OBJECTIVE: Ischemic cardiovascular events increasingly occur during long-lasting HIV infection and are attributed either to the infection itself or to the use of HAART. Endothelial dysfunction and platelet activation are markers of atherosclerosis. Our aim was to assess whether patients with chronic HIV infection present endothelial dysfunction and whether this is the consequence of infection or of HAART. DESIGN: Fifty-six HIV-infected patients were studied in a retrospective cohort study before and 3, 6, 12 and 24 months after starting HAART with protease inhibitors (n = 28) or nonnucleoside reverse transcriptase inhibitors (n = 28), and compared with 28 age-matched and sex-matched healthy controls, and with 10 naive HIV-infected patients studied at diagnosis and after 12 months of untreated infection. METHODS: Soluble endothelial and platelet activation markers were measured in plasma by flow cytometry. RESULTS: Soluble P-selectin, soluble vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and von Willebrand factor were significantly higher in HIV-infected patients than in healthy controls, whereas 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 protease inhibitors and nonnucleoside reverse transcriptase inhibitors treatment. In naive, untreated patients, increased plasma markers of endothelial dysfunction were confirmed at diagnosis, with no changes upon follow-up. CONCLUSION: Chronic HIV infection, and not its pharmacological treatment, induces alterations of markers of endothelial function. Short-term treatment with HAART reduces some markers of endothelial dysfunction, with no differences between protease inhibitors and nonnucleoside reverse transcriptase inhibitors.

HIV type 1 infection, and not short-term HAART, indice endothelial dysfunction.

FRANCISCI, Daniela;BALDELLI, Franco;MALINCARNE, LISA;GRESELE, Paolo
2009

Abstract

OBJECTIVE: Ischemic cardiovascular events increasingly occur during long-lasting HIV infection and are attributed either to the infection itself or to the use of HAART. Endothelial dysfunction and platelet activation are markers of atherosclerosis. Our aim was to assess whether patients with chronic HIV infection present endothelial dysfunction and whether this is the consequence of infection or of HAART. DESIGN: Fifty-six HIV-infected patients were studied in a retrospective cohort study before and 3, 6, 12 and 24 months after starting HAART with protease inhibitors (n = 28) or nonnucleoside reverse transcriptase inhibitors (n = 28), and compared with 28 age-matched and sex-matched healthy controls, and with 10 naive HIV-infected patients studied at diagnosis and after 12 months of untreated infection. METHODS: Soluble endothelial and platelet activation markers were measured in plasma by flow cytometry. RESULTS: Soluble P-selectin, soluble vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and von Willebrand factor were significantly higher in HIV-infected patients than in healthy controls, whereas 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 protease inhibitors and nonnucleoside reverse transcriptase inhibitors treatment. In naive, untreated patients, increased plasma markers of endothelial dysfunction were confirmed at diagnosis, with no changes upon follow-up. CONCLUSION: Chronic HIV infection, and not its pharmacological treatment, induces alterations of markers of endothelial function. Short-term treatment with HAART reduces some markers of endothelial dysfunction, with no differences between protease inhibitors and nonnucleoside reverse transcriptase inhibitors.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11391/37421
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