We read with interest the results of the study by Nef et al.,1 and would like to present a few comments to the paper. The Tako-Tsubo cardiomyopathy (TTC) is a circumferential epicardial damage manifested by very dynamic electrophysiologic and functional changes.2 The TTC occurs mainly in postmenopausal female after strong emotional stress, seldom in fertile female or in male individuals. The subendocardial involvement in the disease process is inconstant.3 In our opinion, the level of oestrogen is a critical factor in the pathophysiologic process of the TTC. There is a growing amount of evidence from the basic laboratory science about the effect of oestrogen on the calcium metabolism in female mammals. Oestrogen has an important regulatory effect on the release of epinephrine in the pre-synaptic cardiac sympathetic nerve fibres.4 Oestrogen is involved in the regulation of three metabolic cascades, which are involved in the entrance of calcium into the sarcomere: (i) the effect on cyclic AMP, which is related to the L-type Ca2+ channel,5 (ii) in the sarco-endoreticular Ca2+ phosphatase (SERCA) 2-phospholamban cascade,6 and (iii) in the activity of the ATP-sensitive K+ channels.7 These physiologic effects play a critical role in the protection of the epicardium against 'adrenergic storm' by shortening of phases 2 and 3 of the action potential. At this phase of the action potential, the calcium enters into the sarcomeres. With less calcium entering into the myocardial cells, reduced muscular contraction results in decreased oxygen consumption. By this mechanism, nature has provided the female mammals with a protection against the strong adrenergic stress during pregnancy and delivery. In the hypooestrogenaemic stage of the postmenopausal female, the epicardium is totally unprotected against the adrenergic storm, predisposing to the TTC.

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