Bezafibrate for the Secondary Prevention of Myocardial Infarction in Patients With Metabolic Syndrome

Abstract

Bezafibrate reduces the incidence of MI in patients with MS during long-term follow-up.

Comparison of effects of bezafibrate and fenofibrate on circulating proprotein convertase subtilisin/kexin type 9 and adipocytokine levels in dyslipidemic subjects with impaired glucose tolerance or type 2 diabetes mellitus: Results from a crossover study

“…Bezafibrate and fenofibrate have some evidence of preventing coronary artery disease in Bezafibrate Infarction Prevention (BIP) [21,22] and Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study [23], respectively. Our present data indicate that fenofibrate treatment (200 mg per day for 8 weeks) produced more favorable effects on cholesterol metabolism than did bezafibrate treatment (400 mg per day for 8 weeks) with regard to lower TC, non-HDL-C, LDL-C and apolipoprotein B levels.…”

Effects of Peroxisome Proliferator-Activated Receptor Ligands, Bezafibrate and Fenofibrate, on Adiponectin Level

“…1 Moreover, further subanalyses demonstrated that the administrations of bezafibrate significantly reduced new-onset diabetes 2,3 and myocardial infarction in the patients with the metabolic syndrome (MS). 4 The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study showed that fenofibrate significantly reduced nonfatal myocardial infarctions and coronary revascularizations, a secondary endpoint, among patients with type 2 diabetes. 5 These favorable clinical outcomes in fibrate studies might be explained by not only its triglyceride-lowering effect but also its various PPAR␣-mediated pleiotropic effects.…”

The metabolic syndrome entanglement: cutting the Gordian knot

“…Emerging varied areas of current MS research interests include heterogeneous topics like adiponectin and biomarkers preserving endothelial health [33,34], angiotensinogen, resistin, and leptin secretion [33], nonalcoholic fatty liver disease and liver steatosis [35], hyperuricemia [36], genetic predisposition [37], the role of adypocytokines and neurohumoral dysregulation [38]; sleep disorders and ethnicity [39], the possible ways for treatment optimization in patients with CVD [40]. Additional related matters are currently investigated, like heart rate (HR) turbulence; it has been shown that this turbulence -a well-established predictor of cardiac autonomic dysfunction -is significantly impaired in MS patients without T2DM in adults [41].…”