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

Background - It is not clear why some plaque ruptures lead to acute coronary syndromes (ACS) but others do not. Methods and Results - 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 mm ², 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). Conclusions - 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.