Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes.

Abstract

It is not clear why some plaque ruptures lead to acute coronary syndromes (ACS) but others do not. We analyzed 80 plaque ruptures in 74 patients and compared culprit lesions of ACS patients with nonculprit lesions of ACS patients and lesions of non-ACS patients; both culprit and nonculprit plaque ruptures were studied in 6 of 54 ACS patients. Intravascular ultrasound findings suggesting thrombus were observed more frequently in culprit lesions of ACS patients (n=35) compared with nonculprit lesions of ACS patients (n=19) and lesions of non-ACS patients (n=26): 60% versus 32% versus 8% (P<0.001). At the minimal lumen site, smaller lumen areas (3.3+/-1.5 versus 5.4+/-2.6 versus 6.1+/-2.0 mm2, P<0.001) and greater area stenosis (61+/-15% versus 50+/-14% versus 46+/-18%, P=0.002) and plaque burden (80+/-8% versus 71+/-8% versus 69+/-10%, P<0.001) were observed in culprit lesions of ACS patients compared with nonculprit lesions of ACS patients and lesions of non-ACS patients. Lesions were longer (18.7+/-6.4 versus 154.9+/-6.1 versus 12.0+/-4.9 mm, P<0.001) and rupture site remodeling indices were greater (1.26+/-0.21 versus 1.24+/-0.21 versus 1.09+/-0.05, P=0.002). Independent predictors of culprit plaque ruptures in ACS patients were smaller minimum lumen areas (P=0.02) and presence of thrombus (P=0.01). Ruptured plaques in culprit lesions of ACS patients have smaller lumens; greater plaque burdens, area stenosis, and remodeling indices; and more thrombus. Plaque rupture itself does not lead to symptoms. The association of plaque rupture with a smaller lumen area and/or thrombus formation causes lumen compromise and leads to symptoms.