Treatment with indinavir, zidovudine, and lamivudine as compared with zidovudine and lamivudine alone significantly slows the progression of HIV-1 disease in patients with 200 CD4 cells or fewer per cubic millimeter and prior exposure to zidovudine.

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As early and effective antiretroviral therapy has become more widespread, HIV has transitioned from a progressive, fatal disease to a chronic, manageable disease marked by elevated risk of chronic comorbid diseases, including cardiovascular diseases (CVDs). Rates of myocardial infarction, heart failure, stroke, and other CVD manifestations, including pulmonary hypertension and sudden cardiac death, are significantly higher for people living with HIV than for uninfected control subjects, even in the setting of HIV viral suppression with effective antiretroviral therapy. These elevated risks generally persist after demographic and clinical risk factors are accounted for and may be partly attributed to chronic inflammation and immune dysregulation. Data on long-term CVD outcomes in HIV are limited by the relatively recent epidemiological transition of HIV to a chronic disease. Therefore, our understanding of CVD pathogenesis, prevention, and treatment in HIV relies on large observational studies, randomized controlled trials of HIV therapies that are underpowered to detect CVD end points, and small interventional studies examining surrogate CVD end points. The purpose of this document is to provide a thorough review of the existing evidence on HIV-associated CVD, in particular atherosclerotic CVD (including myocardial infarction and stroke) and heart failure, as well as pragmatic recommendations on how to approach CVD prevention and treatment in HIV in the absence of large-scale randomized controlled trial data. This statement is intended for clinicians caring for people with HIV, individuals living with HIV, and clinical and translational researchers interested in HIV-associated CVD.

It is currently unknown whether there is an increased risk of coronary heart disease (CHD) in patients with HIV infection. In addition, the contribution of antiretroviral therapy (ART) to CHD risk has not been quantified. We reviewed administrative claims data for HIV-infected and -uninfected individuals from the California Medicaid population and compared the incidence of and relative risk (RR) for CHD using log-linear regression analyses between groups. The association between exposure to ART and CHD incidence was also assessed. Of 3,083,209 individuals analyzed, 28,513 were HIV-infected. The incidence of CHD among young men (up to age 34) and women (up to age 44) with HIV infection was significantly higher than that among non-HIV-infected individuals. The covariate-adjusted RR for the development of CHD in individuals receiving ART compared with those not receiving ART was 2.06 (P < 0.001) in HIV-infected individuals aged 18-33 years. There were no statistically significant associations between ART exposure and CHD in other age groups. CHD incidence appears accelerated among young HIV-infected individuals. Strategies to reduce CHD risk should be incorporated into HIV primary care.