Updated on 2024/04/16

写真a

 
IKEGAMI Riyutaro
 
Organization
Academic Assembly Institute of Medicine and Dentistry IGAKU KEIRETU Assistant Professor
Graduate School of Medical and Dental Sciences Assistant Professor
Title
Assistant Professor
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Degree

  • 医学博士 ( 2019.3   新潟大学 )

Research Interests

  • 動脈硬化

  • 虚血性心疾患

  • 不安定プラーク

  • 脂質

  • 血管内イメージング

Research Areas

  • Life Science / Cardiology  / 動脈硬化

Research History (researchmap)

  • 新潟大学大学院医歯学総合研究科   循環器内科学   助教

    2023.1

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  • 新潟大学医歯学総合病院   循環器内科   専任助教

    2022.4 - 2022.12

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  • 県立新発田病院   循環器内科   医員

    2021.4 - 2022.3

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  • 信楽園病院   循環器内科   医員

    2020.10 - 2021.3

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  • ハーバード大学マサチューセッツ総合病院   Cardiovascular Research Center   リサーチフェロー

    2019.4 - 2020.8

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  • 新潟大学医歯学総合病院   循環器内科   医員

    2013.4 - 2019.3

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  • 新潟市民病院   循環器内科   レジデント

    2010.4 - 2013.3

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  • 鶴岡市立荘内病院   初期研修医

    2008.4 - 2010.3

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Research History

  • Niigata University   Graduate School of Medical and Dental Sciences   Assistant Professor

    2023.1

  • Niigata University   Institute of Medicine and Dentistry, Academic Assembly   Assistant Professor

    2023.1

  • Niigata University   Cardiovascular Medicine, University Medical and Dental Hospital   Assistant Professor

    2022.7 - 2022.12

Education

  • 新潟大学大学院   医歯学総合研究科   生体機能調節医学 循環器内科学

    2014.4 - 2019.3

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  • Nippon Medical School   Medical School   医学科

    2002.4 - 2008.3

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Papers

  • Angioscopic Findings of Calcification in Saphenous Vein Graft. Reviewed

    Shintaro Yoneyama, Naoki Kubota, Kazuyuki Ozaki, Takeshi Okubo, Ryutaro Ikegami, Makoto Hoyano, Takayuki Inomata

    Circulation journal : official journal of the Japanese Circulation Society   2023.9

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    DOI: 10.1253/circj.CJ-23-0421

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  • Angioscopic Finding of Honeycomb-Like Structure in Coronary Artery Disease. Reviewed

    Shintaro Yoneyama, Kazuyuki Ozaki, Naoki Kubota, Takeshi Okubo, Ryutaro Ikegami, Makoto Hoyano, Takao Yanagawa, Takayuki Inomata

    Circulation journal : official journal of the Japanese Circulation Society   87 ( 6 )   852 - 852   2023.5

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    DOI: 10.1253/circj.CJ-23-0042

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  • Efficacy of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitor Treatment for Repeated In-stent Restenosis in a Coronary Artery. Reviewed

    Takumi Akiyama, Kazuyuki Ozaki, Toshiki Takano, Shintaro Yoneyama, Naoki Kubota, Takeshi Okubo, Ryutaro Ikegami, Makoto Hoyano, Takao Yanagawa, Takayuki Inomata

    Internal medicine (Tokyo, Japan)   2023.3

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    A 57-year-old woman experienced chest pain. A coronary angiogram revealed middle left anterior descending artery stenosis. Despite receiving adequate anti-hyperlipidemia treatment and undergoing percutaneous coronary intervention (PCI), she experienced angina and required PCI six more times for in-stent restenosis. As she had high lipoprotein (a) (LP-[a]) levels at the seventh PCI procedure, proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) was administered, and a reduction in the LP-(a) and low-density lipoprotein cholesterol (LDL-C) values was observed. She experienced no recurrence of angina for five years with PCSK9i treatment. PCSK9i can reduce not only LDL-C but also LP-(a) levels, resulting in cardiac event risk reduction.

    DOI: 10.2169/internalmedicine.1609-23

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  • Correlation Between the Japanese Version of the High Bleeding Risk (J-HBR) Criteria and the PRECISE-DAPT Score, and Optimal J-HBR Cut-Off Score to Predict Major Bleeding. Reviewed

    Naoki Kubota, Kazuyuki Ozaki, Takumi Akiyama, Yuzo Washiyama, Shintaro Yoneyama, Takeshi Okubo, Ryutaro Ikegami, Makoto Hoyano, Takao Yanagawa, Naohito Tanabe, Takayuki Inomata

    Circulation reports   4 ( 8 )   363 - 370   2022.8

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    Background: The correlation between the Japanese version of high bleeding risk (J-HBR) criteria and the Predicting Bleeding Complications in Patients Undergoing Stent Implantation and Subsequent Dual Antiplatelet Therapy (PRECISE-DAPT) score is unknown, as is the relationship of both risk scores with ischemic events. Methods and Results: This study enrolled 842 patients who underwent percutaneous coronary intervention (PCI) between January 2016 and December 2020. The 2 bleeding risk scores at the time of PCI and the subsequent risk of bleeding and ischemic events over a 1-year follow-up were examined. The J-HBR score was significantly correlated with the PRECISE-DAPT score (r=0.731, P<0.001). However, 1 year after PCI, the J-HBR was not significantly associated with the incidence of major bleeding and ischemic events (log-rank, P=0.058 and P=0.351, respectively), whereas the PRECISE-DAPT score predicted both the incidence of major bleeding and ischemic events (log-rank, P=0.006 and P=0.019, respectively). According to receiver operating characteristic curve analysis, a J-HBR score ≥1.5 was significantly associated with a higher cumulative incidence of major bleeding, but not ischemic events (log-rank, P=0.004 and P=0.513, respectively). Conclusions: The J-HBR score is highly correlated with the PRECISE-DAPT score. A J-HBR score ≥1.5 can identify high bleeding risk patients without an increased risk of ischemic events.

    DOI: 10.1253/circrep.CR-22-0059

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  • Coagulation factors promote brown adipose tissue dysfunction and abnormal systemic metabolism in obesity. Reviewed International journal

    Yuka Hayashi, Ippei Shimizu, Yohko Yoshida, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Shinya Fujiki, Kazuyuki Ozaki, Manabu Abe, Kenji Sakimura, Shujiro Okuda, Toshiya Hayano, Kazuhiro Nakamura, Kenneth Walsh, Naja Zenius Jespersen, Søren Nielsen, Camilla Scheele, Tohru Minamino

    iScience   25 ( 7 )   104547 - 104547   2022.7

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    Brown adipose tissue (BAT) has a role in maintaining systemic metabolic health in rodents and humans. Here, we show that metabolic stress induces BAT to produce coagulation factors, which then-together with molecules derived from the circulation-promote BAT dysfunction and systemic glucose intolerance. When mice were fed a high-fat diet (HFD), the levels of tissue factor, coagulation Factor VII (FVII), activated coagulation Factor X (FXa), and protease-activated receptor 1 (PAR1) expression increased significantly in BAT. Genetic or pharmacological suppression of coagulation factor-PAR1 signaling in BAT ameliorated its whitening and improved thermogenic response and systemic glucose intolerance in mice with dietary obesity. Conversely, the activation of coagulation factor-PAR1 signaling in BAT caused mitochondrial dysfunction in brown adipocytes and systemic glucose intolerance in mice fed normal chow. These results indicate that BAT produces endogenous coagulation factors that mediate pleiotropic effects via PAR1 signaling under metabolic stress.

    DOI: 10.1016/j.isci.2022.104547

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  • Senolytic vaccination improves normal and pathological age-related phenotypes and increases lifespan in progeroid mice. Reviewed International journal

    Masayoshi Suda, Ippei Shimizu, Goro Katsuumi, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Naomi Matsumoto, Yutaka Yoshida, Ryuta Mikawa, Akihiro Katayama, Jun Wada, Masahide Seki, Yutaka Suzuki, Atsushi Iwama, Hironori Nakagami, Ayako Nagasawa, Ryuichi Morishita, Masataka Sugimoto, Shujiro Okuda, Masanori Tsuchida, Kazuyuki Ozaki, Mayumi Nakanishi-Matsui, Tohru Minamino

    Nature aging   1 ( 12 )   1117 - 1126   2021.12

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    Elimination of senescent cells (senolysis) was recently reported to improve normal and pathological changes associated with aging in mice1,2. However, most senolytic agents inhibit antiapoptotic pathways3, raising the possibility of off-target effects in normal tissues. Identification of alternative senolytic approaches is therefore warranted. Here we identify glycoprotein nonmetastatic melanoma protein B (GPNMB) as a molecular target for senolytic therapy. Analysis of transcriptome data from senescent vascular endothelial cells revealed that GPNMB was a molecule with a transmembrane domain that was enriched in senescent cells (seno-antigen). GPNMB expression was upregulated in vascular endothelial cells and/or leukocytes of patients and mice with atherosclerosis. Genetic ablation of Gpnmb-positive cells attenuated senescence in adipose tissue and improved systemic metabolic abnormalities in mice fed a high-fat diet, and reduced atherosclerotic burden in apolipoprotein E knockout mice on a high-fat diet. We then immunized mice against Gpnmb and found a reduction in Gpnmb-positive cells. Senolytic vaccination also improved normal and pathological phenotypes associated with aging, and extended the male lifespan of progeroid mice. Our results suggest that vaccination targeting seno-antigens could be a potential strategy for new senolytic therapies.

    DOI: 10.1038/s43587-021-00151-2

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  • Empagliflozin maintains capillarization and improves cardiac function in a murine model of left ventricular pressure overload. Reviewed International journal

    Masaaki Nakao, Ippei Shimizu, Goro Katsuumi, Yohko Yoshida, Masayoshi Suda, Yuka Hayashi, Ryutaro Ikegami, Yung Ting Hsiao, Shujiro Okuda, Tomoyoshi Soga, Tohru Minamino

    Scientific reports   11 ( 1 )   18384 - 18384   2021.9

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    Patients with type 2 diabetes treated with Sodium glucose transporter 2 (SGLT2) inhibitors show reduced mortality and hospitalization for heart failure (HF). SGLT2 inhibitors are considered to activate multiple cardioprotective pathways; however, underlying mechanisms are not fully described. This study aimed to elucidate the underlying mechanisms of the beneficial effects of SGLT2 inhibitors on the failing heart. We generated a left ventricular (LV) pressure overload model in C57BL/6NCrSlc mice by transverse aortic constriction (TAC) and examined the effects of empagliflozin (EMPA) in this model. We conducted metabolome and transcriptome analyses and histological and physiological examinations. EMPA administration ameliorated pressure overload-induced systolic dysfunction. Metabolomic studies showed that EMPA increased citrulline levels in cardiac tissue and reduced levels of arginine, indicating enhanced metabolism from arginine to citrulline and nitric oxide (NO). Transcriptome suggested possible involvement of the insulin/AKT pathway that could activate NO production through phosphorylation of endothelial NO synthase (eNOS). Histological examination of the mice showed capillary rarefaction and endothelial apoptosis after TAC, both of which were significantly improved by EMPA treatment. This improvement was associated with enhanced expression phospho-eNOS and NO production in cardiac endothelial cells. NOS inhibition attenuated these cardioprotective effects of EMPA. The in vitro studies showed that catecholamine-induced endothelial apoptosis was inhibited by NO, arginine, or AKT activator. EMPA activates the AKT/eNOS/NO pathway, which helps to suppress endothelial apoptosis, maintain capillarization and improve systolic dysfunction during LV pressure overload.

    DOI: 10.1038/s41598-021-97787-2

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  • Near-Infrared Autofluorescence in Atherosclerosis Associates With Ceroid and Is Generated by Oxidized Lipid-Induced Oxidative Stress. Reviewed International journal

    Mazen S Albaghdadi, Ryutaro Ikegami, Mohamad B Kassab, Joseph A Gardecki, Mie Kunio, Mohammed M Chowdhury, Ramzi Khamis, Peter Libby, Guillermo J Tearney, Farouc A Jaffer

    Arteriosclerosis, thrombosis, and vascular biology   41 ( 7 )   e385-e398   2021.7

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    [Figure: see text].

    DOI: 10.1161/ATVBAHA.120.315612

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  • Conservative treatment with an intra-aortic balloon pump to treat acute myocardial infarction due to spontaneous coronary artery dissection. Reviewed

    Yuji Matsuo, Kazuyuki Ozaki, Ryutaro Ikegami, Kota Nishida, Naoki Kubota, Toshiki Takano, Takeshi Okubo, Makoto Hoyano, Takao Yanagawa, Takeshi Kashimura, Tohru Minamino

    Journal of cardiology cases   23 ( 6 )   274 - 280   2021.6

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    Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome. Treatment for SCAD includes conservative approaches, percutaneous coronary intervention (PCI), and coronary artery bypass graft surgery. Although the success rate of PCI is low, conservative treatment often leads to a good clinical course. Three patients with SCAD who were conservatively treated with intra-aortic balloon pumping without coronary intervention are presented. All three patients continue to do well. <Learning objective: The treatment for spontaneous coronary artery dissection (SCAD) has not yet been established. Intra-aortic balloon pumping (IABP) is a potential conservative treatment for SCAD that increases coronary blood flow. However, IABP could worsen the dissection. In this report, IABP was safely used for SCAD and patients had a good clinical course without worsening the dissection.>.

    DOI: 10.1016/j.jccase.2021.01.004

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  • 透析患者の心房細動治療はどこまで行うべきか

    池上 龍太郎, 三間 渉, 松原 琢

    日本透析医会雑誌   36 ( 1 )   84 - 89   2021.4

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    近年、心房細動(atrial fibrillation;AF)の治療は直接経口抗凝固薬(direct oral anti-coagulations;DOAC)やカテーテルアブレーションの普及により大きく変化してきた。血液透析患者におけるAF有病率は高いが、特有の病態やリスクから非透析患者とは異なる治療戦略が求められ、至適治療について議論が続いている。ワルファリンによる抗凝固療法は一律的な導入は推奨されず、塞栓症既往や弁膜症の有無を考慮し、必要性が高いと判断される症例のみに限定すべきという意見が強い。抗不整脈治療について心拍数コントロールが第一選択であるが、症状や血行動態から洞調率維持が必要な症例では薬物治療やアブレーションも選択されうる。今後のエビデンスの蓄積が待たれるとともに、個々の患者ごとに病態や塞栓症・出血リスクに基づく治療を行っていくことが求められる。(著者抄録)

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  • Cardiac mitofusin-1 is reduced in non-responding patients with idiopathic dilated cardiomyopathy. Reviewed International journal

    Yung Ting Hsiao, Ippei Shimizu, Takayuki Wakasugi, Yohko Yoshida, Ryutaro Ikegami, Yuka Hayashi, Masayoshi Suda, Goro Katsuumi, Masaaki Nakao, Takuya Ozawa, Daisuke Izumi, Takeshi Kashimura, Kazuyuki Ozaki, Tomoyoshi Soga, Tohru Minamino

    Scientific reports   11 ( 1 )   6722 - 6722   2021.3

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    Prognosis of severe heart failure remains poor. Urgent new therapies are required. Some heart failure patients do not respond to established multidisciplinary treatment and are classified as "non-responders". The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Mitofusin-1 (Mfn1), a mitochondrial fusion protein, is significantly reduced in non-responding patients. This study aimed to elucidate the role of Mfn1 in the failing heart. Twenty-two idiopathic dilated cardiomyopathy (IDCM) patients who underwent endomyocardial biopsy of intraventricular septum were included. Of the 22 patients, 8 were non-responders (left ventricular (LV) ejection fraction (LVEF) of < 10% improvement at late phase follow-up). Electron microscopy (EM), quantitative PCR, and immunofluorescence studies were performed to explore the biological processes and molecules involved in failure to respond. Studies in cardiac specific Mfn1 knockout mice (c-Mfn1 KO), and in vitro studies with neonatal rat ventricular myocytes (NRVMs) were also conducted. A significant reduction in mitochondrial size in cardiomyocytes, and Mfn1, was observed in non-responders. A LV pressure overload with thoracic aortic constriction (TAC) c-Mfn1 KO mouse model was generated. Systolic function was reduced in c-Mfn1 KO mice, while mitochondria alteration in TAC c-Mfn1 KO mice increased. In vitro studies in NRVMs indicated negative regulation of Mfn1 by the β-AR/cAMP/PKA/miR-140-5p pathway resulting in significant reduction in mitochondrial respiration of NRVMs. The level of miR140-5p was increased in cardiac tissues of non-responders. Mfn1 is a biomarker of heart failure in non-responders. Therapies targeting mitochondrial dynamics and homeostasis are next generation therapy for non-responding heart failure patients.

    DOI: 10.1038/s41598-021-86209-y

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  • Increased acetylcarnitine does not mediate cardioprotective effects of empagliflozin in a murine heart failure model(和訳中) Reviewed

    仲尾 政晃, 清水 逸平, 吉田 陽子, 勝海 悟郎, 林 由香, 池上 龍太郎, 須田 将吉, 若杉 嵩幸, 南野 徹

    日本抗加齢医学会総会プログラム・抄録集   19回   211 - 211   2019.6

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  • p53 plays a crucial role in endothelial dysfunction associated with hyperglycemia and ischemia. Reviewed International journal

    Masataka Yokoyama, Ippei Shimizu, Ayako Nagasawa, Yohko Yoshida, Goro Katsuumi, Takayuki Wakasugi, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Yusuke Ota, Sho Okada, Marcus Fruttiger, Yoshio Kobayashi, Masanori Tsuchida, Yoshiaki Kubota, Tohru Minamino

    Journal of molecular and cellular cardiology   129   105 - 117   2019.4

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    p53 is a guardian of the genome that protects against carcinogenesis. There is accumulating evidence that p53 is activated with aging. Such activation has been reported to contribute to various age-associated pathologies, but its role in vascular dysfunction is largely unknown. The aim of this study was to investigate whether activation of endothelial p53 has a pathological effect in relation to endothelial function. We established endothelial p53 loss-of-function and gain-of-function models by breeding endothelial-cell specific Cre mice with floxed Trp53 or floxed Mdm2/Mdm4 mice, respectively. Then we induced diabetes by injection of streptozotocin. In the diabetic state, endothelial p53 expression was markedly up-regulated and endothelium-dependent vasodilatation was significantly impaired. Impairment of vasodilatation was significantly ameliorated in endothelial p53 knockout (EC-p53 KO) mice, and deletion of endothelial p53 also significantly enhanced the induction of angiogenesis by ischemia. Conversely, activation of endothelial p53 by deleting Mdm2/Mdm4 reduced both endothelium-dependent vasodilatation and ischemia-induced angiogenesis. Introduction of p53 into human endothelial cells up-regulated the expression of phosphatase and tensin homolog (PTEN), thereby reducing phospho-eNOS levels. Consistent with these results, the beneficial impact of endothelial p53 deletion on endothelial function was attenuated in EC-p53 KO mice with an eNOS-deficient background. These results show that endothelial p53 negatively regulates endothelium-dependent vasodilatation and ischemia-induced angiogenesis, suggesting that inhibition of endothelial p53 could be a novel therapeutic target in patients with metabolic disorders.

    DOI: 10.1016/j.yjmcc.2019.02.010

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  • Peptide vaccine for semaphorin3E ameliorates systemic glucose intolerance in mice with dietary obesity. Reviewed International journal

    Yohko Yoshida, Ippei Shimizu, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Takayuki Wakasugi, Masaaki Nakao, Hironori Nakagami, Ryuichi Morishita, Tohru Minamino

    Scientific reports   9 ( 1 )   3858 - 3858   2019.3

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    We previously demonstrated that cellular aging signals upregulated a secreted class 3 semaphorin E (Sema3E) and its receptor plexinD1 in the adipose tissue of a murine model of dietary obesity and that Sema3E was a chemoattractant, mediating its biological effects by inducing infiltration of plexinD1-positive inflammatory macrophages into the visceral white adipose tissue. This study was performed to develop a peptide vaccine for Sema3E and test its therapeutic potential in a murine model of dietary obesity. Two antigenic peptides were selected to generate neutralizing antibodies for a vaccine. These peptides were conjugated to keyhole limpet hemocyanin (KLH), and were administered with Freund's adjuvant to obese wild-type male mice. The Sema3E antibody titer was analyzed by ELISA, and the biological effects of the peptides were tested in mice with dietary obesity. Among the two candidate peptides, the Sema3E antibody titer was significantly increased by injection of KLH-conjugated HKEGPEYHWS (Sema3E vaccine). Administration of Sema3E vaccine suppressed the infiltration of plexinD1-positive cells, ameliorated chronic inflammation in visceral white adipose tissue, and improved systemic glucose intolerance in mice with dietary obesity, suggesting that Sema3E vaccine has the potential to become a next generation therapy for obesity and diabetes.

    DOI: 10.1038/s41598-019-40325-y

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  • Role of smooth muscle cell p53 in pulmonary arterial hypertension. Reviewed International journal

    Takayuki Wakasugi, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Masaaki Nakao, Makoto Hoyano, Takeshi Kashimura, Kazufumi Nakamura, Hiroshi Ito, Takashi Nojiri, Tomoyoshi Soga, Tohru Minamino

    PloS one   14 ( 2 )   e0212889   2019

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    Pulmonary arterial hypertension (PAH) is characterized by remodeling and narrowing of the pulmonary arteries, which lead to elevation of right ventricular pressure, heart failure, and death. Proliferation of pulmonary artery smooth muscle cells (PASMCs) is thought to be central to the pathogenesis of PAH, although the underlying mechanisms are still being explored. The protein p53 is involved in cell cycle coordination, DNA repair, apoptosis, and cellular senescence, but its role in pulmonary hypertension (PH) is not fully known. We developed a mouse model of hypoxia-induced pulmonary hypertension (PH) and found significant reduction of p53 expression in the lungs. Our in vitro experiments with metabolomic analyses and the Seahorse XF extracellular flux analyzer indicated that suppression of p53 expression in PASMCs led to upregulation of glycolysis and downregulation of mitochondrial respiration, suggesting a proliferative phenotype resembling that of cancer cells. It was previously shown that systemic genetic depletion of p53 in a murine PH model led to more severe lung manifestations. Lack of information about the role of cell-specific p53 signaling promoted us to investigate it in our mouse PH model with the inducible Cre-loxP system. We generated a mouse model with SMC-specific gain or loss of p53 function by crossing Myh11-Cre/ERT2 mice with floxed Mdm4 mice or floxed Trp53 mice. After these animals were exposed to hypoxia for 4 weeks, we conducted hemodynamic and echocardiographic studies. Surprisingly, the severity of PH was similar in both groups of mice and there were no differences between the genotypes. Our findings in these mice indicate that activation or suppression of p53 signaling in SMCs has a minor role in the pathogenesis of PH and suggest that p53 signaling in other cells (endothelial cells, immune cells, or fibroblasts) may be involved in the progression of this condition.

    DOI: 10.1371/journal.pone.0212889

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  • Gamma-Aminobutyric Acid Signaling in Brown Adipose Tissue Promotes Systemic Metabolic Derangement in Obesity. Reviewed International journal

    Ryutaro Ikegami, Ippei Shimizu, Takeshi Sato, Yohko Yoshida, Yuka Hayashi, Masayoshi Suda, Goro Katsuumi, Ji Li, Takayuki Wakasugi, Yasuhiko Minokoshi, Shiki Okamoto, Eiichi Hinoi, Søren Nielsen, Naja Zenius Jespersen, Camilla Scheele, Tomoyoshi Soga, Tohru Minamino

    Cell reports   24 ( 11 )   2827 - 2837   2018.9

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    Brown adipose tissue (BAT) is a metabolically active organ that contributes to the maintenance of systemic metabolism. The sympathetic nervous system plays important roles in the homeostasis of BAT and promotes its browning and activation. However, the role of other neurotransmitters in BAT homeostasis remains largely unknown. Our metabolomic analyses reveal that gamma-aminobutyric acid (GABA) levels are increased in the interscapular BAT of mice with dietary obesity. We also found a significant increase in GABA-type B receptor subunit 1 (GABA-BR1) in the cell membranes of brown adipocytes of dietary obese mice. When administered to obese mice, GABA induces BAT dysfunction together with systemic metabolic disorder. Conversely, the genetic inactivation or inhibition of GABA-BR1 leads to the re-browning of BAT under conditions of metabolic stress and ameliorated systemic glucose intolerance. These results indicate that the constitutive activation of GABA/GABA-BR1 signaling in obesity promotes BAT dysfunction and systemic metabolic derangement.

    DOI: 10.1016/j.celrep.2018.08.024

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  • Catecholamine-Induced Senescence of Endothelial Cells and Bone Marrow Cells Promotes Cardiac Dysfunction in Mice. Reviewed

    Goro Katsuumi, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Takayuki Wakasugi, Masaaki Nakao, Tohru Minamino

    International heart journal   59 ( 4 )   837 - 844   2018.7

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    Previous studies have suggested that cellular senescence plays a central role in the progression of pathologic changes in the failing heart. It is well known that the sympathetic nervous system is activated in patients with heart failure, and this change is associated with poor clinical outcomes. Sympathetic activation increases the levels of various catecholamines, such as epinephrine and norepinephrine, but the contribution of these catecholamines to cellular senescence associated with heart failure remains to be determined. We found that catecholamine infusion induced senescence of endothelial cells and bone marrow cells, and promoted cardiac dysfunction in mice. In C57BL/6NCr mice, the continuous infusion of isoproterenol-induced cardiac inflammation and cardiac dysfunction. Expression of p53, a master regulator of cellular senescence, was increased in the cardiac tissue and bone marrow cells of these mice. Suppression of cellular senescence by genetic deletion of p53 in endothelial cells or bone marrow cells led to improvement of isoproterenol-induced cardiac dysfunction. In vitro studies showed that adrenergic signaling increased the expression of p53 and adhesion molecules by endothelial cells and macrophages. Our results indicate that catecholamine-induced senescence of endothelial cells and bone marrow cells plays a pivotal role in the progression of heart failure. Suppression of catecholamine-p53 signaling is crucial for inhibition of remodeling in the failing heart.

    DOI: 10.1536/ihj.17-313

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  • Amlodipine Inhibits Vascular Cell Senescence and Protects Against Atherogenesis Through the Mechanism Independent of Calcium Channel Blockade. Reviewed

    Hiromi Kayamori, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Masayoshi Suda, Ryutaro Ikegami, Goro Katsuumi, Takayuki Wakasugi, Tohru Minamino

    International heart journal   59 ( 3 )   607 - 613   2018.5

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    Vascular cells have a finite lifespan and eventually enter irreversible growth arrest called cellular senescence. We have previously suggested that vascular cell senescence contributes to the pathogenesis of human atherosclerosis. Amlodipine is a mixture of two enantiomers, one of which (S- enantiomer) has L-type channel blocking activity, while the other (R+ enantiomer) shows ~1000-fold weaker channel blocking activity than S- enantiomer and has other unknown effects. It has been reported that amlodipine inhibits the progression of atherosclerosis in humans, but the molecular mechanism of this beneficial effect remains unknown. Apolipoprotein E-deficient mice on a high-fat diet were treated with amlodipine, its R+ enantiomer or vehicle for eight weeks. Compared with vehicle treatment, both amlodipine and the R+ enantiomer significantly reduced the number of senescent vascular cells and inhibited plaque formation to a similar extent. Expression of the pro-inflammatory molecule interleukin-1β was markedly upregulated in vehicle-treated mice, but was inhibited to a similar extent by treatment with amlodipine or the R+ enantiomer. Likewise, activation of p53 (a critical inducer of senescence) was markedly suppressed by treatment with amlodipine or the R+ enantiomer. These results suggest that amlodipine inhibits vascular cell senescence and protects against atherogenesis at least partly by a mechanism that is independent of calcium channel blockade.

    DOI: 10.1536/ihj.17-265

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  • Percutaneous Coronary Intervention for a Patient with Left Main Coronary Compression Syndrome. Reviewed

    Ryutaro Ikegami, Kazuyuki Ozaki, Takuya Ozawa, Satoru Hirono, Masahiro Ito, Tohru Minamino

    Internal medicine (Tokyo, Japan)   57 ( 10 )   1421 - 1424   2018.5

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    Left main coronary compression syndrome rarely occurs in patients with severe pulmonary hypertension. A 65-year-old woman with severe pulmonary hypertension due to an atrial septal defect suffered from angina on effort. Cardiac computed-tomography and coronary angiography revealed considerable stenosis of the left main coronary artery (LMA) caused by compression between the dilated main pulmonary artery trunk and the sinus of valsalva. Stenting of the LMA under intravascular ultrasound imaging was effective for the treatment of angina. We herein report the diagnosis and management of this condition with a brief literature review.

    DOI: 10.2169/internalmedicine.9534-17

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  • Dual Antiplatelet Therapy Guided by CYP2C19 Polymorphisms after Implantation of Second-Generation Drug-Eluting Stents for Management of Acute Coronary Syndrome. Reviewed

    Takuya Ozawa, Masayoshi Suda, Ryutaro Ikegami, Toshiki Takano, Takayuki Wakasugi, Takao Yanagawa, Komei Tanaka, Kazuyuki Ozaki, Satoru Hirono, Tohru Minamino

    International heart journal   59 ( 1 )   21 - 26   2018.1

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    Prasugrel, a novel P2Y12 receptor inhibitor, is administered to patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI), but it can increase the risk of bleeding. The Japanese exhibit weaker responses to clopidogrel than other races because of CYP2C19 polymorphisms; thus, it is unclear whether these patients should continue dual antiplatelet therapy (DAPT) using prasugrel or switch to clopidogrel in the chronic phase. Here we evaluated the clinical outcomes of DAPT guided by CYP2C19 polymorphisms after implantation of second-generation drug-eluting stents (DESs) for ACS management. Patients with ACS receiving PCI via DES from November 2011 to March 2015 were divided into two groups: conventional DAPT with clopidogrel (n = 41) and gene-guided DAPT (n = 24). In the gene-guided DAPT group, all patients with ACS were given DAPT using prasugrel as soon as possible; extensive and intermediate metabolizers receiving PCI for the first time were switched to clopidogrel at least 2 weeks after discharge, and intermediate metabolizers with repeated ACS and poor metabolizers continued on DAPT using prasugrel. Notably, gene-guided DAPT significantly reduced major adverse cardiovascular/cerebrovascular events (MACCEs; 22.0% versus 4.2%, hazard ratio [HR]: 0.15, 95% confidence interval [CI]: 0.01-0.81; P = 0.0247). Hemorrhagic complications were observed in 3.1% of patients receiving conventional DAPT and absent in the gene-guided group. Moreover, multivariate analysis showed that gene-guided DAPT significantly decreased MACCE incidence (HR: 0.15, 95% CI: 0.01-0.81; P = 0.033). Collectively, these data suggest that CYP2C19 polymorphism analysis may improve treatment decisions in patients with ACS receiving DES-PCI.

    DOI: 10.1536/ihj.17-005

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  • Boysenberry polyphenol inhibits endothelial dysfunction and improves vascular health. Reviewed International journal

    Ryo Furuuchi, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Takayuki Wakasugi, Masaaki Nakao, Tohru Minamino

    PloS one   13 ( 8 )   e0202051   2018

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    Endothelial cells have an important role in maintaining vascular homeostasis. Age-related disorders (including obesity, diabetes, and hypertension) or aging per se induce endothelial dysfunction that predisposes to the development of atherosclerosis. Polyphenols have been reported to suppress age-related endothelial cell disorders, but their role in vascular function is yet to be determined. We investigated the influence of boysenberry polyphenol on vascular health under metabolic stress in a murine model of dietary obesity. We found that administration of boysenberry polyphenol suppressed production of reactive oxygen species (ROS) and increased production of nitric oxide (NO) in the aorta. It has been reported that p53 induces cellular senescence and has a crucial role in age-related disorders, including heart failure and diabetes. Administration of boysenberry polyphenol significantly reduced the endothelial p53 level in the aorta and ameliorated endothelial cell dysfunction in iliac arteries under metabolic stress. Boysenberry polyphenol also reduced ROS and p53 levels in cultured human umbilical vein endothelial cells (HUVECs), while increasing NO production. Uncoupled endothelial nitric oxide synthase (eNOS monomer) is known to promote ROS production. We found that boysenberry polyphenol reduced eNOS monomer levels both in vivo and in vitro, along with an increase of eNOS dimerization. To investigate the components of boysenberry polyphenol mediating these favorable biological effects, we extracted the anthocyanin fractions. We found that anthocyanins contributed to suppression of ROS and p53, in association with increased NO production and eNOS dimerization. In an ex vivo study, anthocyanins promoted relaxation of iliac arteries from mice with dietary obesity. These findings indicate that boysenberry polyphenol and anthocyanins, a major component of this polyphenol, inhibit endothelial dysfunction and contribute to maintenance of vascular homeostasis.

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  • Metabolomic Analysis in Heart Failure. Reviewed

    Ryutaro Ikegami, Ippei Shimizu, Yohko Yoshida, Tohru Minamino

    Circulation journal : official journal of the Japanese Circulation Society   82 ( 1 )   10 - 16   2017.12

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    It is thought that at least 6,500 low-molecular-weight metabolites exist in humans, and these metabolites have various important roles in biological systems in addition to proteins and genes. Comprehensive assessment of endogenous metabolites is called metabolomics, and recent advances in this field have enabled us to understand the critical role of previously unknown metabolites or metabolic pathways in the cardiovascular system. In this review, we will focus on heart failure and how metabolomic analysis has contributed to improving our understanding of the pathogenesis of this critical condition.

    DOI: 10.1253/circj.CJ-17-1184

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  • Inhibition of dipeptidyl peptidase-4 ameliorates cardiac ischemia and systolic dysfunction by up-regulating the FGF-2/EGR-1 pathway Reviewed

    Masayoshi Suda, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Goro Katsuumi, Takayuki Wakasugi, Yutaka Yoshida, Shujiro Okuda, Tomoyoshi Soga, Tohru Minamino

    PLOS ONE   12 ( 8 )   e0182422   2017.8

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    Dipeptidyl peptidase 4 inhibitors are used worldwide in the management of diabetes, but their role in the prevention or treatment of cardiovascular disorders has yet to be defined. We found that linagliptin, a DPP-4 inhibitor, suppressed capillary rarefaction in the hearts of mice with dietary obesity. Metabolomic analysis performed with capillary electrophoresis/mass spectrometry (LC-MS/MS) showed that linagliptin promoted favorable metabolic remodeling in cardiac tissue, which was characterized by high levels of citrulline and creatine. DNA microarray analysis revealed that the cardiac tissue level of early growth response protein 1 (EGR-1), which activates angiogenesis, was significantly reduced in untreated mice with dietary obesity, while this decrease was inhibited by administration of linagliptin. Mature fibroblast growth factor 2 (FGF-2) has a putative truncation site for DPP-4 at the NH2-terminal, and LC-MS/MS showed that recombinant DPP-4 protein cleaved the NH2-terminal dipeptides of mature FGF-2. Incubation of cultured neonatal rat cardiomyocytes with FGF-2 increased Egr1 expression, while it was suppressed by recombinant DPP-4 protein. Furthermore, vascular endothelial growth factor-A had a critical role in mediating FGF-2/EGR-1 signaling. In conclusion, pharmacological inhibition of DPP-4 suppressed capillary rarefaction and contributed to favorable remodeling of cardiac metabolism in mice with dietary obesity.

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  • 医学と医療の最前線 血管老化研究の最前線

    池上 龍太郎, 清水 逸平, 吉田 陽子, 南野 徹

    日本内科学会雑誌   106 ( 8 )   1652 - 1658   2017.8

  • Peripheral Gamma-aminobutyric Acid(gaba) Signaling in Brown Adipose Tissue Induces Metabolic Dysfunction in Obesity Reviewed

    Ryutaro Ikegami, Ippei Shimizu, Takeshi Sato, Shuang Jiao, Yohko Yoshida, Masayoshi Suda, Yuka Hayashi, Goro Katsuumi, Hiromi Kayamori, Tohru Minamino

    CIRCULATION   132   2015.11

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  • Vascular Rarefaction Mediates Whitening of Brown Fat in Dietary Obesity Reviewed

    Ippei Shimizu, Yohko Yoshida, Masayoshi Suda, Yuka Hayashi, Jiao Shuang, Ryutaro Ikegami, Goro Katsuumi, Hiromi Kayamori, Kenneth Walsh, Tohru Minamino

    JOURNAL OF CARDIAC FAILURE   20 ( 10 )   S148 - S148   2014.10

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    DOI: 10.1016/j.cardfail.2014.07.102

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  • 当院におけるペースメーカー埋込み関連感染症の特徴

    佐藤 迪夫, 保阪 幸男, 大久保 健志, 池上 龍太郎, 真田 明子, 矢野 利明, 小林 剛, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    日本心臓病学会誌   8 ( Suppl.I )   307 - 307   2013.9

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  • 閉塞性肥大型心筋症で心室細動を合併し、ICDと経皮的心筋中隔焼灼術(PTSMA)を施行された1例

    青木 亜美, 高橋 和義, 大久保 健志, 池上 龍太郎, 佐藤 迪夫, 矢野 利明, 小林 剛, 保坂 幸男, 尾崎 和幸, 土田 圭一, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   29 - 33   2012.9

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    症例は突然死と肥大型心筋症の家族歴がある45歳の男性。8年前に閉塞性肥大型心筋症と診断された。薬物治療(β遮断薬、カルシウム拮抗薬、抗不整脈薬Ia群)が行われたが、左室流出路圧較差及び労作時息切れの改善は認められなかった。今回、心房細動から心室細動になり、自動体外式除細動器で蘇生された。心臓カテーテル検査で左室流出路圧較差が130mmHgあり、ICD(implantable cardioverter defibrillator)植え込みを行った後に経皮的心筋中隔焼灼術(percutaneous transluminal septal myocardial ablation:PTSMA)を施行され、左室流出路圧較差は110mmHgから26mmHgへ改善した。その後息切れ等なく経過し、6ヵ月後の心臓カテーテル検査で左室流出路圧較差を認められなかった。本症例はPTSMAが奏効した経過良好な症例である。また、PTSMAを施行した後であっても頻脈性不整脈による心停止のリスクはあると報告されており、閉塞性肥大型心筋症で心停止をきたした症例に対してはPTSMAに加えてICDを植え込む必要があると考える。(著者抄録)

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  • 左冠動脈主幹部閉塞の心筋梗塞に対し経皮的心肺補助装置(PCPS)装着下に経皮的冠動脈インターベンション(PCI)を施行し救命しえた1例

    佐藤 里映, 小林 剛, 大久保 健志, 大槻 総, 佐藤 迪夫, 池上 龍太郎, 矢野 利明, 保坂 幸男, 土田 圭一, 尾崎 和幸, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   18 - 22   2012.9

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    症例は45歳男性。仕事中に胸痛の出現とともに意識消失し救急要請となった。救急車内で心室細動を繰り返し電気的除細動および心肺蘇生を受けながら当院へ搬送された。当院到着後も心室細動とPEA(無脈性電気活動)が持続し、救急外来で気管挿管、経皮的心肺補助装置(PCPS)を導入した。急性心筋梗塞を疑い緊急冠動脈造影を施行したところ、左冠動脈主幹部の完全閉塞を認め緊急経皮的冠動脈形成術(PCI)を施行し再灌流を得た。Max CPK 29779IU/L、Max CK-MB 2500IU/Lと非常に大きな心筋梗塞で、術直後の心エコーではEF 5%に低下していた。術後、低体温療法、PCPSとIABP(大動脈内バルーンパンピング)による機械的循環補助、薬物加療(カテコラミン、PDEIII阻害薬、カルペリチド、硝酸イソソルビド、利尿剤)を併用しながら左室収縮能の回復を待つと、下壁領域の壁運動が徐々に改善した。第7病日にPCPSを離脱、第19病日にIABPを抜去することができた。機械的循環補助離脱後も重篤な左心不全の薬物治療に難渋したが、第30病日に人工呼吸器を離脱、心臓リハビリテーションを行い第93病日に独歩退院となった。左冠動脈主幹部閉塞による急性心筋梗塞で心原性ショックを来した際の院内死亡率は55~80%と報告される。PCI手技が成熟した現在も極めて予後不良な疾患であり、いまだ確実な治療方法は確立していない。救命例は貴重であると考え報告する。(著者抄録)

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  • 左冠動脈主幹部閉塞の急性心筋梗塞に対し経皮的心肺補助装置(PCPS)装着下にPCIを施行し救命し得た1例

    佐藤 里映, 小林 剛, 大久保 健志, 大槻 総, 佐藤 迪夫, 池上 龍太郎, 矢野 利明, 保坂 幸男, 土田 圭一, 尾崎 和幸, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   79 - 79   2012.9

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  • 両側肺動脈に限局した大動脈炎症候群の2例

    大槻 総, 池上 龍太郎, 土田 圭一, 大久保 健志, 佐藤 迪夫, 矢野 利明, 小林 剛, 保坂 幸男, 尾崎 和幸, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   71 - 71   2012.9

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  • 心原性院外心肺停止例の予後

    大久保 健志, 大槻 総, 池上 龍太郎, 佐藤 迪夫, 矢野 利明, 小林 剛, 保坂 幸男, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   71 - 72   2012.9

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  • 左冠動脈主幹部(LMT)を責任病変とする重症急性心筋梗塞の1例 当院でのLMT-AMIの治療成績とその臨床的特徴の検討

    池上 龍太郎, 大槻 総, 大久保 健志, 佐藤 迪夫, 矢野 利明, 小林 剛, 保坂 幸男, 土田 圭一, 尾崎 和幸, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   70 - 70   2012.9

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  • 当科におけるRMI症例に対する待機的PCI前の抗凝固療法の有意性の検討

    佐藤 迪夫, 大久保 健志, 大槻 総, 池上 龍太郎, 矢野 利明, 小林 剛, 保坂 幸男, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   70 - 71   2012.9

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  • 心房細動アブレーション治療によりペースメーカ埋込みを回避できた徐脈頻脈症候群の1例 当院における心房細動アブレーション治療成績の検討

    柏 麻美, 保坂 幸男, 大久保 健志, 池上 龍太郎, 佐藤 迪夫, 真田 明子, 矢野 利明, 小林 剛, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   33 ( 1 )   23 - 28   2012.9

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    73歳男性。診断は徐脈頻脈症候群であり、心房細動停止時に症状を伴う心停止が認められた。心房細動に対するアブレーション治療を施行することにより、心房細動発作が消失し、ペースメーカ埋込みを回避することができた。当院ではこれまでに11例の心房細動に対してアブレーション治療を行っている。11症例中10例において心房細動発作の減少、消失を認めており、BNP値、左房径の改善を認めている。心房細動アブレーション治療は、洞調律維持により、抗不整脈薬からの離脱、QOLの向上をもたらすと考えられる。(著者抄録)

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  • Recent Myocardial infarctionにおける待機的PCI前の抗凝固療法の検討

    佐藤 迪夫, 大久保 健志, 池上 龍太郎, 矢野 利明, 小林 剛, 真田 明子, 保坂 幸男, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    日本心臓病学会誌   7 ( Suppl.I )   287 - 287   2012.8

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  • 当院における左室流出路狭窄の臨床像<肥大型心筋症とS字状中隔に注目して>

    尾崎 和幸, 大久保 健志, 佐藤 迪夫, 池上 龍太郎, 真田 明子, 矢野 利明, 小林 剛, 保坂 幸男, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    日本心臓病学会誌   7 ( Suppl.I )   260 - 260   2012.8

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  • 当院での腎動脈狭窄と腎動脈エコーのパラメーターの相関の検討

    小林 剛, 小田 弘隆, 三井田 努, 高橋 和義, 尾崎 和幸, 土田 圭一, 保坂 幸男, 矢野 利明, 池上 龍太郎, 佐藤 迪夫, 大久保 健志

    日本心臓病学会誌   7 ( Suppl.I )   455 - 455   2012.8

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  • 内腸骨動脈瘤に対するcoverd stent治療の検討

    佐藤 迪夫, 池上 龍太郎, 飛田 一樹, 小林 剛, 保坂 幸男, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    新潟医学会雑誌   125 ( 10 )   577 - 577   2011.10

  • 産褥期に発症したタコツボ型心筋症の1例

    飛田 一樹, 小田 弘隆, 大久保 健志, 佐藤 迪夫, 池上 龍太郎, 小林 剛, 保坂 幸男, 土田 圭一, 尾崎 和幸, 高橋 和義, 三井田 努

    新潟市民病院医誌   32 ( 1 )   74 - 74   2011.9

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  • 透析導入に伴う左室流出路狭窄の進行に対して経皮的心室中隔焼灼術が奏功した閉塞性肥大型心筋症の一例

    飯田 久貴, 尾崎 和幸, 佐藤 迪夫, 池上 龍太郎, 飛田 一樹, 羽尾 和久, 小林 剛, 保坂 幸男, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   32 ( 1 )   67 - 68   2011.9

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  • 左前下行枝の器質的狭窄に対する経皮的冠動脈形成術後に左室流出路圧較差が消失した一例 未消失例との比較を含め

    尾崎 和幸, 大久保 健志, 大槻 総, 佐藤 迪夫, 池上 龍太郎, 矢野 利明, 小林 剛, 保坂 幸男, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    日本心臓病学会誌   6 ( Suppl.I )   246 - 246   2011.8

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  • SFA-CTOへの順行性アプローチでワイヤー通過に難渋するも、両方向性アプローチが有効であった症例

    羽尾 和久, 小田 弘隆, 佐藤 迪夫, 池上 龍太郎, 飛田 一樹, 小林 剛, 保坂 幸男, 尾崎 和幸, 土田 圭一, 高橋 和義, 三井田 努

    新潟医学会雑誌   125 ( 4 )   235 - 235   2011.4

  • 膝窩静脈嚢状瘤が原因した重症肺塞栓症に、カテーテル治療が奏功した1例

    飛田 一樹, 佐藤 迪夫, 池上 龍太郎, 羽尾 和久, 小林 剛, 保坂 幸男, 土田 圭一, 尾崎 和幸, 高橋 和義, 三井田 努, 小田 弘隆

    新潟市民病院医誌   31 ( 1 )   21 - 24   2010.9

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    Language:Japanese   Publisher:新潟市民病院  

    症例は50歳代、男性。既往歴は高血圧症、高尿酸血症。自宅にて突然の意識消失から心肺停止となり、家人により直ちに心肺蘇生を行われた。救急隊到着後に自己心拍再開し、当院搬送されたが、循環動態が安定せず、造影CTにて急性肺塞栓症と左膝窩静脈嚢状瘤と診断した。大量肺動脈血栓に対して、経皮的カテーテル治療を施行し、術直後より循環動態は安定した。血行動態が不安定な重症肺動脈塞栓症に対しては、速やかな血栓除去が必要であり、カテーテル治療は極めて有効であった。又、肺塞栓症の原因である膝窩静脈嚢状瘤に対しては、待機的に瘤の切開縫縮術を施行し、術後も抗凝固療法を併用した。しかし、外科的治療の長期有効性には、更なる検討が必要であると思われた。(著者抄録)

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  • 急性心筋梗塞に伴う一過性の左室流出路狭窄 その発症条件に対する考察

    尾崎 和幸, 佐藤 迪夫, 池上 龍太郎, 飛田 一樹, 小林 剛, 羽尾 和久, 保坂 幸男, 土田 圭一, 高橋 和義, 三井田 努, 小田 弘隆

    日本心臓病学会誌   5 ( Suppl.I )   229 - 229   2010.8

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MISC

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Awards

  • 学生表彰(大学院)

    2019.3   新潟大学  

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  • Clinical Research Award YIA

    2018.9   日本循環器学会関東甲信越地方会  

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  • YIA finalist

    2016.12   日本心血管代謝内分泌学会  

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  • YIA

    2016.12   日本抗加齢学会脳心血管抗加齢研究会  

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Research Projects

  • 近赤外線自家蛍光法による不安定プラークの診断および治療法の開発

    Grant number:23K15095

    2023.4 - 2026.3

    System name:科学研究費助成事業

    Research category:若手研究

    Awarding organization:日本学術振興会

    池上 龍太郎

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    Grant amount:\4550000 ( Direct Cost: \3500000 、 Indirect Cost:\1050000 )

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  • 近赤外線蛍光法による動脈硬化質的診断法の開発

    2023.1 - 2024.12

    Awarding organization:公益財団法人アステラス病態代謝研究会

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  • 近赤外線自家蛍光粒子に着目した動脈硬化プラークの質的診断法および治療法の開発

    Grant number:22K20911

    2022.8 - 2024.3

    System name:科学研究費助成事業

    Research category:研究活動スタート支援

    Awarding organization:日本学術振興会

    池上 龍太郎

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    Grant amount:\2860000 ( Direct Cost: \2200000 、 Indirect Cost:\660000 )

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  • 近赤外線蛍光法による冠動脈プラーク質的診断法の開発

    2020.1 - 2021.12

    System name:海外留学リサーチフェローシップ

    Awarding organization:上原記念財団

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  • Effect of osteoporosis therapy with receptor activator for NFkappa B ligand inhibitor on coronary calcifications

    Grant number:18K08030

    2018.4 - 2021.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    OZAWA TAKUYA

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    Grant amount:\4420000 ( Direct Cost: \3400000 、 Indirect Cost:\1020000 )

    The purpose of this study was to investigate the effect of denosumab, a receptor activator for NF-κβ ligand (RANKL), on vascular calcifications in patients with primary osteoporosis and coronary calcification. However, this study was suspended due to difficulty in securing the required number of patients. 84-year-old male with primary osteoporosis was registered. At base line, the coronary artery calcification (CAC) score was 477.4, the volume score was 4.777cm2 and the bone density of femoral bone was 0.57g/cm2. This patient was assigned to receive alendronate. The bone density improved slightly to 0.582g/cm2. The CAC score was 606.8 and the volume score was 6.073cm2. The %ΔCAC/48 weeks and the %Δvolume score/48 weeks were +27% and +27%, respectively. According to past reports, the natural history of coronary artery calcification progression is reported to be around +30%, and these results were consistent with that.

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