Association of Human Immunodeficiency Virus Infection with Exposure to Highly Active Antiretroviral Therapy and Its Adverse Cardiovascular Effects

Human immunodeficiency virus (HIV) infection is a cause of acquired heart disease, particularly of accelerated atherosclerosis, symptomatic heart failure, and pulmonary arterial hypertension. Cardiac complications in persons living with HIV are becoming more relevant as longevity improves. Before the advent of highly active antiretroviral therapy (HAART), the 2- to 5-year incidence of symptomatic heart failure ranged from 4 to 28% in HIV patients. Patients both before and after HAART availability also often have asymptomatic abnormalities in cardiovascular structure. Echocardiographic changes indicate left ventricular (LV) systolic dysfunction, LV hypertrophy, and left atrial dilation in patients followed on HAART therapy. In non-HIV infected infants born to HIV-infected mothers, fetal exposure to antiretroviral therapy is associated with reduced LV dimension, LV mass, and septal wall thickness, and with higher LV fractional shortening and contractility during the first two years of life. Routine, systematic, and comprehensive cardiac evaluation, including a thorough history and directed laboratory assays, are essential for the care of HIV-infected adults and children because cardiovascular illness has become a part of long-term survival in patients with HIV infection. Asymptomatic cardiac disease related to HIV can be fatal, and secondary effects of HIV infection often disguise cardiac symptoms, so systematic echocardiographic monitoring is warranted.