Background:  After complications of HIV, cardiovascular disease (CVD) has the highest age-adjusted mortality rate among individuals living with HIV infection. The major risk factors for CVD in individuals with HIV are similar to those without HIV:  aging, cigarette smoking, male sex, diabetes mellitus, dyslipidemia, hypertension, and family history of premature heart disease. In addition, use of certain ARV medications appears to increase CVD risk. In patients without HIV infection, inflammation has been implicated in atherogenesis, plaque rupture, and acute coronary syndromes, and C-reactive protein, a non-specific marker of inflammation, is an independent predictor of CVD risk. In HIV⁺ patients, it is likely that persistent inflammation, viremia, and immune activation cause arterial injury and may predict CVD risk. Indeed, C-reactive protein and a wide range of markers of inflammation and immune activation have been associated with CVD events and markers of arterial disease in patients with HIV infection.   However, the vast majority of studies showing such associations have been small and observational, although intriguing data from some longitudinal and interventional investigations support the hypothesis that inflammation and immune activation adversely influence atherogenesis and CVD risk in HIV⁺ individuals. 

Conclusions:  This talk will briefly review the role of traditional risk factors for predicting CVD risk in patients with HIV and the risks associated with certain ART medications, such as protease inhibitors and abacavir. Its focus, however, will be on the roles of inflammation and immune activation in atherogenesis and CVD risk in patients with HIV. It will draw on research presented at CROI 2012, and attempt to determine whether the causes of atherosclerosis and its complications in patients with HIV are any different than observed in individuals without HIV.  The talk will conclude with a brief discussion of future research needs related to CVD pathogenesis, CVD risk prediction, and prevention of CVD among HIV⁺ individuals.