The trouble with sudden cardiac death (SCD) is just that—it is sudden and individually unpredictable. Recent data from the Centers for Disease Control showed that SCD accounted for >460 000 deaths, or about 63% of deaths due to cardiac disease, in 1999.1 Typically, a cardiac arrest results from sustained ventricular tachycardia (VT) or ventricular fibrillation that progresses to death if effective resuscitative efforts are not started within several minutes of the arrest.2 It is not surprising that the overall survival rate of patients with out-of-hospital cardiac arrest in the United States is low, estimated to be <5%.3 Although more widespread use of automated external defibrillators could lead to a reduction in SCD,3 it is unrealistic to expect too much from this technology, especially because most cardiac arrests either are unwitnessed or occur in a location without ready access to an automated external defibrillator. The epidemic proportions of SCD have led to decades of research and randomized clinical trials designed to predict which individuals are at risk of SCD and to determine what methods prevent it. See p 1082 Coronary artery disease (CAD) causes ≈70% of SCD,1 and most clinical trials have evaluated this patient population. The emphasis of this Focused Perspective is on antiarrhythmic drug and device trials, but the reader should remember that selective use of β-adrenergic–blockers and angiotensin-converting enzyme inhibitors has reduced SCD.2,4,5 It has been known for decades that patients at highest risk for SCD after myocardial infarction (MI) have substantial left ventricular dysfunction, frequent premature ventricular complexes (PVCs) or nonsustained VT, or both conditions.2 Early efforts to prevent SCD employed the PVC suppression method. The Cardiac Arrhythmia Suppression Trial (CAST) was a randomized, placebo-controlled study that tested the hypothesis that PVC suppression after MI would reduce arrhythmic death.6 …
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