期刊
CELL BIOCHEMISTRY AND BIOPHYSICS
卷 70, 期 1, 页码 687-696出版社
HUMANA PRESS INC
DOI: 10.1007/s12013-014-9973-9
关键词
C-reactive protein; Endothelial progenitors cells; Ezetimibe; Inflammation; Microparticles; Statins
资金
- FAPESP (Foundation for Research of the State of Sao Paulo, Brazil) [2009/50052-1]
- CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior, Brazil)
Imbalance on endothelial turnover can predict cardiovascular outcomes. We aimed at evaluating the effects of lipid-modifying therapies on circulating endothelial progenitor cells (EPCs), endothelial microparticles (EMPs), and platelet microparticles (PMPs) in high cardiovascular risk subjects with elevated C-reactive protein (CRP). Sixty-three individuals with coronary heart disease (CHD) or CHD risk equivalent on stable statin therapy, with LDL-cholesterol < 100 mg/dL and CRP a parts per thousand yen2.0 mg/L were selected. After a 4-week run-in period with atorvastatin 10 mg, those with persistent CRP a parts per thousand yen2.0 mg/L were randomized to another 4-week treatment period with atorvastatin 40 mg, ezetimibe 10 mg or atorvastatin 40 mg/ezetimibe 10 mg. EPC (CD34(+)/CD133(+)/KDR+), EMP (CD51(+)), and PMP (CD42(+)/CD31(+)) were quantified by flow cytometry. Atorvastatin 40 mg and atorvastatin 40 mg/ezetimibe 10 mg reduced LDL-cholesterol (P < 0.001, paired T test, vs. baseline). Combined therapy, but not ezetimibe reduced CRP. CD34(+)/KDR+ EPC were reduced after ezetimibe alone (P = 0.011 vs. baseline, Wilcoxon test) or combined with atorvastatin (P = 0.016 vs. baseline, Wilcoxon test). In addition, ezetimibe increased CD51(+) EMP (P = 0.017 vs. baseline, Wilcoxon test). No correlations between these markers and LDL-cholesterol or CRP were observed. These results contribute to understand the link between inflammation and vascular homeostasis and highlight the broader benefit of statins decreasing inflammation and preventing microparticles release, an effect not observed with ezetimibe alone.
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