Stress-Induced Cardiomyopathy: Advance & Catecholamine-Induced Inflammation

Stress-Induced Cardiomyopathy: Advance & Catecholamine-Induced Inflammation
SHORT FEATURES and FACES ARTICLE

A recent Editorial published in the March 2012 issue of Expert Review of Cardiovascular Therapy outlines some new insights and research trends related to stress-induced cardiomyopathy.

Stress-induced cardiomyopathy, also known as “Takotsubo” cardiomyopathy, broken heart syndrome and apical ballooning syndrome, was first described in Japan, in 1990, by Sato et al.

The syndrome is characterized by a bulging out of the left ventricular apex with a hyper-contractile base of the left ventricle. The term “Takotsubo” is a Japanese word for a round-bottomed pot with a narrow neck used for trapping octopuses.

Stress-induced cardiomyopathy represents a transient left ventricle systolic dysfunction with electrocardiographic changes that can mimic acute myocardial infarction and minimal release of myocardial enzymes in the absence of obstructive coronary artery disease. This cardiomyopathy is more commonly seen in post-menopausal women and most likely accounts for 1% to 2% of all cases of suspected acute myocardial infarction.

Data from patients who underwent myocardial biopsy indicate interstitial infiltrates consisting primarily of mononuclear lymphocytes, leukocytes, macrophages, myocardial fibrosis; and contraction bands with or without overt myocyte necrosis. Mechanisms suggested being involved in the etiology and pathophysiologies of stress-induced cardiomyopathy include: coronary microcirculatory abnormalities, multi-vessel epicardial spasm and regionally stunned myocardium, high circulating levels of catecholamines (mostly epinephrine/adrenaline) and related catecholamine-mediated cardiotoxicity.

A neurogenic stunned myocardium has also been linked with a much higher concentration of adrenoceptors in the left ventricular apex, and thus, to a pronounced myocardial responsiveness to adrenergic stimulation in the apex. Takotsubo cardiomyopathy might be due to a locally high toxic concentration of catecholamines, not coronary artery or microvascular disease (for review, see Yoshihiro J. et al., Circulation, 2008, 118:2754).

Interestingly, immobilization in rats, a well-established stress model and condition inducing high epinephrine and norepinephrine levels, has also been shown to be associated with characteristic ECG changes, including ST-segment elevation and reversible left ventricular apical ballooning, strikingly reproducing the abnormalities seen in Takotsubo cardiomyopathy.

In the Expert Review of Cardiovascular Therapy editorial Matthias Friedrich and Myra Cocker discuss new advances and studies using cardiovascular magnetic resonance. This method enables a comprehensive analysis of regional and global myocardial function, combined with a multi-parametric myocardial tissue characterization.

The most intriguing finding obtained from these studies indicates that myocardial inflammation is an important component of the pathophysiology behind stress-induced cardiomyopathy. Furthermore, the authors discuss recent evidence suggesting that stress-induced inflammation, and particularly catecholamine-induced inflammation, might represent the driving force leading to the development of acute symptoms and transiently altered ventricular contractility.

The authors conclude that future research will have to identify key determinants of individual susceptibility to stress-induced inflammation, and that cardiovascular magnetic resonance is expected to play a major role in advancing our understanding of myocardial stress.

SOURCE:  Expert Rev Cardiovasc Ther, 2012, 10: 271.

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Source: Cover Image: Left ventriculography during systole showing apical ballooning akinesis with basal hyperkinesis in a characteristic takotsubo ventricle. From: Takotsubo cardiomyopathy in a patient with esophageal cancer: a case report. Authors: Tara C. Gangadhar et al. Credit: Wikimedia Commons.

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