Abstract 4145973: Pemafibrate Provides Multiple Antiatherothrombotic Effects for Patients with Dyslipidemia Receiving Statin

Background: Statin is thought to be highly effective against complex atherothrombogenic processes, but further therapies for the residual risk after statin have not been established. Hypothesis: We assessed hypothesis that treatment with pemafibrate, a selective peroxisome proliferator-activated receptor α (PPARα) modulator, inhibits atherothrombotic progression in patients with coronary artery disease and dyslipidemia receiving statin, one of the best possible antiatherosclerotic treatment. Methods: Thirty dyslipidemic patients with stable coronary artery disease were randomized to group-P where they received pemafibrate (0.2mg/day), or to group-C where they continued antidyslipidemic therapy without a fibrate for 3 months. We quantified flow-mediated endothelium-dependent dilation of right brachial artery after 5 minutes forearm occlusion (BFMD), and we also quantified intima-media thickness of brachial artery (BIMT) using high-resolution ultrasonography. Changes in BFMD, BIMT, and other serum variables were compared between the two study groups. Results: Group-P (n=20) manifested good compliance to the treatment with pemafibrate and improvements in clinical variables represented by triglycerides and D-dimer after medication of pemafibrate, while there were no improvements in group-C. BFMD (%) improved after medication in group-P (from 4.1±1.6 to 5.4±2.5, p<0.01) and BIMT (mm) decreased in group-L (from 0.33±0.10 to 0.30±0.11, p=0.03), while both remained unchanged in group-C (BFMD; from 4.0±2.1 to 3.9±1.8, p=0.58, BIMT; from 0.33±0.14 to 0.34±0.18, p=0.44). Changes of BFMD or BIMT in group-P did not correlate to those of triglycerides (FMD: r=0.18, p=0.62, BIMT: r=0.11, p=0.80). Conclusion: This study suggests that pemafibrate safely improves arterial function and inhibits progression of wall thickness independent of reversal for dyslipidemic status, and has novel potential benefit for residual risk management of atherothrombosis in dyslipidemics receiving statin.