Cardiac repolarization. The long and short of it

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.