Abstract

Abstract Background Lipid-rich plaque is an important substrate causing acute coronary events. Near-infrared spectroscopy (NIRS) imaging has been shown to visualize lipidic coronary plaque at non-culprit site associated with future coronary events. Given that histopathological studies reported that the unstable plaque underlying the implanted drug-eluting stent (DES) could cause neoatherosclerosis formation, we hypothesized that NIRS-based evaluation of lipidic plaque burden behind the implanted DES may clinically predict the occurrence of stent failure in patients with CAD receiving PCI. Purpose We aimed to investigate the relationship of stent-related events' risk with lipidic plaque materials behind the implanted DES imaged by NIRS/intravascular ultrasound (NIRS/IVUS) imaging. Methods The REASSURE-NIRS registry is an on-going multi-center registry to enroll CAD subjects receiving NIRS/IVUS-guided PCI. In this registry data, 406 lesions in 379 CAD subjects (ACS/non-ACS=150/229) receiving new-generation DES were analyzed. Minimum stent area (MSA) after PCI and maximum lipid-core-burden index in any 4mm-segment within the implanted stents (in-stent maxLCBI4mm) were measured. A 3-year lesion-oriented composite outcome [LOCO: culprit lesion-related MI + ischemia-driven target lesion revascularization (ID-TLR)] was compared in subjects stratified according to the tertile of in-stent maxLCBI4mm. Results The mean value of in-stent maxLCBI4mm was 221, and 17% of lesions exhibited in-stent maxLCBI4mm >400. Patients with a greater in-stent maxLCBI4mm were more likely to exhibit a higher LDL-C level (p=0.026) with a longer stent length (p<0.001) and a smaller MSA (p=0.033) (Picture 1). Over 95% of entire study subjects received a statin. During the observational period (median=726 days), the frequency of LOCO up to 3 years was 3.4% in entire study subjects (culprit lesion-related MI=1.0%, ID-TLR=2.8%). Kaplan-Meier curve analysis demonstrated that the occurrence of LOCO did not increase in association with in-stent maxLCBI4mm (log-rank p-value=0.25, Picture 2). In addition, in-stent maxLCBI4mm did not associate with each component of LOCO (culprit lesion-related MI: p=0.502, ID-TLR: p=0.872). Receiver Operating Characteristic analysis revealed that the predictive ability of in-stent maxLCBI4mm for the occurrence of LOCO was unsatisfactorily (c-statistics=0.486). Conclusion The amount of underlying lipidic materials at culprit lesions receiving new-generation DES implantation did not necessarily predict future stent-related events. Clinical significance of maxLCBI4mm behind the implanted DES may be different from that at naïve non-culprit plaques. Funding Acknowledgement Type of funding sources: None. Background and lesion characteristicsKaplan-Meier analysis for LOCO

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