Article

Journal of Thrombosis and Thrombolysis

, Volume 18, Issue 3, pp 177-185

Losartan and Simvastatin Inhibit Platelet Activation in Hypertensive Patients

  • Shosaku NomuraAffiliated withFirst Department of Internal Medicine, Kansai Medical UniversityFirst Department of Internal Medicine, Kansai Medical University Email author 
  • , Akira ShouzuAffiliated withSecond Department of Internal Medicine, Kansai Medical University
  • , Seitarou OmotoAffiliated withSecond Department of Internal Medicine, Kansai Medical University
  • , Mitsushige NishikawaAffiliated withSecond Department of Internal Medicine, Kansai Medical University
  • , Shirou FukuharaAffiliated withFirst Department of Internal Medicine, Kansai Medical University
  • , Toshiji IwasakaAffiliated withSecond Department of Internal Medicine, Kansai Medical University

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Abstract

Background: Diabetic patients also show hypercoagulability and platelet hyperaggregability, with increased levels of platelet activation-markers such as P-selectin (CD62P) and platelet-derived microparticles. We investigated the effects of losartan and simvastatin on circulating levels of platelet activation markers, microparticles, soluble selectins, and soluble cell adhesion molecules in hypertensive and hyperlipidemic patients with or without Type 2 diabetes.

Methods: The subjects included 25 normotensive healthy controls and 41 hypertensive patients. The 41 hypertensive patients were divided into three groups: group A had hypertension and hyperlipidemia (n = 11), group B had hypertension and Type 2 diabetes (n = 14), and group C had hypertension, hyperlipidemia, and diabetes (n = 16). Losartan was administered to all of the patients at a dose of 50 mg/day for 24 weeks. In addition, simvastatin was administered to the hyperlipidemic patients at a dose of 10 mg/day for 24 weeks.

Results: There were significant differences in the levels of CD62P, CD63, PAC-1, platelet microparticles, endothelial microparticles, sE-selectin, and sVCAM-1 between the hypertensive patients and healthy controls. These markers were all significantly increased in hypertensive and hyperlipidemic patients with Type 2 diabetes. In hypertensive patients with diabetes, CD62P, CD63, PAC-1, platelet and endothelial microparticles, and soluble adhesion markers were all decreased by losartan monotherapy. The decrease of each marker in hypertensive and hyperlipidemic patients given combined therapy with losartan plus simvastatin was greater among those with than without Type 2 diabetes. Low-density lipoprotein was decreased significantly by simvastatin and was correlated with CD62P or platelet microparticles in all of the patients.

Conclusion: Administration of losartan plus simvastatin to hypertensive and hyperlipidemic patients with Type 2 diabetes may prevent the development of cardiovascular complications caused by activated platelets and microparticles via another mechanism in addition to reduction of the blood pressure or lipid levels.

Key Words

platelet activation markers hypertension hyperlipidemia type 2 diabetes mellitus losartan simvastatin