Seroreverters (uninfected children of HIV-infected mothers) have exhibited left ventricular (LV) dysfunction. Mitochondrial toxicity associated with in utero or postnatal exposure to highly active antiretroviral therapy (HAART) is a possible mechanism. Adult and animal models have demonstrated associations between LV abnormalities, cardiomyopathy, and components of HAART. Yet, outcomes in children are poorly understood. In this study, we explore HAART-associated LV abnormalities in seroreverters exposed to HAART (n = 144) or never exposed (n = 252). Subjects are drawn from the Women and Infants Transmission Study and the Pediatric Pulmonary and Cardiovascular Complications of HIV Study, respectively. Data include (1) echocardiographic studies of LV structure and function and (2) serologic cardiac biomarkers (cardiac troponin, probrain natriuretic peptide, high-sensitivity C reactive protein), both collected during the first month of life, and again at 6, 12, 24, 36, and 48 months postnatally. Planned analyses include several regression models. At this time, we have access to data for all 252 unexposed children, and 53 exposed subjects are enrolled. The cohorts are similar in terms of gender and race and the recruited subjects are representative of all eligible subjects in terms of exposure to HAART. Recruitment will continue into 2006.
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