I. Introduction
The long-QT syndrome (LQTS) characterized by the appearance of long QT intervals and wide T waves in the electrocardiogram (ECG) is associated with an atypical type of polymorphic ventricular tachycardia (VT) that may lead to sudden cardiac death [1]. Reentry is the main form of arrhythmia. The presence of ring road of conductance route, unidirectional conduction block and slow conduction velocity are the conditions for producing reentrant excitation. The heterogeneity of repolarization is the source of reentry. Optical mapping experiments showed that the unique topographical distribution of mid-myocardial cells (M cells) caused unidirectional block and reentrant excitation. By using optical mapping, Akar's group studied the distribution of M cells across the transmural surface [2]. Their experiments showed that M cells exhibited an island-like distribution but not sandwich-like. The island-like distribution of M cells extended toward endocardial or epicardial surfaces. M cells exhibited the longest APDs, but epicardial cells exhibited the shortest APDs. The distribution of APDs is the substrate of the heterogeneity of repolarization. The genetic mutations of LQTS result in a loss of ionic channel function with slow action potential repolarization and prolonged APDs[3]. It is important that M cell has many unique electrophysiological properties. M cells have a steeper APD-rate relation and a longer action potential duration (APD) than epicardial or endocardial cells. M cells display greater responsiveness to interventions that prolong APD (eg, agents with class III antiarrhythmic action) and a higher susceptibility to the development of early afterdepolarizations (EADs). These properties suggest that M cells play an important role in arrhythmias associated with abnormal repolarization in the congenital or acquired long-QT syndrome (LQTS) [4].