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A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography.

A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Research Abstract Details 

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  • A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Abstract Text:

    tetsuro yoshidaTetsuro Yoshida,takeshi hibinoTakeshi Hibino,nobuo kakoNobuo Kako,shunsuke muraiShunsuke Murai,mitsutoshi oguriMitsutoshi Oguri,kimihiko katoKimihiko Kato,kazuhiro yajimaKazuhiro Yajima,nobuyuki ohteNobuyuki Ohte,kiyoshi yokoiKiyoshi Yokoi,genjiro kimuraGenjiro Kimura,

    AIMS; Our study aims to investigate the pathophysiologic mechanism underlying tako-tsubo cardiomyopathy using F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET). METHODS AND RESULTS: Fifteen patients with tako-tsubo cardiomyopathy were enrolled in this study. Plasma catecholamines, cardiac troponin T (cTnT), and D-dimer were serially evaluated in all patients. Thallium-201 ((201)Tl) single-photon emission computed tomography (SPECT) and F-18 FDG PET were performed in 10 and eight patients, respectively. Emotional or physical stress occurred in 12 (80.0%) patients. ST-T segment abnormalities existed in all patients. Thirteen patients exhibited mildly elevated cTnT, although coronary angiography did not reveal significant stenosis in any patient. Endomyocardial biopsy specimens (n = 9) demonstrated contraction-band necrosis (n = 4) and mononuclear cell infiltration (n = 3). The levels of norepinephrine and epinephrine peaked on admission (744 +/- 452 and 140 +/- 166 pg/mL, respectively). There was severely reduced uptake at the apex on F-18 FDG PET image, despite slightly reduced uptake of (201)Tl. Elevation of D-dimer was observed in nine patients. CONCLUSION: The extent of metabolic defect involving apical akinetic area was more severe than perfusion abnormality. Our data suggest that sudden emotional or physical stress may cause a catecholamine-induced metabolic disorder in the myocardium, which is probably central to this syndrome.

    A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Publishing Authors By Initials

    t yoshidaT Yoshida,t hibinoT Hibino,n kakoN Kako,s muraiS Murai,m oguriM Oguri,k katoK Kato,k yajimaK Yajima,n ohteN Ohte,k yokoiK Yokoi,g kimuraG Kimura,

    For similar abstracts research abstracts see: abstracts research

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    A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: European heart journal

    VOLUME: 28

    Page Numbers: 2598-604

    Journal Abbreviation: Eur. Heart J.

    ISSN: 0195-668X

    DAY: 7

    MONTH: 10

    YEAR: 2007

    A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Information

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    LANGUAGE: eng

    NlmUniqueID: 8006263

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    Grant and Affiliation Information for A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography.

    AFFILIATION: Department of Cardiovascular Medicine, Gifu Prefectural Government Tajimi Hospital, 5-161 Maehata, Tajimi, Gifu 5078522, Japan. tetsuro-moet@nifty.com

    Country: England

    England Research PublicationEngland Research Publication

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    MEDLINETA: Eur Heart J

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