• Erika F R da Silva, Francisco A H Fonseca, Carolina N França, Paulo R A Ferreira, Maria C O Izar, Reinaldo Salomão, Luciano M Camargo, Simone B Tenore, and David S Lewi.
• Infectious Diseases Division, Federal University of São Paulo, Brazil. erikaferrari@uol.com.br
• AIDS. 2011 Aug 24; 25 (13): 1595-601.

BackgroundCardiovascular events have been reported among HIV-infected patients following antiretroviral therapy. However, the role of HIV itself in determining vascular damage is less described. Chronic inflammatory state might impair some regulatory endothelium properties leading to its activation, apoptosis or erosion.ObjectivesTo evaluate the balance between endothelial progenitor cells and microparticles in HIV-infected antiretroviral drug-naive patients.DesignA case-control study comparing HIV-infected patients (n = 35) with sex-matched and age-matched healthy controls (n = 33).MethodsEndothelial progenitor cells populations expressing CD34, CD133 and KDR were quantified by flow cytometry. Endothelial-derived microparticles, expressing CD51, and platelet-derived microparticles, expressing CD31/CD42, were also measured. Endothelial function was estimated by flow-mediated dilation.ResultsLower percentages of endothelial progenitor cells (CD34/KDR) were observed in HIV-infected individuals compared with controls (0.02 vs. 0.09%, P = 0.045). In addition, endothelial microparticles concentration was higher in HIV-infected individuals (1963 vs. 436 microparticles/μl platelet-poor plasma, P = 0.003), with similar number of platelet-derived microparticles among groups. Furthermore, flow-mediated dilation was lower among HIV-infected individuals compared with controls [mean (SEM): 10 (1) and 16% (2), respectively; P = 0.03].ConclusionOur findings suggest an imbalance between endothelial progenitor cells mobilization and endothelial apoptosis. The alteration in the turnover of endothelial cells may contribute to cardiovascular events in HIV-infected patients.

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