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Angiographic coronary morphology in survivors of cardiac arrest
1Division of Cardiology, Stanford Medical Center, Calif.
Insights
Ruptured atherosclerotic plaques, identified as type II lesions, were more common in cardiac arrest survivors lacking ventricular tachycardia substrates. This suggests ruptured plaques may contribute to sudden cardiac arrest in these patients.
Area of Science:
- Cardiology
- Pathology
- Electrophysiology
Background:
- Autopsy studies link intramyocardial platelet aggregates and myonecrosis to sudden coronary death.
- Ruptured atherosclerotic plaques often appear as irregular (type II) angiographic lesions.
Purpose of the Study:
- To investigate the role of ruptured plaques in arrhythmic death.
- To analyze clinical, angiographic, and electrophysiologic data in cardiac arrest survivors.
Main Methods:
- Studied 49 survivors of cardiac arrest without acute myocardial infarction.
- Assessed coronary artery stenoses and lesion morphology (type II vs. non-type II).
- Evaluated inducibility of sustained monomorphic ventricular tachycardia and presence of akinetic/dyskinetic segments.
Main Results:
- Type II morphology was more prevalent in patients without inducible sustained monomorphic ventricular tachycardia (50% vs. 19%).
- Type II morphology was also more prevalent in patients without akinetic or dyskinetic segments (57% vs. 24%).
- These findings were statistically significant (p<0.05 and p<0.06).
Conclusions:
- Type II plaque morphology is more common in patients lacking a clear substrate for reentrant ventricular tachycardia.
- This indirectly implicates ruptured plaques in the pathogenesis of cardiac arrest in this patient group.
Abstract:
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 greater than or equal to 50% stenoses of greater than or equal to 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 tachycardia (11 of 22 or 50%) than in those with it (five of 27 or 19%), p less than 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 less than 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.