Abstract 11417: Impact of Eicosapentanoic Acid and Statin Therapy on Coronary Thin-cap Fibroatheroma: Assessment by Optical Coherence Tomography
Background Thin-cap fibroatheroma (TCFA) is a major form of vulnerable plaque. Pentraxin 3 (PTX3) is a novel inflammatory marker mainly produced by macrophages in atherosclerosis and is known to be associated with plaque vulnerability. We assessed the impact of eicosapentanoic acid (EPA) and statin therapy on the stabilization of vulnerable plaque by serial OCT and PTX3 measurement.
Methods Forty non-culprit TCFA lesions from 24 patients with untreated dyslipidemia were enrolled. Patients were randomly assigned to either 1) EPA group (concomitant use of EPA 1,800mg/day and rosuvastatin: 19 lesions in 12 patients) or 2) Statin group (rosuvastatin alone: 21 lesions in 12 patients). The dose of rosuvastatin was adjusted with a goal of LDL > 70 mg/dl. Baseline and nine-month follow-up OCT was performed to evaluate the change of fibrous-cap thickness, lipid arc, plaque length, and macrophage accumulation (defined as a heterogeneous bright spot in the fibrous-cap) in non-culprit TCFA. Serum EPA/Arachidonic acid (EPA/AA) ratio and PTX3 were evaluated at the time of follow-up OCT.
Results Despite similar follow-up LDL- and HDL-cholesterol level, EPA group had a significantly greater increase in fibrous-cap thickness with a tendency toward a greater decrease in TCFA length than Statin group. Also, macrophage accumulation was less frequently detected in EPA group than Statin group by follow-up OCT. EPA group had a significantly higher serum EPA/AA ratio and lower PTX3 than Statin group. When all patients were divided into tertiles by PTX3 (T1; > 2.38ng/ml, T2; 2.38-3.85, T3; >3.85), there was a stepwise association between the PTX3 and the incidence of macrophage accumulation (T1; 0%, T2; 25.0%, T3; 41.2%, P=0.048).
Conclusions The concomitant use of EPA and rosuvastatin stabilizes a vulnerable plaque more strongly than statin alone in patients with untreated dyslipidemia, probably due to a greater suppress of local inflammation afforded by EPA therapy.
- © 2012 by American Heart Association, Inc.