KCNH2 and chronic obstructive pulmonary disease: The majority of research efforts have focused classically on reduction of IKr as an approach for understanding arrhtymogenesis because it is well recognized that reduction of Ikr means decrease in net repolarizing current that results in prolongation of action potential duration (APD) and QT interval in the ECG and development of early afterdepolarization-induced triggered activity following torsade de pointes (TdP).[13] On the other hand, much attention has been paid to upregulation of KCNH2 in recent years because of its causal relationship to cardiac arrhythmias.