Abstract 16462: Phenotypic Features of Lipidic Plaque in Patients With Polyvascular Disease: Findings From the Reassure Near-Infrared Spectroscopy Imaging Multi-Center Registry

Abstract

Introduction: Polyvascular disease (PolyVD) is a high-risk atherosclerotic phenotype presenting worse cardiovascular outcomes. However, its atherosclerotic features remain to be fully elucidated yet. Near-infrared spectroscopy (NIRS) imaging quantifies lipidic plaque associated with clinical outcome. Hypothesis: Given a clustering of atherogenic risks in PolyVD, PolyVD may exhibit a distinct plaque phenotype, which accounts for their outcome. Methods: 224 culprit lesions in 203 CAD patients receiving PCI were evaluated by NIRS imaging. PolyVD was defined as those with additional ASCVD (stroke and/or LEAD). NIRS-derived lipidic plaque feature (maxLCBI 4mm ) and clinical outcome (all-cause death+non-fatal MI+stroke) were compared in PolyVD and non-PolyVD subjects. Results: 28.6% of study subjects exhibited PolyVD. They were older (77 v. 71 years, p=0.02) with a greater frequency of CKD (61 v. 45%, p=0.03). Under the use of statin (81 v. 71%, p=0.15) and ezetimibe (32 v. 21%, p=0.09), PolyVD patients had a lower LDL-C level (73 v. 84 mg/dL, p=0.01). Despite their LDL-C control, maxLCBI 4mm did not differ in two groups (median: 458 v. 576, p=0.19). Moreover, 64% of PolyVD patients still showed maxLCBI 4mm ≧400 (69% in non-PolyVD, p=0.44). On multivariate analysis, ACS independently predicted maxLCBI 4mm ≧400 (Figure) in PolyVD patients. Of note, PolyVD presenting ACS had a higher maxLCBI 4mm (790 v. 411, p=0.001) compared to those without ACS, whereas this relationship did not exist in non-PolyVD (622 v. 561, p=0.19, Figure). During the 3-year observational period, PolyVD was associated with an elevated risk of MACE (p=0.002). Conclusions: Despite lowering LDL-C levels, PolyVD harbored a large amount of lipidic materials, accompanied by worse cardiovascular outcomes. Given the relationship of ACS with maxLCBI 4mm in PolyVD, additional therapies which modulates ACS-related inflammatory activity may be warranted to alter their disease substrate and outcomes.