Human Immunodeficiency Virus Infection-Associated Cardiomyopathy and Heart Failure

The landscape of human immunodeficiency virus (HIV) epidemiology and treatment is ever-changing, with the widespread and evolving use of antiretroviral therapy (ART). With timely ART, people living with HIV (PLWH) are nearing the life expectancies and the functionality of the general population; nevertheless, the effects of HIV and ART on cardiovascular health remain under investigation. The pathophysiology of HIV-related cardiomyopathy and heart failure (HF) have historically been attributed to systemic inflammation and changes in cardiometabolic function and cardiovascular architecture. Importantly, newer evidence suggests that ART also plays a role in modulating the process of HIV-related cardiomyopathy and HF. In the short term, newer highly active ART (HAART) seems to have cardioprotective effects; however, emerging data on the long-term cardiovascular outcomes of certain HAART medications, i.e., protease inhibitors, raise concerns about the potential adverse effects of these drugs in the clinical course of HIV-related HF. As such, the traditional phenotypes of dilated cardiomyopathy and left ventricular systolic failure that are associated with HIV-related heart disease are incrementally being replaced with increasing rates of diastolic dysfunction and ischemic heart disease. Moreover, recent studies have found important links between HIV-related HF and other clinical and biochemical entities, including depression, which further complicate cardiac care for PLWH. Considering these trends in the era of ART, the traditional paradigms of HIV-related cardiomyopathy and HF are being called into question, as is the therapeutic role of interventions such as ventricular assist devices and heart transplantation. In all, the mechanisms of HIV-related myocardial damage and the optimal approaches to the prevention and the treatment of cardiomyopathy and HF in PLWH remain under investigation.