Human immunodeficiency virus per se exerts atherogenic effects.

Objective: Premature atherosclerosis in HIV-infected patients has been attributed to highly active antiretroviral therapy (HAART) and the associated metabolic complications. Whether HIV per se plays a role is an unresolved issue. The purpose of this study was to evaluate whether HIV per se exerts atherogenic effects.Methods: We measured carotid intima-media thickness (IMT) and brachial endothelial-dependent (FMD) and endothelial-independent (NMD) vasodilation in 38 naive untreated HIV-infected patients and 41 healthy control subjects.Results: Control subjects were selected as to match the HIV patients for metabolic risk factors. Mean carotid IMT was higher in HIV patients (0.85 +/- 0.2 mm; p < 0.001) than in controls (0.63 +/- 0.1 mm). In a stepwise multiple regression model, the changes in carotid IMT were predicted by the duration of HIV infection (p < 0.001)and CD4T-cells (p = 0.035). Brachial FMD was impaired in HIV patients (8.8 +/- 3% versus 12.2 +/- 3% in controls; p < 0.001). In contrast, NMD values practically overlapped in the HIV patients and controls. Analysis of the data in relation to viral load showed that FMD was significantly more impaired in the subgroup of patients with viral load values above the median (p < 0.001). In addition, there was a highly significant, inverse correlation between FMD and the HIV-RNA copies (p < 0.001).Conclusion: HIV infection causes functional and structural vascular alterations in a very early stage of the infection independent of HAART and metabolic factors. The data lend support to the viral infectious theory of atherosclerosis. Early assessment of the vascular status in HIV-infected patients is suggested.