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GW24-e1288 Captopril and atorvastatin inhibit platelet activation in hypertensive, hypercholesterolemic and diabetic patients
  1. Li Xiaoyan,
  2. Zhang Ping
  1. The Third Affiliated Hospital Of Sun Yat-sen University

Abstract

Objectives Hypertension, hypercholesterolemia accompanied with type 2 diabetes mellitus (T2DM) showed hypercoagulability and platelet hyperaggregability, so the present trail was designed to investigate the effects of captopril with atorvastatin on circulating levels of soluble selectins, soluble cell adhesion molecules, platelet activation markers and microparticles in hypertensive hyperlipidemic patients with or without T2DM.

Methods A total of 47 hypertensive, hyperlipidemic patients were divided into two groups: A group (hypertensive, hyperlipidemic patients combine with T2DM) and B group (hypertensive, hyperlipidemic patients without T2DM), in addition to 25 normotensive healthy patients were distributed into controls. Captopril (50 mg/day) and atorvastatin (80 mg/day) was administered to all of the patients for 24 weeks.

Results The plasma levels of CD63, CD62P, PAC-1, PDMP, EDMP, and sVCAM-1, sE-selectin were significantly increased in A group more than B groups and healthy controls (CD63: 21.2 ± 3.4 vs 13.6 ± 1.3 vs 11.2 ± 1.1; CD62P:19.4 ± 4.3 vs 11.6 ± 2.8 vs 9.2 ± 0.8; PAC-1:15.9 ± 1.2 vs 9.3 ± 1.0 vs 7.9 ± 0.4; PDMP: 9898 ± 172 vs 8243 ± 389 vs 7034 ± 156; EDMP: 908 ± 72 vs 546 ± 23 vs 321 ± 27; sVCAM-1: 790 ± 54 vs 521 ± 32 vs 423 ± 24; sE-selectin: 82.9 ± 7.6 vs 66.8 ± 2.9 vs 48.7 ± 5.7, P < 0.01, respectively). Atorvastatin and captopril combined with atorvastatin decreased those more than captopril alone, and the effect of captopril combined with atorvastatin was more than atorvastatin alone (P < 0.01, respectively). In all patients, Low-density lipoprotein was reduced obviously by atorvastatin had correlation between with CD62P or platelet microparticles.

Conclusions In hypertensive, hyperlipidemic with T2DM patients, combined therapy of captopril with atorvastatin may ameliorate the development of cardiovascular complications by decreasing levels of platelet activation-markers.

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