European Heart Journal Advance Access originally published online on January 31, 2008
European Heart Journal 2008 29(5):681; doi:10.1093/eurheartj/ehm635
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A pathophysiological study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography
Department of Internal Medicine
University of Arizona College of Medicine
1501 N Campbell Avenue
Tucson, AZ 85724
USA
Tel: +1 520 437 1635
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Email: drkutty2{at}gmail.com
An interesting observational study by Yoshida et al.1 using F-18 fluorodeoxyglucose positron emission tomography identified that the extent of metabolic defect involving apical akinetic area was more severe than perfusion abnormality in tako-tsubo cardiomyopathy. There are few questions worth answering in stress cardiomyopathy.
Does the abnormal catecholamine flux in the cardiac apex during the emotional and physical stress account for abnormal glucose metabolism?
It has been already known that adrenoceptor density is higher in the cardiac apex, compared with other areas of the myocardium, which may account for the apical ballooning during the catecholamine stress in tako-tsubo cardiomyopathy.2 There can also be abnormal coronary flow in the absence of obstructive disease in patients with stress-related myocardial dysfunction. Study by Akashi et al.3 using 123I- metaiodobenzyl guanidine myocardial scintigraphy showed a unique pattern of ventricular asynergy, suggesting the existence of cardiac sympathetic hyperactivity with maintained coronary blood flow. Therefore, there is a possibility that abnormal glucose metabolism at the cardiac apex may be due to the increased density of adrenal receptors in the apex.
Do the sex hormones play a role in pathogenesis of tako-tsubo cardiomyopathy?
From the available medical literature so far, women—especially middle-aged or elderly—are the most commonly affected. The same gender difference is again demonstrated in the study by Yoshida et al.1 Mostly, this disease affects young women and men, but the vast majority of these patients are post-menopausal women. Indeed, >90% of the patients suffering from stress cardiomyopathy are females.4 The basis for this predisposition is unknown. Sex hormones exert important influences on the sympathetic neurohormonal axis as well as on coronary vasoreactivity,5 but sex-related differences in catecholamine metabolism and responsiveness are complex and remain poorly understood.
References
- Yoshida T, Hibino T, Kako N, Murai S, Oguri M, Kato K, Yajima K, Ohte N, Yokoi K, Kimura G. A pathophysiologic study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Eur Heart J (2007) 28:2598–2604.
[Abstract/Free Full Text] - Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion HC. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med (2005) 352:539–548.
[Abstract/Free Full Text] - Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Musha H, Sasaka K. 123I-MIBG myocardial scintigraphy in patients with ‘takotsubo’ cardiomyopathy. J Nucl Med (2004) 45:1121–1127.
[Abstract/Free Full Text] - Ramaraj R. Stress cardiomyopathy: aetiology and management. Postgrad Med J (2007) 83:543–546.
[Abstract/Free Full Text] - Sader MA, Celermajer DS. Endothelial function, vascular reactivity and gender differences in the cardiovascular system. Cardiovasc Res (2002) 53:597–604.
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