Abstract Body (Do not enter title and authors here): Background: Hypertriglyceridemia is associated with an increased risk of adverse cardiovascular outcomes in patients with coronary artery disease (CAD). Although pemafibrate is effective in reducing triglyceride levels, its impact on fibrinogen, a key biomarker linked to thrombotic risk, in those patients remains unclear. This study aimed to evaluate the effect of pemafibrate on fibrinogen levels in CAD patients with hypertriglyceridemia undergoing antiplatelet monotherapy and statin therapy.
Methods: This multicenter, randomized, controlled trial enrolled 101 patients with hypertriglyceridemia (fasting triglycerides ≥150 mg/dL) and CAD receiving antiplatelet monotherapy and statin therapy. After exclusion, 98 participants were randomly assigned to receive either pemafibrate 0.1 mg twice daily (intervention group) or standard care without additional lipid-lowering therapy (control group), and 96 patients were finally analyzed. Fibrinogen levels were assessed at baseline and after 3 months of treatment. The primary outcome was the change in fibrinogen levels from baseline to 3 months. Secondary outcomes included the thrombogenicity by Total Thrombus-formation Analysis System (T-TAS).
Results: Among 96 patients (median age of 72 years, male; 81%), the median baseline fasting triglyceride level was 175 mg/dL, HDL cholesterol level 45 mg/dL, LDL cholesterol level 72 mg/dL, and fibrinogen level 299 mg/dL. Regarding lipid levels at 3 months, triglyceride level was significantly lower in intervention group than those in control group (99 mg/dL vs. 186 mg/dL, p<0.001), whereas LDL cholesterol level was significantly higher in intervention group than those in control group (81 mg/dL vs. 71 mg/dL, p=0.003). No difference was observed in HDL cholesterol level at 3 months. At 3 months, the intervention group showed a significant reduction in fibrinogen levels compared to the control group (241 mg/dL vs. 300 mg/dL, p < 0.001). However, the intervention group showed a significant increase in AR-AUC and PL-AUC levels compared to the control group (p < 0.001, p=0.004, respectively).
Conclusions: Pemafibrate significantly reduced fibrinogen levels in patients with CAD and hypertriglyceridemia, highlighting its primary benefit in lowering thrombotic risk. While increases in AR-AUC and PL-AUC were observed as secondary outcomes, their implications require further investigation to fully understand potential effects on thrombogenicity.