Autopsy studies in victims of sudden coronary death revealed intramyocardial platelet aggregates with microscopic myonecrosis downstream from ruptured atherosclerotic plaques. Ruptured plaques usually manifest angiographically as irregularly bordered (type II) lesions. To investigate the possible pathogenic role of ruptured plaques in arrhythmic death, we analyzed clinical, angiographic, and electrophysiologic data from 49 survivors of cardiac arrest without acute myocardial infarction. All patients had ≥50% stenoses of ≥one coronary artery; 16 had type II morphology, and 33 did not. Type II morphology was more prevalent in patients without inducible sustained monomorphic ventricular tachycardla (11 of 22 or 50%) than in those with it (five of 27 or 19%), p < 0.05, and patients without akinetic or dyskinetic segments (eight of 14 or 57%) than in those with them (eight of 34 or 24%), p < 0.06. Thus type II morphology is more prevalent in patients without a demonstrable anatomic and/or electrophysiologic substrate for reentrant ventricular tachycardia, indirectly implicating ruptured plaques in the pathogenesis of cardiac arrest in this subset of patients.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine