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Affiliation |
Faculty of Medicine School of Medicine Department of Medical Sciences, Cardiovascular Physiology |
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External Link |
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WATANABE Nozomi
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Papers 【 display / non-display 】
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Furugen M., Watanabe N., Nishino S., Kimura T., Ashikaga K., Kuriyama N., Shibata Y.
Journal of Cardiology 78 ( 5 ) 423 - 430 2021.11
Language：English Publishing type：Research paper (scientific journal) Publisher：Journal of Cardiology
Background: Previous studies have proposed that osteogenic and apoptotic processes of valve interstitial cells contribute to the mineralization and then calcification of the aortic valve. Osteoblast-like cells subsequently mediate calcification of the aortic valve as part of a highly regulated process analogous to skeletal bone formation. The objective of this study was to evaluate the pathogenesis of the sclerotic/calcific changes in the aortic valve from histological and biological findings, and investigate the role of osteoblasts in the calcified pathway of aortic stenosis. Methods: Preoperative echocardiography in 550 consecutive patients with osteoporotic hip fracture were retrospectively examined (475 females, mean 25th–75th, 89 [85–93] years). One hundred sixteen patients were under medical treatment with anti-osteoporosis drugs. We evaluated the prevalence and degree of degenerative changes in the aortic valve and examined the associations of bone turnover biomarkers N-terminal pro-peptide of type 1 collagen (P1NP) and serum tartrate-resistant acid phosphatase (TRACP-5b) with degenerative calcific changes in the aortic valve. Results: Of 550 patients, 112 patients (20.9%) showed no leaflet calcification; 296 (53.8%), 1 leaflet calcification; and 142 (25.8%), 2 ≥ leaflets calcification. Significant (peak velocity ≥ 3.0m/s) Aortic stenosis was found in 43 patients (7.8%). In patients who were not taking anti-osteoporotic drugs, P1NP was higher in the 2 ≥ leaflets calcification group than in the other groups (p < 0.01). TRACP-5b was not significantly different among the three groups (p = 0.15). Conclusions: Degenerative changes in the aortic valve were related to bone biomarker activation in osteoporotic hip fracture patients.
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Haruki Shinomiya, Hisakazu Kato, Yuki Kuramoto, Nozomi Watanabe, Toshihiro Tsuruda, Tadaaki Arimura, Yohei Miyashita, Yoshiki Miyasaka, Tomoji Mashimo, Ayako Takuwa, Daisuke Motook, Daisuke Okuzaki, Ken Matsuoka, Osamu Tsukamoto, Hideyuki Hakui,Noriaki Yamada,Jong-Kook Lee,Hidetaka Kioka,Masafumi Kitakaze,Seiji Takashima,Yasushi Sakata,Yoshihiro Asano
FASEB Journal 35 ( 11 ) e21994 2021.10
Language：English Publishing type：Research paper (scientific journal) Publisher：FASEB Journal
Arrhythmogenic cardiomyopathy (ACM) caused by TMEM43 p.S358L is a fully penetrant heart disease that results in impaired cardiac function or fatal arrhythmia. However, the molecular mechanism of ACM caused by the TMEM43 variant has not yet been fully elucidated. In this study, we generated knock-in (KI) rats harboring a Tmem43 p.S358L mutation and established induced pluripotent stem cells (iPSCs) from patients based on the identification of TMEM43 p.S358L variant from a family with ACM. The Tmem43-S358L KI rats exhibited ventricular arrhythmia and fibrotic myocardial replacement in the subepicardium, which recapitulated the human ACM phenotype. The four-transmembrane protein TMEM43 with the p.S358L variant (TMEM43S358L) was found to be modified by N-linked glycosylation in both KI rat cardiomyocytes and patient-specific iPSC-derived cardiomyocytes. TMEM43S358L glycosylation increased under the conditions of enhanced endoplasmic reticulum (ER) stress caused by pharmacological stimulation or age-dependent decline of the ER function. Intriguingly, the specific glycosylation of TMEM43S358L resulted from the altered membrane topology of TMEM43. Moreover, unlike TMEM43WT, which is mainly localized to the ER, TMEM43S358L accumulated at the nuclear envelope of cardiomyocytes with the increase in glycosylation. Finally, our comprehensive transcriptomic analysis demonstrated that the regional differences in gene expression patterns between the inner and outer layers observed in the wild type myocardium were partially diminished in the KI myocardium prior to exhibiting histological changes indicative of ACM. Altogether, these findings suggest that the aberrant accumulation of TMEM43S358L underlies the pathogenesis of ACM caused by TMEM43 p.S358L variant by affecting the transmural gene expression within the myocardium.
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Non-rheumatic giant left atrium: An illustrative case successfully treated by surgical intervention Reviewed
Honda Y., Watanabe N., Nishino S., Matsuura H., Nishimura M., Yano M., Kataoka H., Shibata Y.
Journal of Cardiology Cases 24 ( 2 ) 79 - 83 2021.8
Language：English Publishing type：Research paper (scientific journal) Publisher：Journal of Cardiology Cases
A 45-year-old male presented to us with decompensated heart failure. He had been diagnosed as having atrial fibrillation when he was 31 years old. Transthoracic and transesophageal echocardiography revealed an excessive left atrial (LA) enlargement with left ventricular dysfunction and severe functional mitral regurgitation. There were no specific findings of rheumatic valve disease. He underwent surgical mitral valve replacement and LA volume reduction surgery after optimal medical therapy. Surgically-removed specimens of the LA and the anterior mitral leaflet were examined and there were no specific histopathological findings suggesting the specific etiology of the giant LA in this patient. The patient's condition significantly improved after the surgery without any cardiac events ever since. <Learning objective: Non-rheumatic giant left atrium (LA) is rare but can cause decompensated heart failure with various types of complications and hemodynamic problems. Mitral annular dilation and changes in the valve morphology often cause functional mitral regurgitation in giant LA, which adversely affect the hemodynamic condition. Valve surgery and surgical reduction of LA was effective in the present case.>
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Matsuura H., Watanabe N., Shibata Y., Asada Y.
Journal of Echocardiography 19 ( 2 ) 86 - 94 2021.6
Language：Japanese Publishing type：Research paper (scientific journal) Publisher：Journal of Echocardiography
Myocarditis is a fatal inflammatory disease of myocardium, diagnosed with clinical and histopathological findings by endomyocardial biopsy (EMB). Myocarditis has a variety of clinical presentations and a dynamic and sometimes rapid process of severity. Echocardiography plays an important role in the management of myocarditis because it has noninvasiveness and portability. Once acute myocarditis is suspected by an echocardiography, pathological information should be required as early as possible. In our cardiovascular center, emergency EMB suspecting myocarditis was performed in 19 cases (1.3%) among consecutive 1469 cases (70.1 ± 12.6 years old, male 67.5%) undergoing emergency coronary angiograms from April 2014 to September 2017. Hematoxylin–eosin stain of the biopsy specimens were prepared with microwave-accelerated histoprocessing within 3–5 hours after EMB for rapid pathological diagnosis of myocarditis. We reviewed the value of emergency echo-EMB combination leading to the early decision making of intensive care, corticosteroids and proper mechanical circulatory support prior to the possible sudden collapse in patients with myocarditis.
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ST-Elevation Myocardial Infarction With Cardiogenic Shock and Severe Acute Ischemic Mitral Regurgitation Rescued by Primary Coronary Intervention Under Hemodynamic Support With Impella. Reviewed
Koiwaya H, Watanabe N, Nishihira K, Goriki Y, Shibata Y
Circulation reports 3 ( 5 ) 304 - 305 2021.4
Language：English Publishing type：Research paper (scientific journal)
Books 【 display / non-display 】
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ASE’s Comprehensive Echocardiography Third edition
Nozomi Watanabe（ Role： Joint author , Chapter 75 Takotsubo Cardiomyopathy）
SAUNDERS 2021
Language：English Book type：Textbook, survey, introduction
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ハートバルブ・カンファレンス : 弁膜症診療の“キモ"がわかる : 徹底討論!
川副 浩平, 泉 知里, 渡邉 望, 渡辺 弘之（ Role： Joint author）
メジカルビュー社 2021 （ ISBN:9784758319676 ）
Language：Japanese Book type：Scholarly book
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ガイドラインを心エコーに生かす：ケースから学ぶ指針の解釈と活用
渡邉 望（ Role： Joint author , 二次性（機能性）僧帽弁閉鎖不全症：左室収縮能低下）
メジカルビュー社 2020
Language：Japanese Book type：Textbook, survey, introduction
Presentations 【 display / non-display 】
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心臓外科医と診る僧帽弁形成術の周術期心エコー図
渡邉 望
第19回KCH-CVS心臓疾患研究会 2021.10.9
Event date： 2021.10.9
Language：Japanese Presentation type：Oral presentation (general)
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インターベンション医と診る心エコー：最新モダリティを活かしたチーム医療のために Invited
渡邉 望
第27回日本心血管インターベンション治療学会(CVIT)中国・四国地方会 2021.9.14
Event date： 2021.9.14
Language：Japanese Presentation type：Oral presentation (invited, special)
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Case, Case, Case!! 症例から学ぶ心エコー Vol.2 Invited
渡邉 望
第13回実地医家のための心エコー図勉強会 2021.9.14
Event date： 2021.9.14
Language：Japanese Presentation type：Symposium, workshop panel (nominated)
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心筋病理と診る心エコー図 Invited
渡邉 望
知っておくべきファブリー病 in 東海 2021.8.19
Event date： 2021.8.19
Language：Japanese Presentation type：Oral presentation (general)
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循環器診断における心エコーの役割：薬物治療から最先端治療まで Invited
渡邉 望
第29回宮崎心エコー研究会 2021.8.2
Event date： 2021.8.2
Language：Japanese Presentation type：Oral presentation (invited, special)
Awards 【 display / non-display 】
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8. 9th Cardiovascular Clinical Research Investigator's Award "Clinical Research Investigator
2020.3 Japanese Circulation Society
Award type：Award from international society, conference, symposium, etc.