"Ischemic cardiovascular events increasingly occur during long-lasting HIV infection and are attributed either to the infection itself or to the use of HAART [highly active antiretroviral therapy]. Endothelial dysfunction and platelet activation are markers of atherosclerosis," noted the researchers. For the current retrospective cohort study, they assess whether patients with chronic HIV infection present endothelial dysfunction and whether this is a consequence of HAART or of infection.
Fifty-six HIV-infected patients were studied at baseline and at three, six, 12, and 24 months after starting HAART with protease inhibitors (PI) (n=28) or nonnucleoside reverse transcriptase inhibitors (NNRTI) (n=28). These participants were compared with 28 age-matched and sex-matched healthy controls, and with 10 treatment-naïve HIV-infected patients studied at diagnosis and after 12 months of untreated infection. Flow cytometry was used to measure soluble endothelial and platelet activation markers.
Compared to healthy controls, soluble P-selectin, soluble vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and von Willebrand factor were significantly higher in HIV-infected patients; soluble CD40 ligand and tissue type plasminogen activator were within normal range. During follow-up, soluble vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and von Willebrand factor but not soluble P-selectin decreased progressively, without significant differences between PI and NNRTI. In untreated patients, increased plasma markers of endothelial dysfunction were confirmed at diagnosis, with no changes at follow-up.
"Chronic HIV infection, and not its pharmacological treatment, induces alterations of markers of endothelial function," the authors concluded. "Short-term treatment with HAART reduces some markers of endothelial dysfunction, with no differences between [PI] and [NNRTI]."
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