Journal of atherosclerosis and thrombosis · 2026
The Effects of Pemafibrate on Fibrinogen and Thrombogenicity in Patients with Coronary Artery Disease.
СтатьяРандомизированное исследованиеМногоцентровое исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Ishii Masanobu, Fujisue Koichiro, Kaikita Koichi, Yamanaga Kenshi, Hanatani Shinsuke, Matsuzawa Yasushi, Miura Mitsutoshi, Kudo Takashi, Shimomura Hideki, Takae Masafumi, Shirahama Yuichiro, Yamamoto Nobuyasu, Ito Teruhiko, Tsunoda Ryusuke, Horio Eiji, Sakamoto Tomohiro, Rokutanda Taku, Morihisa Kenji, Noda Katsuo, Tanaka Hiroki, Matsuura Yunosuke, Yamamoto Eiichiro, Izumiya Yasuhiro, Tsujita Kenichi, PEMA-TAS Investigators
Аннотация
AIMS: Pemafibrate effectively reduces the triglyceride levels in patients with coronary artery disease (CAD). However, its effect on the fibrinogen levels in these patients remains unclear. This study aimed to investigate the effects of pemafibrate on thrombogenicity and the plasma fibrinogen levels in patients complicated by hypertriglyceridemia.
METHODS: This multicenter, randomized, controlled trial enrolled 101 patients with hypertriglyceridemia (fasting triglycerides ≥ 150 mg/dL) and CAD who received 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 any additional lipid-lowering therapy (control group), and 96 patients were analyzed. The fibrinogen levels were assessed at the baseline and after 12 weeks of treatment. The primary endpoint was the change in the fibrinogen level from baseline to week 12. The secondary endpoints included thrombogenicity measured using the Total Thrombus-formation Analysis System (T-TAS).
RESULTS: Among the 96 patients, the median baseline fasting triglyceride, HDL cholesterol, LDL cholesterol, and fibrinogen levels were 175 mg/dL, 45 mg/dL, 72 mg/dL, and 299 mg/dL, respectively. The median decrease in triglycerides from baseline to 12 weeks was greater in the pemafibrate group than in the control group (-62 mg/dL vs. -5 mg/dL, p＜0.001), as was the median decrease in fibrinogen (-58 mg/dL vs. 9 mg/dL, p＜0.001).
CONCLUSIONS: Pemafibrate significantly reduced fibrinogen levels in patients with CAD and hypertriglyceridemia, thus highlighting its primary benefit in lowering thrombotic risk.
METHODS: This multicenter, randomized, controlled trial enrolled 101 patients with hypertriglyceridemia (fasting triglycerides ≥ 150 mg/dL) and CAD who received 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 any additional lipid-lowering therapy (control group), and 96 patients were analyzed. The fibrinogen levels were assessed at the baseline and after 12 weeks of treatment. The primary endpoint was the change in the fibrinogen level from baseline to week 12. The secondary endpoints included thrombogenicity measured using the Total Thrombus-formation Analysis System (T-TAS).
RESULTS: Among the 96 patients, the median baseline fasting triglyceride, HDL cholesterol, LDL cholesterol, and fibrinogen levels were 175 mg/dL, 45 mg/dL, 72 mg/dL, and 299 mg/dL, respectively. The median decrease in triglycerides from baseline to 12 weeks was greater in the pemafibrate group than in the control group (-62 mg/dL vs. -5 mg/dL, p＜0.001), as was the median decrease in fibrinogen (-58 mg/dL vs. 9 mg/dL, p＜0.001).
CONCLUSIONS: Pemafibrate significantly reduced fibrinogen levels in patients with CAD and hypertriglyceridemia, thus highlighting its primary benefit in lowering thrombotic risk.