Evolution of nonculprit coronary atherosclerotic plaques assessed by serial virtual histology intravascular ultrasound in patients with ST-segment elevation myocardial infarction and chronic total occlusion.

OBJECTIVE: The pathophysiology and natural course of coronary nonculprit plaques remain unclear. We investigated whether the short-term natural course of nonculprit plaques differs between ST-segment elevation myocardial infarction (STEMI) and chronic total occlusion (CTO) patients.

METHODS: We performed serial virtual histology intravascular ultrasound on nonculprit plaques in 26 STEMI and 11 CTO lesions at baseline and the 6-month follow-up.

RESULTS: At baseline, more lesions in the STEMI group were virtual histology intravascular ultrasound-derived thin-cap fibroatheromas (TCFA; 76.9 vs. 18.1%, P=0.002). During the follow-up period, the plaque composition changed dynamically in the STEMI group (fibrofatty: 9.8±1.9 to 17.3±2.9%, P=0.030; dense calcium: 12.7±1.8 to 8.1±1.7%, P=0.026; necrotic core: 21.1±1.8 to 15.4±2.2%, P=0.052), with a consistent plaque size. In the CTO group, the plaque composition and plaque size remained consistent without a significant change. Also, more lesions in the STEMI group remained as or progressed to TCFA, compared with the CTO group (67 vs. 11%, P=0.089). Factors associated with a persistent TCFA or with a new development of TCFA were a large necrotic core volume index and the diagnosis of STEMI, whereas new statin usage was a protective factor.

CONCLUSION: Nonculprit lesions in STEMI patients were more unstable at the baseline compared with those in CTO patients. During follow-up, nonculprit lesions in STEMI and CTO patients showed a distinct pattern of change; the former were stabilized in plaque composition, whereas the latter remained consistent. The diagnosis of STEMI and a large necrotic core volume were predictors of evolution to a TCFA, and new statin usage was a protective factor.