[HIV-related cardiovascular risk factors]

Abstract

Evidence from experimental and observational studies suggests that HIV infection per se and the associated proinflammatory state can increase the risk of cardiovascular disease. HIV infection can activate several inflammatory pathways in the vascular wall with cytokine release and expression of endothelial adhesion molecules. Many of these alterations can be suppressed by highly-active antiretroviral therapy (HAART). The role of HIV in cardiovascular risk has been demonstrated in studies of treatment interruption, mainly in the SMART trial, in which greater cardiovascular mortality was observed in the group interrupting HAART. The abrupt change to a more proinflammatory state produced by sudden resumption of viral replication could induce an increase in platelet adhesion and migration of inflammatory cells with plaque instability. Some studies suggest that HIV can also produce endothelial damage; a decrease in markers of endothelial activation and improvement of endothelial function after initiation of HAART have been described, and these changes have been correlated with the decrease in HIV viral load. Finally, HIV can induce cardiovascular disease through its effect on high-density lipoprotein cholesterol, which can decrease in patients with uncontrolled infection. Although the association of HIV with cardiovascular risk is controversial, coinfection with hepatitis C infection has been associated with a higher frequency of insulin resistance and acute myocardial infarction in some cohorts.