Advances in antiretroviral treatment has increased the life expectancy of patients with HIV significantly, AIDS-related deaths have fallen by 30% since they peaked in 2005.
HIV infection predisposes to a chronic inflammatory and immunologic dysfunctional state, subsequent highly active antiretroviral treatment (HAART) results in metabolic changes and dyslipidemia.
In the post-HAART era, CAD is now considered to be the main cause of heart failure in HIV-infected patients, superseding the prior most common etiologies myocarditis and opportunistic infections.
The presentation of CAD in HIV-infected patients is largely similar to that in the general population with the exception is that they present at a younger age.
Certain antiretroviral agents specifically protease inhibitors have conventionally been associated with lipid dysfunction, further complicating the HIV-infected patients milieu.
Recent research has shown that a C-C chemokine receptor-type 5 (CCR5) antagonists has emerged as a potential target both as an antiretroviral agent as well as in the process of arresting atherogenesis, but warrants more research.
