Ventricular arrhythmias: mechanisms and actions of antiarrhythmic drugs

Choosing the correct drug therapy of ventricular arrhythmias is difficult, even when, for discussion, reentry is arbitrarily considered the mechanism for arrhythmias. To counter ventricular arrhythmia with its many possible reentry circuits, an antiarrhythmic drug should lengthen the refractory period but not affect conduction velocity. Antiarrhythmic drugs for ventricular rhythm disturbances do work by prolonging the refractory period, slowing conduction, or both. However, in anatomically and functionally determined circuits, drugs may stop or decelerate tachycardia; but in some cases antiarrhythmics, particularly class I drugs, can theoretically accelerate tachycardia. Individual drug level determinations are important; what is therapeutic in one patient may worsen the arrhythmia in another. The changeable electrophysiologic milieu in early stages of ischemic heart disease makes controlled investigations difficult. However, individual variance calls for further systematic investigation of new ways to interrupt, isolate, or destroy the reentry pathway, and such investigation probably should be conducted in patients with inducible ventricular tachycardia.