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

Abstract

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.