Cardiac repolarization. The long and short of it

Cardiac repolarization. The long and short of it
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DOI:
10.1016/j.eupc.2005.05.010
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发表时间:
2005-09-01
期刊:
影响因子:
6.1
通讯作者:
Antzelevitch, C
Antzelevitch, C
中科院分区:
医学2区
文献类型:
--
作者:
Antzelevitch, C

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心脏透壁心室复极的异质性与多种心律失常表现有关。心室肌中的电异质性是由于三种主要细胞类型(心内膜细胞、M 细胞和心外膜细胞)之间的离子差异造成的。净复极电流的减少通常会导致 M 细胞动作电位优先延长。净复极电流的增加可导致右心室心外膜或左心室心内膜的动作电位优先缩短。这些变化可能导致再电导的跨壁异质性放大,从而容易发生潜在致命的折返性心律失常。 Tong QT、短 QT、Brugada 和儿茶酚胺能 VT 综合征都是具有截然不同的表型和病因的病理学例子,但在导致猝死方面具有共同的最终途径,即通过心室心肌内的跨壁放大或其他空间分散的再启动。这些相同的机制可能导致多种其他心肌病中危及生命的心律失常,包括心力衰竭和肥大,其可能涉及与Tong QT综合征非常相似的机制,到缺血和梗塞,其可能涉及与Brugada综合征的机制更相似的机制。 (c) 2005 年欧洲心脏病学会。由爱思唯尔有限公司出版。保留所有权利。
Heterogeneity of transmural ventricutar repolarization in the heart has been linked to a variety of arrhythmic manifestations. Electrical heterogeneity in ventricular myocardium is due to ionic distinctions among the three principal Cell types: Endocardial, M and Epicardial cells. A reduction in net repolarizing current generally leads to a preferential prolongation of the M cell action potential. An increase in net repolarizing current can lead to a preferential abbreviation of the action potential of right ventricutar epicardium or left ventricutar endocardium. These changes can result in amplification of transmural heterogeneities of repotarization and thus predispose to the development of potentially lethal reentrant arrhythmias. The tong QT, short QT, Brugada and catecholaminergic VT syndromes are all examples of pathologies that have very different phenotypes and aetiotogies, but share a common final pathway in causing sudden death via amplification transmural or other spatial dispersion of repotarization within the ventricular myocardium. These same mechanisms are likely to be responsible for life-threatening arrhythmias in a variety of other cardiomyopathies ranging from heart failure and hypertrophy, which may involve mechanisms very similar to those operative in tong QT syndrome, to ischaemia and infarction, which may involve mechanisms more closely resembling those responsible for the Brugada syndrome. (c) 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.