Intravascular Ultrasound Assessment of the Mechanisms and Predictors of Restenosis Following Coronary Angioplasty

Restenosis occurs after 30% to 50% of transcatheter coronary procedures; its mechanisms remain incompletely understood. Intravascular ultrasound (IVUS) studies were analyzed in 360 non-stented native coronary artery lesions in which follow-up quantitative angiographic and/or IVUS data was available. Pre-intervention, post-intervention, and follow-up, the external elastic membrane (EEM) and lumen cross-sectional areas (CSA) were measured; plaque + media (P + M = EEM - lumen CSA), and cross-sectional narrowing (CSN = P + M/EEM CSA) were calculated. The anatomic slice selected for serial analysis had an axial location within the lesion at the smallest follow-up lumen CSA. At follow-up, 73% of the decrease in lumen CSA was due to a decrease in EEM CSA; 27% was due to an increase in P+M CSA. The change in lumen CSA correlated more strongly with the change in EEM CSA than with the change in P + M CSA. The change in EEM CSA was bidirectional; 47 lesions (22%) showed an increase in EEM CSA. Despite a greater increase in P + M CSA, lesions exhibiting an increase in EEM CSA had (1) no change in lumen CSA, (2) decreased restenosis, and (3) a 49% frequency of late lumen gain. The independent clinical, angiographic, and IVUS predictors of angiographic restenosis (3 50% diameter stenosis at follow-up) were the IVUS reference lumen CSA, angiographic pre-intervention diameter stenosis, and post-intervention IVUS CSN. Restenosis appeared to be determined primarily by the direction and magnitude of the change in EEM CSA. An increase in EEM CSA was adaptive while a decrease in EEM CSA contributed to restenosis. The most powerful predictor of restenosis was the IVUS post-procedural CSN. The importance of the post-procedural CSN was related to the change in EEM CSA as a mechanism of restenosis.