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Absence of post-extrasystolic potentiation in takotsubo cardiomyopathy: Another piece of the puzzle?

作者信息

Aoi Shunsuke, Misumida Naoki, Carabello Blase, Rachko Maurice

机构信息

Department of Internal Medicine, Mount Sinai Beth Israel, 16th Street and 1st Avenue, New York, NY 10003, USA.

Department of Internal Medicine, Mount Sinai Beth Israel, 16th Street and 1st Avenue, New York, NY 10003, USA.

出版信息

Int J Cardiol. 2016 Dec 15;225:9-13. doi: 10.1016/j.ijcard.2016.09.058. Epub 2016 Sep 17.

Abstract

BACKGROUND

Takotsubo cardiomyopathy (TCM) is an intriguing phenomenon characterized by transient and reversible left ventricular (LV) dysfunction despite angiographically unobstructed coronary arteries. The detailed pathophysiology of stunned, viable myocardium in TCM remains to be determined. Post-extrasystolic potentiation (PESP), the phenomenon of enhanced LV contractility following extrasystole, has been used to assess myocardial viability.

METHODS

Utilizing a local database, we identified 74 cases that met the modified Mayo Clinic criteria for TCM between October 2004 and March 2016. The patients undergoing left ventriculography were assessed for the presence of fortuitously provoked extrasystoles and the presence or absence of PESP.

RESULTS

The baseline characteristics of TCM were 93.2% female patients with median age of 69 and majority cases were apical type (77%). In-hospital mortality was observed in 3 cases (4.1%), all of which were apical type. We observed improved ejection fraction after extrasystole compared to baseline, however stunned myocardium had minimal PESP whereas unaffected myocardium showed marked potentiation.

CONCLUSION

Extrasystoles in TCM failed to elicit PESP in affected LV segments despite viability in those segments, in turn implicating a calcium handling abnormality in TCM. Potential explanations of our results may be that catecholamine excess caused maximum calcium release so that an extrasystole could not enhance contractility any further, or that there is a regional insensitivity to calcium release due to a disturbance of the calcium regulatory system at the molecular level despite the bolus of calcium availability provided by the extrasystole.

摘要

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