Acute myocardial infarction (MI) stems from a disruption of the plaque in the coronary artery. Based on postmortem examinations, such plaque disruption has been classified as either a rupture or an erosion. Unfortunately, it has been difficult to clinically identify plaque ruptures and plaque erosions during the development of acute MI. To elucidate the relationships between clinical features and the morphological characteristics of the infarct-related lesions, we observed the culprit lesions in patients with acute MI by coronary angioscopy and intravascular ultrasound.

We examined culprit lesions in 107 patients with acute MI using coronary angioscopy and intravascular ultrasound immediately before performing percutaneous coronary intervention. The lesions were then classified as plaque ruptures or nonruptured erosions, and their clinical features were compared.

Among the lesions studied, 44 were classified as plaque ruptures, 28 were classified as plaque erosions, and 35 were unclassified. Patients with nonruptured eroded plaques had more preinfarction angina before the onset of MI than those with ruptured plaques (53.6% vs 22.7%, P = .0074). They also had less ST-segment elevation MI (71.4% vs 93.2%, P = .0185), lower peak creatine kinase levels (2029 ± 1517 vs 4033 ± 2699 IU/L, P = .0009), less distal embolization after percutaneous coronary intervention (3.6% vs 36.4%, P = .0014), and less Q-wave MI 1 month after onset (40.7% vs 88.4%, P < .0001).

Patients with eroded plaque lesions have smaller infarctions than those with ruptured plaque lesions, suggesting that an eroded plaque is less potently thrombogenic than a ruptured plaque.