ABSTRACT
The T wave in a surface electrocardiogram (ECG) indicates the diastolic phase in the cardiac cycle. Even though the cellular basis of T-wave morphology in surface ECG remains unclear in clinical cardiology, the morphology may be determined by the transmural voltage gradient during the repolarization period that underlies the changes in the T wave and QT interval. The heterogeneous distribution of electrophysiological activity across the heart is essential for normal cardiac function. However, excessive heterogeneity may contribute to arrhythmogenesis and sudden cardiac death. This paper will provide an overview of T wave genesis and the contribution to action potential duration (APD), in which ion channels are involved in the repolarization period, with special emphasis on K+ channels involved in phase 3 repolarization. These channels are primarily Kv11.1 (hERG1), Kv7.1 (KCNQ1), and Kir2.1 (KCNJ2), which are the α-subunits responsible for conducting I(Kr), I(Ks), and I(K1). Changes in the T wave and QT interval that are affected by both functional loss and gain of these currents are associated with various arrhythmogenic diseases. This review also briefly discusses arrhythmogenesis in diseases that are manifested by changes in the T wave and QT interval.