The role of silent ischemia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death

AbstractTo study the role of silent ischemia and the arrhythmic substrate in the genesis of sudden cardiac death, 67 patients were studied (mean age 62 ± 12 years). Of these, 14 patients (Group 1) had an in-hospital episode of ventricular tachycardia or fibrillation while wearing a 24 h Holter ambulatory electrocardiographic (ECG) monitor, 33 (Group II) had a documented episode of sustained ventricular tachycardia or fibrillation, or both, and 20 (Group III) had angina pectoris but no ventricular tachycardia or fibrillation. Eight Group I survivors underwent programmed electrical stimulation or ECG signal averaging, or both. All Group II patients underwent 24 h Holter monitoring and ECG signal averaging to detect late potentials before programmed electrical stimulation. Group III patients underwent both 24 h Holter recording and coronary angiography. The 24 h ECG tapes were analyzed for ST segment changes, prematurity index and characteristics of ventricular premature depolarizations. Any ST depression ≥1mm for >30 s was considered to be a reflection of silent ischemia, and the induction of ventricular tachycardia or fibrillation by programmed electrical stimulation or the presence of late potentials, or both, was considered to be a reflection of the arrhythmia substrate.Silent ischemia preceded ventricular tachycardia in only 2 (14%) of the 14 Group I patients. The prematurity index was <1 in only 18% of ventricular tachycardia episodes. However, 14 (64%) of 22 episodes of ventricular tachycardia in 9 (64%) of the 14 patients were initiated by a ventricular premature depolarization preceded by a short-long sequence (sinus beat-ventricular premature depolarization-sinus beat) with a ratio of 0.5 ± 0.1. Six (75%) of eight in-hospital survivors of ventricular tachycardia or fibrillation (Group 1) had an arrhythmic substrate. A significantly (p < 0.0001) higher percent of the 33 Group II patients had an arrhythmic substrate (93%) than had silent ischemic episodes (45%). Silent ischemia resulted in ventricular tachycardia in only 1(7%) of 15 Group II patients. There was no significant difference between the incidence of silent ischemia (45% versus 35%) and the extent of coronary artery disease between Groups II and III.It is concluded that: 1) Silent ischemia was not a major determinant of ventricular tachycardia. 2) Although silent ischemia was common in survivors of ventricular tachycardia or fibrillation, its incidence was not significantly different from that in patients with angina pectoris and no sustained ventricular arrhythmias. 3) A high percent of patients (75% to 93%) with ventricular tachycardia and fibrillation have an arrhythmic substrate. 4) In the absence of acute myocardial infarction, sudden cardiac death is frequently triggered by a ventricular premature depolarization, with a preceding short-long cycle that likely produces dispersion of refractoriness in the arrhythmic substrate