S0002-9149(97)89189-8

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPAN HEART JOURNAL, SECOND DEPT OF INTERNAL MED  

The patient was a 50-year-old woman with primary chylopericardium. Triglyceride rich chyloid fluid was continuously drained from the pericardial space through an indwelling catheter. A surgical procedure was scheduled since a medium chain triglyceride diet was insufficient to control the fluid accumulation. Before the operation, inflammatory signs were apparent around the indwelling catheter and the catheter was removed immediately. The inflammation was easily treated with antibiotics, and the pericardial effusion no longer accumulated during a follow-up period of 10 months.
The inflammatory process may have caused fibrin production and tissue adhesion in the pericardial cavity, and these might have prevented an accumulation of chyloid fluid and occluded the connection between the thoracic duct and the pericardial cavity.

DOI： 10.1536/ihj.37.271