Several reports have indicated that HIV-positive patients have an increased risk of cardiovascular disease (CVD). Some studies have demonstrated a relationship between antiretroviral use and increased risk of cardiovascular events. More recent studies disclosed that the use of abacavir was associated with an excess risk of CVD, and patients with low CD4+ cell count could be at higher risk of subclinical arterial lesions or CVD. This prompted the hypothesis that mechanisms other that those linked to lipid changes and “classic” risk factors for atheroma may be at work in HIV-positive patients. Atherogenesis is mainly an inflammatory disease, so it is not surprising that endothelial injury is associated with the progression and severity of HIV infection. Another question is: do antiretroviral drugs increase or reduce endothelial injury? Various studies support the hypothesis that highly active antiretroviral therapy (HAART) does stimulate endothelial function. Thus, the HIV virus together with immune reconstitution and HAART itself promote premature endothelial activation. Such a prominent role played by the inflammatory events also seems to affect the structure of the arterial lesions in HIV patients that could differ from classical atheroma. We hypothesize that the atherosclerotic lesions in HIV patients develop in two distinct phases: the first characterized by an inflammation of the vascular wall, the second in which the lesions could evolve towards the classic feature of atheroma. The initial lesions are probably determined by immune deficiency, immune reconstitution, and the effect of HAART, whereas subsequent lesions could be maintained by the classic risk factors.
Keywords: Atherosclerosis; HIV; Antiretroviral therapy; Endothelium; Arteritis.
Articolo presente in – HAART and correlated pathologies n. 1 –