Katsumata, Yoshinori

写真a

Affiliation

School of Medicine, Institute for Integrated Sports Medicine (Shinanomachi)

Position

Senior Assistant Professor (Non-tenured)/Assistant Professor (Non-tenured)

Career 【 Display / hide

  • 2005.04
    -
    2006.03

    Keio University School of Medicine, 臨床初期研修医

  • 2006.04
    -
    2007.03

    National Hospital Organization Saitama National Hospital, 臨床初期研修医

  • 2007.04
    -
    2008.03

    Keio University School of Medicine, 内科, 後期研修医

  • 2008.04
    -
    2009.03

    SANOKOUSEI General Hospital, 内科, 後期研修医

  • 2009.04
    -
    2014.09

    Keio University School of Medicine, Department of Cardiology

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Academic Background 【 Display / hide

  • 1999.04
    -
    2005.03

    Keio University, Medical Department

    Japan, University, Graduated, Doctoral course

  • 2009.04
    -
    2013.03

    Keio University, Medical Department

    Graduate School, Graduated

Academic Degrees 【 Display / hide

  • 医学博士, Keio University, Coursework, 2014.09

    Endogenous Prostaglandin D2 and Its Metabolites Protect the Heart Against Ischemia-Reperfusion Injury by Activating Nrf2

Licenses and Qualifications 【 Display / hide

  • Medical License, 2005.04

  • Board Certified Member of the Japanese Society of Internal Medicine, 2008.09

  • Fellow of the Japanese Society of Internal Medicine (FJSIM), 2011.12

  • A heart rehabillitation guidance person, 2013.09

  • Board Certified Member of The Japanese Circulation Society, 2014.04

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Research Areas 【 Display / hide

  • General medical chemistry

  • Cardiovascular medicine

Research Keywords 【 Display / hide

  • arrhythmia

  • metabolome

  • exercise

  • Genetic cardiac desease

Research Themes 【 Display / hide

  • ウェアラブル機器を用いた運動中の心拍変動解技術の開発と運動療法への応用, 

    2017
    -
    Present

  • 心血管疾患の包括的遺伝子診断システムの構築研究, 

    2017
    -
    Present

  • ベルト電極式骨格筋電気刺激法を用いた心不全急性期の廃用予防に関する研究, 

    2017
    -
    Present

  • 心血管疾患の精密医療実現に向けた研究開発、人における、オミックス解析の実現化, 

    2016
    -
    Present

  • 心臓における代謝の空間的・時間的マップ作製に向けた研究開発, 

    2012
    -
    2017

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Books 【 Display / hide

  • これからの日本の健康・医療戦略:日本医療研究開発機構(AMED)をめぐって

    Katsumata Yoshinori, 南江堂, 2015.12

     View Summary

    「日本医療研究開発機構(Japan Agency for Medical Research and Development: 以下「AMED」と表記)」が2015年4月1日に創設され,これまで文部科学省,厚生労働省および経済産業省がそれぞれに実施してきた医療分野の研究費配分等の機能をAMEDに集約することにより,された。これにより、基礎から実用化までの切れ目ない研究開発の推進,成果の円滑な実用化や研究開発のための環境整備等の総合的かつ効率的な運営を開始した。
    政府の「日本再興戦略(2013年6月)」 の中で重点的な取組と位置付けられた政策の1つが,健康長寿社会の実現であった。「日本再興戦略」では、医療分野も日本の戦略的産業と位置付けており、高度な医療の育成により「健康長寿社会」が実現され、国民一人ひとりに幸せをもたらすとしている。また、「健康長寿社会の実現」は、高齢者の社会参画による労働力の確保、増加する社会保障費の抑制といった効果も期待できる。

Papers 【 Display / hide

  • Visualization of the electrophysiologically defined junction between the superior vena cava and right atrium

    Nishiyama N., Hashimoto K., Yamashita T., Miyama H., Fujisawa T., Katsumata Y., Kimura T., Fukuda K., Takatsuki S.

    Journal of Cardiovascular Electrophysiology (Journal of Cardiovascular Electrophysiology)  31 ( 8 ) 1964 - 1969 2020.08

    ISSN  10453873

     View Summary

    © 2020 Wiley Periodicals LLC Introduction: An electrical superior vena cava (SVC) isolation from the right atrium (RA) sometimes can be challenging. For a safe and efficient SVC isolation, we aimed to visualize the accurate position of the SVC-RA junction on a three-dimensional (3D) mapping system using the decremental conduction properties of the SVC-RA junction in patients with atrial fibrillation (AF). Methods: This study consisted of 15 consecutive AF patients (11 males, age 59 ± 10 years). A 3D mapping catheter was positioned in the SVC-RA junction region while delivering a single extra-stimulus from the right atrial appendage (RAA), to discriminate the RA and SVC potentials. The electrophysiological SVC-RA junction was defined as the most proximal points where the SVC potentials were recorded, which were tagged on the 3D mapping system around the SVC-RA junction, where radiofrequency energy applications were applied. Results: Around the SVC-RA junction, 9 ± 2 points were tagged on the 3D mapping system. The highest and lowest SVC-RA junction points were located on the anterior wall and posterior wall, respectively. The difference in the level between the highest and lowest SVC-RA junction points was 16.2 ± 6.3 mm. A successful SVC isolation was obtained in all patients without any complications. Conclusion: The plane of the electrophysiologically defined SVC-RA junction was not perpendicular to the body axis, but slanted due to the anterior side being higher. Recognizing the precise location of the SVC-RA junction would contribute to a safe and efficacious SVC isolation.

  • Discrepancy in recognition of symptom burden among patients with atrial fibrillation

    Katsumata Y., Kimura T., Kohsaka S., Ikemura N., Ueda I., Fujisawa T., Nakajima K., Nishiyama T., Aizawa Y., Oki T., Suzuki M., Heidenreich P.A., Fukuda K., Takatsuki S.

    American Heart Journal (American Heart Journal)  226   240 - 249 2020.08

    ISSN  00028703

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    © 2020 Elsevier Inc. Our aim was to investigate the variability in physician recognition of atrial fibrillation (AF)-related symptoms, which greatly contributes to the management of AF patients. Methods and Results: A total of 1493 newly-referredAF patients (67 ± 11 y/o, 1057 men) consecutively registered in an outpatient-based Japanese multicenter database (KiCS-AF) from September 2012 to December 2016 were analyzed. Self-reportedAF symptom burden was assessed via symptom and daily activities domains within the Atrial Fibrillation Effect on QualiTy-of-life (AFEQT) questionnaire. Physician symptom under-recognition (UR) was defined as no subjective complaints recorded in the medical records despite AFEQT score of <80; and physician's apparent over-recognition (OvR) was defined as documentation of subjective complaints despite total AFEQT score of ≥80. There was poor agreement between patient-reported and physicians-estimated symptom burden (kappa 0.28, 95% CI 0.23 to 0.33). In the logistic regression analysis, age> 75 (odds ratio [OR], 1.72; 95% confidence interval [CI], 1.13–2.62), male sex (OR, 1.82; 95% CI, 1.22–2.74), and persistent/permanent AF (OR 2.54/3.36; CI, 1.63–3.99/1.91–5.89, respectively) were predictors of UR. Conversely, heart failure (OR, 2.46; 95% CI, 1.44–4.25) and treatment in an ablation facility (OR, 1.43; 95% CI, 1.02–2.02) were associated with greater odds of OvR in addition to age, sex, and type of AF. Conclusions: Discordance in recognition of AF symptom burden by physicians was frequent in AF patients seen in outpatient management and involved both patient- and physician-related factors.

  • Successful Surgical Treatment Combined With Infliximab in a Patient With Acute Aortic Regurgitation Caused by Behçet Disease

    Kawakubo Y., Katsumata Y., Komuro J., Shiraishi Y., Yuasa S., Itabashi Y., Kohno T., Fukuda K.

    Canadian Journal of Cardiology (Canadian Journal of Cardiology)  36 ( 7 ) 1161.e3 - 1161.e5 2020.07

    ISSN  0828282X

     View Summary

    © 2020 Canadian Cardiovascular Society Standard aortic valve replacement for aortic regurgitation caused by Behçet disease (BD) is frequently complicated by postoperative recurrent prosthetic valve detachment. Tumour necrosis factor (TNF) α is known to be associated with higher inflammation activities. Therefore, the concomitant use of immunomodulatory agents with TNFα inhibitors may be the key to a better outcome. This is a case report of a 46-year-old woman with severe acute aortic regurgitation due to BD. Immunosuppressive therapy including the TNFα inhibitor infliximab, which has not been reported for perioperative use to date, resulted in the prompt remission of inflammation, leading to the success of Bentall surgery.

  • Pharmacokinetics of a single inhalation of hydrogen gas in pigs

    Sano M., Ichihara G., Katsumata Y., Hiraide T., Hirai A., Momoi M., Tamura T., Ohata S., Kobayashi E.

    PLoS ONE (PLoS ONE)  15 ( 6 )  2020.06

     View Summary

    © 2020 Sano et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The benefits of inhaling hydrogen gas (H2) have been widely reported but its pharmacokinetics have not yet been sufficiently analyzed. We developed a new experimental system in pigs to closely evaluate the process by which H2 is absorbed in the lungs, enters the bloodstream, and is distributed, metabolized, and excreted. We inserted and secured catheters into the carotid artery (CA), portal vein (PV), and supra-hepatic inferior vena cava (IVC) to allow repeated blood sampling and performed bilateral thoracotomy to collapse the lungs. Then, using a hydrogen-absorbing alloy canister, we filled the lungs to the maximum inspiratory level with 100% H2. The pig was maintained for 30 seconds without resuming breathing, as if they were holding their breath. We collected blood from the three intravascular catheters after 0, 3, 10, 30, and 60 minutes and measured H2 concentration by gas chromatography. H2 concentration in the CA peaked immediately after breath holding; 3 min later, it dropped to 1/40 of the peak value. Peak H2 concentrations in the PV and IVC were 40% and 14% of that in the CA, respectively. However, H2 concentration decay in the PV and IVC (half-life: 310 s and 350 s, respectively) was slower than in the CA (half-life: 92 s). At 10 min, H2 concentration was significantly higher in venous blood than in arterial blood. At 60 min, H2 was detected in the portal blood at a concentration of 6.9–53 nL/mL higher than at steady state, and in the SVC 14–29 nL/mL higher than at steady state. In contrast, H2 concentration in the CA decreased to steady state levels. This is the first report showing that inhaled H2 is transported to the whole body by advection diffusion and metabolized dynamically.

  • Palmitate induces cardiomyocyte death via inositol requiring enzyme-1 (IRE1)-mediated signaling independent of X-box binding protein 1 (XBP1)

    Yamamoto T., Endo J., Kataoka M., Matsuhashi T., Katsumata Y., Shirakawa K., Isobe S., Moriyama H., Goto S., Shimanaka Y., Kono N., Arai H., Shinmura K., Fukuda K., Sano M.

    Biochemical and Biophysical Research Communications (Biochemical and Biophysical Research Communications)  526 ( 1 ) 122 - 127 2020.05

    ISSN  0006291X

     View Summary

    © 2020 The Authors Overloading of the saturated fatty acid (SFA) palmitate induces cardiomyocyte death. The purpose of this study is to elucidate signaling pathways contributing to palmitate-induced cardiomyocyte death. Palmitate-induced cardiomyocyte death was induced in Toll-like receptor 2/4 double-knockdown cardiomyocytes to a similar extent as wild-type cardiomyocytes, while cardiomyocyte death was canceled out by triacsin C, a long-chain acyl-CoA synthetase inhibitor. These results indicated that palmitate induced cytotoxicity after entry and conversion into palmitoyl-CoA. Palmitoyl-CoA is not only degraded by mitochondrial oxidation but also taken up as a component of membrane phospholipids. Palmitate overloading causes cardiomyocyte membrane fatty acid (FA) saturation, which is associated with the activation of endoplasmic reticulum (ER) unfolded protein response (UPR) signaling. We focused on the ER UPR signaling as a possible mechanism of cell death. Palmitate loading activates the UPR signal via membrane FA saturation, but not via unfolded protein overload in the ER since the chemical chaperone 4-phenylbutyrate failed to suppress palmitate-induced ER UPR. The mammalian UPR relies on three ER stress sensors named inositol requiring enzyme-1 (IRE1), PKR-like endoplasmic reticulum kinase (PERK), and activating transcription factor 6 (ATF6). Palmitate loading activated only IRE1 and PERK. Knockdown of PERK did not affect palmitate-induced cardiomyocyte death, while knockdown of IRE1 suppressed palmitate-induced cardiomyocyte death. However, knockdown of X-box binding protein 1 (XBP1), the downstream effector of IRE1, did not affect palmitate-induced cardiomyocyte death. These results were validated by pharmacological inhibitor experiments. In conclusion, we identified that palmitate-induced cardiomyocyte death was triggered by IRE1-mediated signaling independent of XBP1.

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Reviews, Commentaries, etc. 【 Display / hide

Presentations 【 Display / hide

  • Development of in vivo four-dimensional [4D] metabolism imaging

    Katsumata Yoshinori

    The 2nd JCS Council Forum on Basic Cardiovascular Research, 2018.09, Oral Presentation(general)

     View Summary

    We aimed to continuously grasp temporal changes in local cardiac metabolism using an in vivo micro-dialysis method in mice hearts 10 min after ligation of the left anterior descending artery. An additional goal was to establish in vivo 4D metabolism imaging technology by combining this micro-dialysis technique and quantitative metabolic flux imaging (spatial grasp of metabolism) technology using isotope elements (13C palmitate, 13C glucose, 13C lactate, 13C acetoacetic acid, 13C glutamate, and 2H2).

  • Effect under-recognition of symptom on treatment strategy and quality of life in outpatients with atrial fibrillation

    Katsumata Yoshinori

    Japanese heart rhythm scientific session 2017, YIA session, 2018.07, Oral Presentation(general)

  • Change in the Quality of Life after Catheter Ablation on ‘Asymptomatic’ Patients with Atrial Fibrillation

    Katsumata Yoshinori

    Japanese heart rhythm scientific session 2017, 2017.09, Oral Presentation(general)

  • Change in the Quality of Life after Catheter Ablation on ‘Asymptomatic’ Patients with Atrial Fibrillation

    Katsumata Yoshinori

    heart rhythm scientific session 2017, 2017.05, Oral Presentation(general)

  • Change in the Quality of Life after Catheter Ablation on ‘Asymptomatic’ Patients with Atrial Fibrillation

    Katsumata Yoshinori

    The 81th annual scientific meeting of the Japanese Circulation Society, 2017.03, Oral Presentation(general)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 心臓における、警告シグナルとしてのグルタチオンの新たな機能の解明

    2021.04
    -
    2024.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 勝俣 良紀, Grant-in-Aid for Scientific Research (C), Principal Investigator

  • Development of in vivo four-dimensional [4D] metabolism imaging

    2019.04
    -
    2021.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 勝俣 良紀, Grant-in-Aid for Early-Career Scientists , Principal Investigator

  • 日本循環器学会2018年度基礎研究助成

    2018
    -
    Present

    一般社団法人日本循環器学会, 勝俣良紀, Research grant, Principal Investigator

     View Summary

    心臓におけるin vivo 四次元代謝イメージング技術の開発と応用

  • Takeda Japan Medical Affairs Funded Research Grant 2018

    2018
    -
    Present

    武田薬品工業株式会社, 勝俣良紀, Research grant

     View Summary

    リアルタイム心拍変動解析と運動強度の自己管理システムの開発

  • 平成29年度 日本心臓リハビリテーション学会学術研究助成

    2017
    -
    Present

    日本心臓リハビリテーション学会, 勝俣良紀, Principal Investigator

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    心臓自律神経反射機能リアルタイム画像を用いた自動有酸素運動通知システムおよび新規運 動療法の開発

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Awards 【 Display / hide

  • Young investigator award優秀賞受賞

    2018.07, 日本不整脈心電学会, Effect Under-recognition of Symptom on Treatment Strategy and Quality of Life in Outpatients with Atrial Fibrillation

  • 第4回循環器イメージング賞優秀賞

    2017.03, 日本循環器学会, Visualization of In Vivo Metabolic Flows Reveals Accelerated Utilization of Glucose and Lactate in Penumbra of Ischemic Heart

    Country: 日本

     View Description

    第4回 循環器イメージング賞優秀賞は26名の応募者の中から書類審査で選考された3名が受賞した。本研究はマウス心臓の代謝イメージングに関するものである。質量分析計の開発改良に伴い、近年、臓器の代謝イメージングが実現可能となってきたが、心臓は死後の代謝変化が著しく、解糖系やクエン酸回路などの中心代謝産物の正確な代謝イメージングは難しかった。そこで、死後の代謝変化を最小限にするため、マイクロウェーブによる固定法を開発した。さらに、炭素13(13C)でラベルした基質を用いて、心筋梗塞モデルのグルコースおよび乳酸のトレースイメージングも成功した。虚血の中心部ではグルコースを乳酸に変換するとともに、乳酸を積極的にTCAサイクルで代謝していること、虚血の周辺部位ではグルコースを積極的にTCAサイクルで代謝していることがトレースイメージングにより明らかとなった。

 

Memberships in Academic Societies 【 Display / hide

  • The Japan Society of Human Genentics, 

    2015.10
    -
    Present
  • Japan Cardiac Rehabilitation Society, 

    2011
    -
    Present
  • Japanese Heart Rhythm Society, 

    2011
    -
    Present
  • Japanese Circulation Society, 

    2008
    -
    Present
  • The Japanese Society of Internal Medicine, 

    2006
    -
    Present