Antiarrhythmic Drugs:

When the North American Society of Pacing and Electrophysiology (NASPE) was founded 25 years ago, treatments were empiric and targeted diseases or symptoms whose underlying mechanisms were poorly understood, if at all. Therapies available and widely used for arrhythmias in the late 1970s included pacemakers, external defibrillation for cardiac arrest, and drugs: lidocaine, procainamide, quinidine, and disopyramide.1 Generally accepted indications for antiarrhythmic drug therapy included prevention (of recurrent cardiac arrest, of recurrent atrial fibrillation [AF]) and treatment of symptoms. Frequent premature ventricular contractions (PVCs), whether symptomatic or not, were a common indication for therapy since ventricular ectopy was by then becoming established as a marker for an increased risk of sudden death following myocardial infarction (MI). Few drugs were available, and these were incompletely effective at best, plagued by a high incidence of serious and nuisance adverse affects, and the mechanisms whereby they actually suppressed arrhythmias were poorly defined. Efficacy was judged by clinical anecdotes, like acute termination of an ongoing tachyarrhythmia by drug administration, and extrapolation to other settings. Few large controlled clinical trials had been performed. Studies had shown that lidocaine administered in the coronary care unit reduced the incidence of ventricular fibrillation but survival appeared unaffected;2 later analysis of much larger databases suggests an adverse effect of lidocaine on survival in this setting.3 Studies of β-blockers, including some of the first cardiology megatrials,4,5 suggested antiarrhythmic efficacy in some settings. Similarly, the striking efficacy of verapamil in supraventricular arrhythmias was beginning to be appreciated, and it was supplanting “traditional therapies,” like phenylephrine or