Purpose of review: Cardiovascular disease is increasingly recognized to be a significant cause of morbidity and mortality among patients with chronic HIV infection in the current era of effective antiretroviral therapy. HIV-infected patients treated with antiretroviral therapy have increased traditional cardiovascular risk factors, but whether HIV infection in and of itself confers a significant increase in cardiovascular risk is largely unknown. This review summarizes recent data investigating cardiovascular risk in HIV patients and the evidence for an effect of HIV per se. The potential physiological mechanisms by which HIV might contribute to coronary artery disease are reviewed.
Recent findings: Several interesting studies in the last year have evaluated cardiovascular endpoints and surrogate measures such as carotid intima-media thickness and endothelial function in HIV-infected patients compared with uninfected control groups. Several studies to date using surrogate measurements such as carotid intima-media thickness and endothelial dysfunction suggest a possible independent HIV effect on cardiovascular risk, but some studies have yielded conflicting results. Numerous potential mechanisms by which HIV might contribute to coronary artery disease exist. These mechanisms include effects of HIV proteins to attract monocytes to the intimal wall, and impair cholesterol efflux, and effects of activated monocytes to induce an inflammatory response.
Summary: More definitive prospective studies are needed to fully answer whether HIV infection per se promotes cardiovascular disease, but ample evidence suggests that HIV and related inflammatory responses could contribute to increased cardiovascular disease.