Abstract Body

Background: Adolescents and young adults (AYA) infected with HIV early in life may be at increased risk of atherosclerotic cardiovascular disease (CVD). Chronic inflammation and circulating adhesion molecules may play a role in the early pathogenesis of atherosclerosis, however, the mechanism of vascular injury in this population is still unclear. The aim of this study was to measure biomarkers of cardiovascular injury and immune activation in relationship to coronary plaque burden in patients infected with HIV early in life.

Methods: 35 AYA who acquired HIV early in life and 11 healthy controls were examined in this prospective cross-sectional study. All participants were free of active CVD at the time of evaluation. CT angiography was utilized for coronary plaque quantification. Number of atherosclerotic plaques, calcified and non-calcified, was determined in each of the 17 American Heart Association coronary segments.

Results: We studied HIV+ subjects (mean age 22; 15-29 years; 54% male) and control subjects (mean age 25; 22-29 years; 27% male). No calcified plaque was found in either group. No significant difference in number of plaque lesions between groups (HIV+ median 0, range 0-4, Control median 0, range 0-7, p=0.08). Activated CD8 T cells in the periphery, as measured by %CD8+CD38+DR+, was associated with increased coronary plaque in the HIV+ group (Table 1). Levels of activated peripheral CD8 T-cells (%CD8+CD38+DR+, p =0.025) were significantly associated with coronary plaque in HIV, but not levels of activated CD4 T-cells (%CD4+CD38+DR+). E-selectin was significantly associated with plaque in HIV+ subjects (p=0.006). In a multivariate analysis only %CD8+CD38+DR+ was significant (Table 1). Although P-selectin, sICAM-3, VCAM-1, TIMP-1, and MCP-1 levels were significantly elevated in HIV, these biomarkers did not relate to plaque, nor did lipopolysaccharide binding protein.

Conclusions: Prior investigation in HIV+ adults identified an association between increased carotid lesions and T-cell activation markers. We identify a significant relationship between increased coronary plaque and levels of activated T-cells in AYA with life-long HIV. Further, soluble E-selectin, which has also been linked with carotid artery plaque and atherosclerosis, was positively correlated with coronary plaque in the present study. The presence of increased circulating adhesion molecules and markers of immune activation may be early predictors of atherosclerosis in AYA infected with HIV early in life.