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To the Editor: Kume et al provide an elegant mechanistic analysis of the coronary microcirculation in the increasingly recognized entity of takotsubo-like left ventricular (LV) dysfunction (stress-induced cardiomyopathy).1 Despite a growing awareness and increase in reported cases, the mechanisms responsible for stress-induced cardiomyopathy remain unclear and warrant further study. Kume and colleagues demonstrated that in the acute phase of takotsubo-like LV dysfunction, coronary flow velocity reserve in all 3 major coronary arteries is decreased, and significantly improves during the follow-up phase 3 weeks later. In neurally mediated cardiomyopathies, approximately one-quarter of patients develop LV dysfunction, however, in 2 distinct patterns: one of apical sparing and the other apical-affected.2 In multivariate analysis, younger patient age is associated with the apical-sparing pattern, a characteristic feature supported by a recent case series showing a similar apical-sparing pattern in young patients with acute cerebral disorders. The cardiac syndrome in these patients was termed “inverted takotsubo”.3 This divergence in wall motion pattern provides insight to the differing types of stress-induced cardiomyopathy. The density of sympathetic nerve terminals is greatest at the base of the heart and reduced towards the apex.4 Accordingly, it is possible that younger patient populations are more susceptible to the apical-sparing type of stress-induced cardiomyopathy, and represent a more pure form of neurally mediated myocardial injury. In older subjects, specifically postmenopausal women, with a greater prevalence of coronary risk factors,5 the mechanism of the disease seems to involve exaggerated sympathetic activity, 6 but also necessitate abnormalities in the coronary microcirculation. 1,7

Takotsubo-Like Left Ventricular Dysfunction and Coronary Microvascular Dysfunction: Fulminant Cardiac Syndrome X?