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Haemostatic effects of simvastatin in subjects with impaired glucose tolerance

R Krysiak1, B Okopien

  • 1Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland. r.krysiak@interia.pl

Internal Medicine Journal
|December 2, 2010
PubMed

Insights

Simvastatin improves blood clotting and clot breakdown in prediabetic individuals with impaired glucose tolerance (IGT), independent of its cholesterol-lowering effects. This action may help prevent atherosclerosis progression in this at-risk group.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Pharmacology

Background:

  • Limited understanding of statin's non-lipid effects in prediabetes.
  • Prediabetic individuals often exhibit dysregulated glucose metabolism.

Purpose of the Study:

  • To investigate simvastatin's impact on coagulation and fibrinolysis in patients with impaired glucose tolerance (IGT).
  • To compare these effects with simvastatin's actions in patients with isolated hypercholesterolemia.

Main Methods:

  • Assessed coagulation and fibrinolysis markers (fibrinogen, PAI-1, vWF, factor VII) in IGT, hypercholesterolemia, and control groups.
  • Measured lipid profiles, glucose metabolism markers (HOMA, HbA1c), and clotting times before and after 90 days of simvastatin treatment (20 mg/day).

Main Results:

  • IGT and hypercholesterolemia patients showed similar baseline hemostatic abnormalities (elevated fibrinogen, PAI-1, vWF, factor VII activity).
  • Simvastatin normalized these hemostatic markers and prolonged prothrombin and partial thromboplastin times in both patient groups.
  • Simvastatin reduced LDL-cholesterol and other lipid markers but did not alter glucose metabolism indicators.

Conclusions:

  • Hemostasis is similarly disturbed in IGT and isolated hypercholesterolemia.
  • Simvastatin demonstrates beneficial, lipid-independent effects on coagulation and fibrinolysis in IGT patients.
  • These effects may contribute to preventing atherosclerosis initiation and progression in prediabetic states.
Abstract

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