Abstract
Sudden death from ventricular arrhythmias is an important source of mortality in patients with congestive heart failure. Rapid ventricular arrhythmias also occur in small animal models of heart failure. Prolongation of the action potential in failing hearts is thought to be an important arrhythmia mechanism. Prolongation of the ventricular action potential plateau sometimes causes reactivation of the voltage-dependent calcium current leading to an “early afterdepolarization” (EAD).1 Experimental methods of producing EADs include the use of cesium or a class III antiarrhythmic drug (such as quinidine or sotalol) to block repolarizing potassium current, the use of catecholamines to increase the calcium current, or the use of veratrine to prevent the inactivation of fast sodium channels and increase the sodium-channel “window current.”
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