Abstract
The QT interval on surface electrocardiogram represents the sum of depolarization and repolarization process of the ventricles. The ventricular recovery process, reflected by ST segment and T wave, mainly depends on the transmembrane outward transport of potassium ions to reestablish the endocellular electronegativity. Outward potassium channels represent a heterogeneous family of ionic carriers, whose global kinetics is modulated by heart rate and autonomic nervous activity. Several cardiac and noncardiac drugs and disease conditions, and several mutations of genes encoding ionic channels, generating distinct genetic channellopathies, may affect the ventricular repolarization, provoke QT interval prolongation and shortening, and increase the susceptibility to ventricular arrhythmias.
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