In dyslipidemic or hyperlipidemic patients
etofibrate (CAS 31637-97-5, active principle of
Lipo-Merz-retard) improves plasma
lipoprotein profiles by reducing
low density lipoprotein cholesterol and
triglycerides. Experimentally, it also promotes fibrinolysis and thrombolysis and reduces the susceptibility of
lipoproteins to oxidative stress. In order to investigate the possible efficacy of
etofibrate on
atherosclerosis, a study in African Green Monkeys was performed. To accelerate
atherogenesis, balanced groups of adult male Vervetes (Cercopithecus aethiops) were fed an atherogenic diet, with and without
etofibrate, while negative controls received a prudent diet. Total dietary risk exposure was 38 months, with
etofibrate treatment during the final 27 months. The
etofibrate dose achieved plasma concentrations of
clofibric acid comparable to the one achieved clinically. Necropsy demonstrated lesions equivalent to human
atherosclerosis types I-VII, which were compared between treatments both macroscopically and microscopically. Peripheral
atherosclerosis was significantly less frequent after
etofibrate treatment than in positive controls. In aortas,
etofibrate probably ameliorated
atherogenesis, as defined by proliferation of smooth muscle and foam cells, and accumulation of
cholesterol crystals. Effective reduction of plasma
cholesterol by
etofibrate was confirmed. In conclusion, anti-atherogenic efficacy of
etofibrate was demonstrated in a non-human primate model of accelerated
atherogenesis. The results on peripheral
atherosclerosis confirm the preliminary clinical data in patients suffering from peripheral vascular occlusion.