Intravascular Ultrasound‐Guided Stenting in Long Lesions: An Insight into Possible Mechanisms of Restenosis and Comparison of Angiographic and Intravascular Ultrasound Data from the MUSIC and RENEWAL Trials

Abstract

The high restenosis rates in long stents may be related to suboptimal stent deployment. In an attempt to understand the potential components associated with restenosis in long stents, this study compares angiographic and intravascular ultrasound (IVUS) data from the MUSIC and RENEWAL studies where IVUS was used to optimize stent deployment in short (< 15 mm) and long (> 20 mm) coronary lesions, respectively. The RENEWAL study, a randomized trial, compared the NIR stent and Wallstent in long (> 20 mm) coronary lesions and used on-line visual IVUS criteria to optimize stent expansion. Detailed analysis of IVUS data was performed off line. Angiographic and IVUS data from this study was compared to that from the MUSIC study. Initial stent deployment was deemed optimal by the operator after visual angiographic and IVUS assessment in 50 of 70 lesions. In the remaining 20 lesions further balloon inflations were required to optimize stent apposition that led to an average gain in minimal in-stent luminal area (MISA) of 15.9% (P < 0.01). Off-line IVUS data analysis showed that the number reaching "MUSIC criteria" for optimal stent deployment preredilatation was 8 (11.4%) of 70 and 14 (20%) of 70 postredilatation. The ratio of MISA/MRAprox (mean proximal reference area) was 0.69 in RENEWAL. At 6-month follow-up, the angiographic restenosis rate in RENEWAL was 36% and target lesion revascularization (TLR) rate was 7.8%, compared with MUSIC's 9.7% and 4.5%, respectively. In conclusion, angiographic assessment of stent deployment in long lesions is limited. On-line visual IVUS with further balloon inflations to improve stent apposition led to a significant gain in MISA, but the MISA/MRAprox ratio remained suboptimal. Therefore, suboptimal stent deployment due to constraint by lesion resistance may be an important mechanism underlying the high restenosis rates in long stents.