Haemostatic effects of simvastatin in subjects with impaired glucose tolerance.

摘要

BACKGROUND: Very little is known about extra-lipid effects of statins in prediabetic subjects. Aim: Our study has assessed the effect of simvastatin on coagulation and fibrinolysis in patients with impaired glucose tolerance (IGT), comparing this effect with that exhibited by simvastatin in isolated hypercholesterolaemia. METHODS: Lipid profile, fasting and 2-h post-glucose challenge plasma glucose levels, the homeostatic model assessment (HOMA) ratio, glycated haemoglobin, the prothrombin and partial thromboplastin time, plasma fibrinogen, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (vWF), factor X levels and factor VII coagulant activity were assessed at baseline, and after 30 and 90 days of simvastatin treatment (20 mg daily) in 28 patients with IGT and 28 subjects with primary isolated hypercholesterolaemia. The control group included 26 age-, sex- and weight-matched dyslipidaemia-free individuals with normal glucose tolerance. The experiments comply with the current law of Poland. RESULTS: Compared to the control subjects, hypercholesterolaemic and IGT patients exhibited increased baseline plasma levels of fibrinogen, PAI-1 and vWF, and increased factor VII activity, with no difference between the two groups of patients. All these haemostatic abnormalities were alleviated or normalized after simvastatin treatment, which was accompanied by a prolongation of the prothrombin and partial thromboplastin time. In both treatment groups simvastatin reduced total and low-density lipoprotein (LDL)-cholesterol, oxidized LDL and apoprotein B but did not affect glucose metabolism marker levels. CONCLUSIONS: Our study shows that haemostasis is disturbed to a similar degree in IGT and isolated hypercholesterolaemia. Simvastatin exhibits a multidirectional, lipid-independent favourable action on coagulation and fibrinolysis in IGT patients, which may play a role in the prevention of initiation and progression of atherosclerosis in this prediabetic state.