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European Heart Journal Advance Access published online on October 7, 2007

European Heart Journal, doi:10.1093/eurheartj/ehm401
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

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

Tetsuro Yoshida1,*, Takeshi Hibino1, Nobuo Kako2, Shunsuke Murai1, Mitsutoshi Oguri1, Kimihiko Kato1, Kazuhiro Yajima1, Nobuyuki Ohte3, Kiyoshi Yokoi1 and Genjiro Kimura3

1 Department of Cardiovascular Medicine, Gifu Prefectural Government Tajimi Hospital, 5-161 Maehata, Tajimi, Gifu 5078522, Japan
2 Department of Radiology, Kizawa Memorial Hospital, Minokamo, Japan
3 Department of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

* Corresponding author. Tel: +81 572 22 5311; fax: +81 572 25 1246. E-mail address: tetsuro-moet{at}nifty.com

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 (201Tl) 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 201Tl. 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.

Key Words: Tako-tsubo cardiomyopathy • Catecholamine-induced metabolic disorder • F-18 fluorodeoxyglucose positron emission tomography


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