PVCs (trigger mechanisms) and the vulnerability of the myocardium to sustain a life-threatening ventricular tachycardia (substrate) are two variables in the sudden death equation. Physicians treating patients at risk for sudden death should consider PVC frequency and vulnerability as interrelated variables. Risk assessment must take into consideration both variables. Antiarrhythmic drug efficacy can be assessed in terms of a reduction in trigger mechanisms (PVCs) as well as decreasing myocardial vulnerability (induction of VT at PES). Flecainide acetate, at a reduced dosage of 100 mg twice daily, is effective in both aspects, markedly decreasing PVC frequency and preventing VT induction at PES testing. Holter monitoring and electrophysiologic testing evaluate different aspects of the problem. With the addition of an agent as potent as flecainide, which is devoid of many of the bothersome side effects previously limiting antiarrhythmic therapy, an agent is now available that may be useful to treat both the trigger mechanism and the substrate in sudden death. We must be careful not to worsen the situation through the profound effects of flecainide on depolarization and refractoriness that in some patients cause life-threatening arrhythmias to be more frequent.