Abstract 14864: Risk Markers for Coronary Plaque Progression and Destabilization Beyond LDL-Cholesterol in Patients with Acute Coronary Syndrome

Abstract

Introduction and Purpose: In acute coronary syndrome (ACS) patients, it is important to stabilize pan-coronary vulnerable plaques as early as possible in ACS patients, in addition to revascularization of the culprit lesion by percutaneous coronary intervention (PCI). Although statins are effective for regression and stabilization of vulnerable plaques in ACS patients, several patients experience plaque progression and/or destabilization despite aggressive control of low-density lipoprotein (LDL)-cholesterol by statins. Therefore, we should do further efforts to research new risk markers beyond LDL-cholesterol and to intervene in them. Methods and Results: In 57 patients with ACS, who underwent emergent percutaneous coronary intervention (PCI), we performed a virtual histology (VH)-IVUS for a non-culprit lesion, at baseline and at the follow-up time (8-10 months), to assess plaque regression/progression and plaque stabilization/destabilization. At the follow-up time, we measured specific biomarkers. All of the patients received aggressive treatment with statins. Change in the total plaque volume by the gray scale IVUS was correlated positively with derivatives of reactive oxygen metabolites (d-ROMs) level (0.32, P<0.05). Change in the volume of destabilized components, i.e., necrotic core plus fibro-fatty compositions, was correlated negatively with the eicosapentaenoic acid to arachidonic acid (EPA/AA) ratio (R=-0.39, P<0.01) and positively with the levels of interleukin (IL)-8 (R=0.31, P<0.01) and d-ROMs (0.32, P<0.01). Multivariate logistic regression analysis showed that only the d-ROMs level was an independent discriminative biomarker for plaque progression (hazard ratio; 1.018, 95% confidence interval; 1.005-1.032, P<0.01) and plaque destabilization (hazard ratio; 1.022, 95% confidence interval; 1.005-1.038, P<0.01). Conclusions: The d-ROMs would be a powerful biomarker to predict plaque progression and destabilization as the residual risk marker beyond LDL-cholesterol. Intervention to oxidative stress state would be the most important residual target beyond LDL cholesterol lowering for plaque regression and stabilization.