Abstract
Although the total number of deaths attributed to cardiovascular disease has decreased during recent decades, an increase in the percentage of cardiac deaths occurring suddenly (from 56% in 1989 to 63% in 1998) has actually resulted in an increase in the total number of sudden deaths in the United States.1 The problem of sudden death spans all racial and cultural groups and is equally important in men and women. It is now 40 years since continuous ECG monitoring revealed that ventricular tachycardia and ventricular fibrillation (VT/VF) are responsible for the majority of sudden deaths. Dissemination of this information resulted in a marked change in practice. Until the 1970s, physicians treated only symptomatic VTs. Therapeutic options were limited to a few antiarrhythmic drugs, administered empirically. With the advent of telemetric ECG monitoring and continuous ambulatory (Holter) ECG monitoring came the recognition that frequent and multiform ventricular ectopy often preceded episodes of VF in the acute phase of myocardial infarction (MI). Ventricular ectopy and nonsustained VT was documented 1 to 2 weeks after MI in many patients. The presence of frequent ventricular premature complexes and runs of nonsustained VT in patients with significant left ventricular dysfunction were then demonstrated to be an independent predictor of sudden cardiac death late after MI. This information then led to the practice of administering antiarrhythmic drugs to suppress ventricular ectopy under the presumption that suppression of asymptomatic ectopy would prevent sudden death. This fashion lasted almost 20 years, until the results of the Cardiac Arrhythmia Suppression Trial (CAST) trial demonstrated the harm caused by this approach.2 Thus, a sea change in the practice of cardiology had occurred, from treating only symptomatic patients to therapy aimed at primary prevention of sudden death. The initial efforts using antiarrhythmic drugs failed to reduce mortality. While many physicians …
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