Background— Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI).

Methods and Results— We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries [IRAs] with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P&M) area. Positive remodeling was defined as lesion/mean reference EEM >1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5±10.1, 9.8±4.0, and 10.3±5.7 mm, respectively; P<0.0001), had larger EEM area (15.0±6.0, 11.5±5.7, and 12.6±5.6 mm², respectively; P=0.0353) and P&M area (13.0±6.0, 7.5±3.7, 9.3±4.3 mm², respectively; P<0.0001), smaller lumens (2.0±0.9, 4.1±3.1, and 3.4±2.5 mm², respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging.

Conclusions— Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.