Effects of simvastatin/ezetimibe on microparticles, endothelial progenitor cells and platelet aggregation in subjects with coronary heart disease under antiplatelet therapy

It is not known whether the addition of ezetimibe to statins adds cardiovascular protection beyond the expected changes in lipid levels. Subjects with coronary heart disease were treated with four consecutive 1-week courses of therapy (T) and evaluations. The courses were: T1, 100 mg aspirin alone;...

Full description

Bibliographic Details
Main Author: Camargo, Luciano M.[UNIFESP] (author)
Other Authors: França, Carolina Nunes [UNIFESP] (author), Izar, Maria Cristina de Oliveira [UNIFESP] (author), Bianco, Henrique Tria [UNIFESP] (author), Lins, Liliane S. (author), Barbosa, Simone Pinto de Melo [UNIFESP] (author), Pinheiro, Luiz Fernando Muniz [UNIFESP] (author), Fonseca, Francisco Antonio Helfenstein [UNIFESP] (author)
Format: article
Language:eng
Published: 2015
Subjects:
Online Access:https://doi.org/http://dx.doi.org/10.1590/1414-431X20143628
https://doi.org/10.1590/1414-431X20143628
Country:Brazil
Oai:oai:k-repositorio.unifesp.br:11600/8378
Description
Summary:It is not known whether the addition of ezetimibe to statins adds cardiovascular protection beyond the expected changes in lipid levels. Subjects with coronary heart disease were treated with four consecutive 1-week courses of therapy (T) and evaluations. The courses were: T1, 100 mg aspirin alone; T2, 100 mg aspirin and 40 mg simvastatin/10 mg ezetimibe; T3, 40 mg simvastatin/10 mg ezetimibe, and 75 mg clopidogrel (300 mg initial loading dose); T4, 75 mg clopidogrel alone. Platelet aggregation was examined in whole blood. Endothelial microparticles (CD51), platelet microparticles (CD42/CD31), and endothelial progenitor cells (CD34/CD133; CDKDR/CD133, or CD34/KDR) were quantified by flow cytometry. Endothelial function was examined by flow-mediated dilation. Comparisons between therapies revealed differences in lipids (T2 and T3<T1 and T4 for total cholesterol, LDL-C, and triglycerides; P<0.002 for all), as well as for endothelial function (T2>T1 and T4, P=0.001). Decreased platelet aggregation was observed after aspirin (arachidonic acid, T1<T3 and T4, P=0.034) and clopidogrel (adenosine, T3 and T4<T1 and T2, P<0.0001) therapy. Simvastatin/ezetimibe diphosphate did not change platelet aggregation, the amount of circulating endothelial and platelet microparticles, or endothelial progenitor cells. Cardiovascular protection following therapy with simvastatin/ezetimibe seems restricted to lipid changes and improvement of endothelial function not affecting the release of microparticles, mobilization of endothelial progenitor cells or decreased platelet aggregation.