Stress cardiomyopathy: a syndrome of catecholamine-mediated myocardial stunning?

Abstract

During the past few years, a novel syndrome of heart failure and transient left ventricular systolic dysfunction precipitated by acute emotional or physical stress has been described. While patients with "stress cardiomyopathy"(SCM) typically present with signs and symptoms that resemble an acute coronary syndrome, it has become clear that this syndrome has unique clinical features that can readily be distinguished from acute infarction.In particular, in contrast to the irreversible myocardial injury seen with infarction, the myocardial dysfunction of SCM is completely reversible and occurs in the absence of plaque rupture and coronary thrombosis. There is increasing evidence that exaggerated sympathetic stimulation may play a pathogenic role in the development of SCM. Plasma catecholamine levels have been found to be markedly elevated in some patients with SCM, and the syndrome has been observed in other clinical states of catecholamine excess such as central neurologic injury and pheochromocytoma.Further, intravenous catecholamines can precipitate SCM in humans and can reproduce the syndrome in animal models. The precise mechanism in which excessive sympathetic stimulation may result in transient left ventricular dysfunction remains controversial. Abnormal myocardial blood flow due to sympathetically mediated microvascular dysfunction has been suggested and is supported by decreased coronary flow reserve during the acute phase of this syndrome. An alternative explanation is the direct effect of catecholamines on cardiac myocytes, possibly through cyclic AMP-mediated calcium overload. This manuscript will review the clinical and diagnostic features of SCM and will summarize the evidence supporting a sympathetically mediated pathogenesis. Clinical risk factors that appear to increase susceptibility to SCM, possibly by modulating myocyte and microvascular sensitivity to catecholamines, will also be highlighted.

Fig. 1

Left ventriculography during systole of the three different variants of stress cardiomyopathy. On the left is the “apical ballooning” variant with apical and mid-ventricular akinesis with sparing of the base. In the middle is the “mid-ventricular ballooning” variant with akinesis of the mid-ventricle but normal contractility of the apex and base. On the right is the “basal ballooning” pattern with basal and mid-ventricular akinesis and normal apical contractility. Reproduced with kind permission from Springer Science + Business Media (Wittstein , Fig. 1)

Fig. 2

Possible mechanistic link between acute stress and the syndrome of stress cardiomyopathy. Increased sympathetic stimulation may mediate myocardial stunning through a variety of possible pathophysiologic effects that include microvascular dysfunction and myocyte calcium overload. Risk factors that may increase individual susceptibility to these pathophysiologic responses are also shown. Modified from Bhattacharyya et al. (2007), copyright © 2007, with permission from Elsevier (Bhattacharyya and Steptoe , Fig. 1)

Fig. 3

A proposed model to explain how stress cardiomyopathy can be precipitated by triggers of variable intensity. The amount of stress needed to induce the clinical syndrome is dependent on individual risk factors that likely influence myocyte and microvascular sensitivity to sympathetic stimulation (see text). SCM stress cardiomyopathy