© 2007 European Society of Cardiology
Tako-Tsubo cardiomyopathy
Middelheim Hospital, University of Antwerp Lindendreef 1, 2020, Antwerp, Belgium
* Tel.: +32 3 280 32 23; fax: +32 3 280 32 25 E-mail address: dirk.brutsaert{at}skynet.be.
Received May 20, 2007; Tako-Tsubo cardiomyopathy is characterized by a typically transient hypo-to-akinesis with ballooning of the apical portion of the left ventricle (LV) in the absence of major vascular impairment [1]. Compensatory hyperkinetic wall motion of the basal portion of the LV chamber has been described in a recent issue of this Journal [2]. Although emotional or physical stresses are commonly invoked as possible triggers in a majority of reported cases, the pathophysiology of the underlying mechanisms has remained largely elusive. Sudden systemic sympathetic activation with transiently excessive levels of plasma catecholamines, causing either metabolic or microvascular impairment in the LV apical zone, has been suggested [3]. Regional dysfunction of right ventricular (RV) wall motion may also be involved [4].
In the absence of any definitive explanation, we would like to call attention to the additional possibility that a transient dysfunction of the endocardial endothelium lining the apical, highly trabeculated LV myocardium could also be a plausible cause of a reversible dysfunction of the apical LV myocardium.
Previous work has shown that endocardial and capillary endothelial-to-myocardial interactions are obligatory for normal cardiac function [5,6]. Interaction of the endocardial endothelium with circulating substances and constituents in the blood may thereby modulate subjacent myocardial performance [7-9]. The transmural inner cavitary half of the apical portion of the LV wall is highly trabeculated; in fact, the apical LV myocardium is the thinnest and most densely trabeculated — or, most non-compaction — myocardium of the LV. The more trabeculated the myocardium in any given portion of the ventricular wall, the higher the surface-to-volume ratio, and hence the more exposed the endocardial endothelial surface lining that area. Accordingly, along with the intensively trabeculated RV surface, the apical trabeculated LV wall may become a most vulnerable target when exposed to excessive plasma levels of substances, like catecholamines, known to affect or damage the endocardial endothelial cells [7,10].
In Tako-Tsubo cardiomyopathy, catecholamine-induced endocardial endothelial dysfunction could, therefore, be expected to preferentially affect these LV areas with the highest surface-to-volume ratio, and hence contribute to a transient impairment of the contractile performance of the subjacent, apical LV myocardium, as well as of some zones in the RV.
Although this conjecture can presently hardly be proven experimentally, as there are as yet no in vivo markers of endocardial endothelial (dys)function available, we suggest to nevertheless add it to the already exhaustive list of putative mechanisms.
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- Kurisu S., Inoue I., Kawagoe T., Ishihara M., Shimatani Y., Nakama Y., et al. Pressure tracings in obstructive Tako-Tsubo cardiomyopathy. Eur J Heart Fail (2007) 9:317–319. Epub 2006.
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- Haghi D., Athanasiadis A., Papavassiliu T., Suselbeck T., Fluechter S., Mahrholdt H., et al. Right ventricular involvement in Takotsubo cardiomyopathy. Eur Heart J (Oct. 2006) 27(20):2433–2439. Epub 2006 Sep 25.
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[Abstract/Free Full Text] - Rona G., Hüttner I., Boutet M. Microcirculatory changes in myocardium with particular reference to catecholamine-induced cardiac muscle cell injury. In: Handbuch der Allgemeinen Pathologie. Microzirkulation/Microcirculation—Mussen H., ed. (1977) Berlin: Springer Verlag. 791–888. sect. III.
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