Cardiac effects in perinatally HIV‐infected and HIV‐exposed but uninfected children and adolescents: a view from the United States of America. Issue 1 (18th June 2013)

• Record Type: Journal Article
• Authors: Lipshultz, Steven E; Miller, Tracie L; Wilkinson, James D; Scott, Gwendolyn B; Somarriba, Gabriel; Cochran, Thomas R; Fisher, Stacy D
• Is Part Of: Journal of the International AIDS Society. Volume 16:Issue 1(2013)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2013-06-18
• Subjects: HIV -- AIDS -- child -- cardiac outcomes -- antiretroviral therapies -- therapeutic complications -- cardiovascular risk; AIDS (Disease) -- Periodicals; HIV infections -- Periodicals; 616.9792005
• DOI: 10.7448/IAS.16.1.18597
• Languages: English
• ISSNs: 1758-2652

Abstract

Abstract : Introduction: Human immunodeficiency virus (HIV) infection is a primary cause of acquired heart disease, particularly of accelerated atherosclerosis, symptomatic heart failure, and pulmonary arterial hypertension. Cardiac complications often occur in late‐stage HIV infections as prolonged viral infection is becoming more relevant as longevity improves. Thus, multi‐agent HIV therapies that help sustain life may also increase the risk of cardiovascular events and accelerated atherosclerosis. Discussion: Before highly active antiretroviral therapy (HAART), the two‐to‐five‐year incidence of symptomatic heart failure ranged from 4 to 28% in HIV patients. Patients both before and after HAART also frequently have asymptomatic abnormalities in cardiovascular structure. Echocardiographic measurements indicate left ventricular (LV) systolic dysfunction in 18%, LV hypertrophy in 6.5%, and left atrial dilation in 40% of patients followed on HAART therapy. Diastolic dysfunction is also common in long‐term survivors of HIV infection. Accelerated atherosclerosis has been found in HIV‐infected young adults and children without traditional coronary risk factors. Infective endocarditis, although rare in children, has high mortality in late‐stage AIDS patients with poor nutritional status and severely compromised immune systems. Although lymphomas have been found in HIV‐infected children, the incidence is low and cardiac malignancy is rare. Rates of congenital cardiovascular malformations range from 5.6 to 8.9% in cohorts of HIV‐uninfected and HIV‐infected children with HIV‐infected mothers. In non‐HIV‐infected infants born to HIV‐infected mothers, foetal exposure to ART 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. Conclusions: Routine, systematic, and comprehensive cardiac evaluation, including a thorough history and directed laboratory assays, is essential for the care of HIV‐infected adults and children as cardiovascular illness has become a part of care for long‐term survivors of HIV infection. The history should include traditional risk factors for atherosclerosis, prior opportunistic infections, environmental exposures, and therapeutic and illicit drug use. Laboratory tests should include a lipid profile, fasting glucose, and HIV viral load. 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.