Purpose of review: Inflammation and immune activation associated with untreated HIV infection may increase the risk for cardiovascular disease (CVD) and are not entirely reversed by antiretroviral therapy (ART). Although older ART regimens were associated with drug-specific risks for CVD, this may not be true for modern ART. Thus, with regard to CVD risk, the net benefit of initiating ART at higher CD4 T-cell counts remains unclear.
Recent findings: In addition to the well established risk of coronary heart disease, emerging evidence now suggests that chronic HIV infection is associated with higher risk of ischemic stroke, heart failure, and arrhythmias. These epidemiologic studies have associated immunodeficiency and active viral replication with higher CVD risk. Novel methods of imaging subclinical vascular disease continue to implicate inflammation and immune activation as likely mediators of CVD among patients with HIV. Newer generation protease inhibitors, chemokine receptor 5 antagonists, and integrase inhibitors do not appear to be associated with the adverse cardiometabolic risks of older drugs.
Summary: Recent evidence suggests that treating HIV infection with ART may reduce the risk of CVD, even at higher CD4 T-cell counts; however, the definitive answer to this question will come from clinical trials and long-term observational studies.