[The electrophysiological mechanism of the long QT syndrome]

There are several functions to modulate if action potential prolongation and early and late after depolarizations are expected to appear, namely: calcium/sodium channels gating modes, potassium channels rectification, 3Na+/1Ca+2 exchange function, left/to/right balance of the sympathetic innervation of the heart. Based upon chronological correspondence of electrophysiological events and surface ecg waves, heterogeneous prolonged repolarization and after depolarizations are two possible explanations for QT interval prolongation and dispersion in both acquired and congenital long QT syndromes. Pauses commonly trigger arrhythmias in acquired LQTS, and imbalanced sympathetic drive commonly triggers arrhythmias in the congenital type of the syndrome.