Heart failure in HIV infection: focus on the role of atherosclerosis

Since the advent of highly active antiretroviral treatment, accelerated atherosclerosis resulting in coronary artery disease (CAD) has become an area of increasing concern among patients infected with HIV. As CAD has replaced myocarditis and opportunistic infection as the most common cause of heart failure in this population, it is necessary to re-evaluate the specific risks of cardiovascular disease in HIV-infected patients taking into consideration the processes driving atherogenesis.

Recent data illustrating that atazanavir is not associated with an increased risk of CAD argue against a class-wide association of protease inhibitors in HIV treatment and adverse cardiovascular outcomes. C-C chemokine receptor-type 5 has been identified as a potential target for pharmacological therapy to manage the process of atherosclerosis while simultaneously having an antiretroviral effect. Additionally, as the use of statins has recently been associated with new-onset diabetes in the general population, further investigation of this risk in HIV-infected patients is necessary.

HIV-infected patients have an increased risk of CAD and subsequently heart failure. This is likely because of a confluence of several factors including: conventional risk factors, HIV-specific processes driving inflammation, coagulatory pathway and endothelial dysfunction. The benefits of antiretroviral drugs in terms of overall survival rates outweigh the risks of dyslipidemia. The focus of the management of cardiovascular risk remains in the domains of primary and secondary prevention. More accurate risk stratification, which accounts for HIV-specific risk factors, is now increasingly warranted.