title: Fenofibrate improves endothelial function and decreases thrombin-activatable fibrinolysis inhibitor concentration in metabolic syndrome.
abstract: Procoagulant state, inflammation, and endothelial dysfunction have been documented in metabolic syndrome. Endothelial dysfunction is a strong predictor of cardiovascular events. Studies on the association of thrombin-activatable fibrinolysis inhibitor and thrombosis are still controversial, but substantial evidence suggests that increased thrombin-activatable fibrinolysis inhibitor or thrombin-activatable fibrinolysis inhibits or protects against arterial thrombosis. This study aimed to assess concomitantly the effects of fenofibrate therapy on thrombin-activatable fibrinolysis inhibitor concentrations and endothelial functions in patients with metabolic syndrome. Twenty-five patients (16 women; mean age 50.4 +/- 7.0) were enrolled in the study. Plasma thrombin-activatable fibrinolysis inhibitor, C-reactive protein, and fibrinogen levels were measured before fenofibrate administration and after 8 weeks of fenofibrate treatment. Endothelial function was assessed by endothelial-dependent flow-mediated dilatation from brachial artery. Pretreatment (baseline) thrombin-activatable fibrinolysis inhibitor level was 52.3 (1.2-119.7) decreasing to 7.7 (0.9-51.2; P < 0.001) after 8 weeks of fibrate treatment. Endothelial functions, which were measured with flow-mediated dilatation, were significantly improved after treatment (mean flow-mediated dilatation was 6.76 +/- 2.21 at baseline and 10.66 +/- 1.17% after 8 week of fenofibrate treatment, P < 0.001). Fenofibrate decreases thrombin-activatable fibrinolysis inhibitor levels and improves endothelial function in metabolic syndrome and, thus, suggests a potential for protection against cardiovascular effects. Further studies are warranted to confirm the effects of fibrates on thrombin-activatable fibrinolysis inhibitor and for conclusive evidence on the association between thrombin-activatable fibrinolysis inhibitor and thrombosis.
authors.affiliation: Hacettepe University Faculty of Medicine, Department of Internal Medicine, Ankara, Turkey. alparslanmd@gmail.com
authors.forename: Alpaslan
authors.initials: A
authors.lastname: Kilicarslan
authors.forename: Bunyamin
authors.initials: B
authors.lastname: Yavuz
authors.forename: Gulay Sain
authors.initials: GS
authors.lastname: Guven
authors.forename: Enver
authors.initials: E
authors.lastname: Atalar
authors.forename: Levent
authors.initials: L
authors.lastname: Sahiner
authors.forename: Yavuz
authors.initials: Y
authors.lastname: Beyazit
authors.forename: Murat
authors.initials: M
authors.lastname: Kekilli
authors.forename: Necla
authors.initials: N
authors.lastname: Ozer
authors.forename: Gul
authors.initials: G
authors.lastname: Oz
authors.forename: Ibrahim C
authors.initials: IC
authors.lastname: Haznedaroglu
authors.forename: Tumay
authors.initials: T
authors.lastname: Sozen
mesh_terms: D000328:Adult; D025901:Carboxypeptidase B2 / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000187:drug effects*; D005260:Female; D011345:Fenofibrate / Q000494:pharmacology*; D005340:Fibrinogen / Q000187:drug effects; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology*; D008297:Male; D024821:Metabolic Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D008875:Middle Aged; D011446:Prospective Studies; D011673:Pulsatile Flow / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000960:Hypolipidemic Agents; D005340:Fibrinogen; D025901:Carboxypeptidase B2; D011345:Fenofibrate