Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients sustained ventricular tachycardia after myocardial infarction

Abstract

After the acute phase of myocardial infarction, patients who developed sustained ventricular arrhythmias present with either sudden death or ventricular tachycardia (VT). Although current evidence suggests that VT frequently precedes ventricular fibrillation (VF) in patients presenting with sudden death, the factors resulting in rapid deterioration of VT to VF have not been delineated in humans. To determine whether left ventricular function, coronary anatomy, or electrophysiologic characteristics could differentiate patients with sudden death from those with VT without sudden death, we compared results of cardiac angiography and programmed electrical stimulation in 42 patients referred for evaluation of sustained VT or surviving ‘aborted’ sudden death for more than 9 days after myocardial infarction. By univariate analysis there were no differences between patients with sudden death and those with VT in age, time from myocardial infarction to VT or sudden death, ejection fraction (0.31 ±0.12 vs 0.29 ± 0.09), or the number of patients with a major area of contracting myocardium supplied by an artery with a 50% or greater or a 70% or greater stenosis (84% vs 64% and 68% vs 41%). Thirty-six percent of patients with sudden death but no patient with VT had two separate areas of infarction. During programmed electrical stimulation, a sustained ventricular arrhythmia was initiated in 100% of patients with VT and 73% of patients with sudden death and rapidly produced syncope in 67% of patients with sudden death but in only 5% of those with VT. This difference was due to the more frequent initiation of rapid polymorphic VT or VF (27% of patients) and to the shorter VT cycle length (242 ±31 vs 319 ± 69 ms) when monomorphic VT was induced in the group with sudden death. No difference was found in the number of extrastimuli required for initiation of a sustained ventricular arrhythmia. We conclude that (1) resting ventricular function and the potential for ischemia remote from the infarct fail to distinguish patients with sudden death from those with VT without sudden death, (2) electrophysiologic properties determining VT rate and stability are major determinants of the clinical presentation of VT after myocardial infarction, and (3) two separate areas of infarction may predispose to sudden death.