Background:  To date, there are no data on cardiovascular disease (CVD) risk of HIV⁺ children treated with ART.

Methods:  We assessed cardiovascular markers in HIV⁺ children with HIV-1 RNA £5000 copies/mL on stable ART for ≥6 months. Healthy children overall matched for age, gender, race, and body mass index were used as controls. Diabetes and family history of premature CVD were exclusionary. Carotid intima-media thickness (IMT) was measured and reported separately as internal carotid artery (ICA) and common carotid artery (CCA) thickness, and left and right sides were also separately measured. Two cardiovascular markers, myeloperoxidase, and high-sensitivity CRP (HS-CRP) were also measured. Groups were compared using distributionally appropriate 2-sample tests.

Results:  Overall, 44 subjects were enrolled (27 HIV⁺). All HIV⁺ children acquired HIV by vertical transmission; 67% were female, 67% African American, median age was 10 years, and body mass index 18.3 kg/m²; median nadir was CD4 310 (13%) ; at study entry median CD4 was 931 (32%) and 89% had HIV-1 RNA <50 copies/mL; 41% were on ritonavir-enhanced protease inhibitors (RTV/PI), 52% on non-nucleoside reverse transcriptase inhibitors (NNRTI), and 7% on NNRTI + RTV/PI. Median duration of ART and of PI therapy was 74 and 29 months, respectively. None of the subjects had a history of hypertension or smoking. There were no differences in age, body mass index, waist-to-hip ratio, HOMA-IR, insulin, or blood pressure between groups. In contrast, median fasting total cholesterol, triglycerides, and non-HDL cholesterol (mg/dL) were significantly higher in HIV⁺ group than in controls (172 vs 148, p = 0.002; 84 vs 50, p = 0.01; 134 vs 102, p <0.001; respectively). Median myeloperoxidase (pmoles/L) was higher in the HIV⁺ group (1299 vs 746, p = 0.01). Median HS-CRP (mg/L) was also higher in the HIV⁺ group but did not reach statistical significance (0.67 vs 0.43, p = 0.15). CCA IMT was similar in both groups, whereas ICA thickness (in mm) was increased in HIV⁺ group vs controls (median 0.50 [0.35 to 0.73] vs 0.45 [0.25 to 0.50], p = 0.038 for left ICA; and 0.50 [0.40 to 0.70] vs 0.45 [0.30 to 0.55], p = 0.08 for right ICA). IMT measurements correlated with body mass index, HOMA-IR, and myeloperoxidase.

Conclusions:  Higher cardiovascular markers and IMT were seen in ART-treated HIV⁺ children when compared with matched healthy controls. This suggests that HIV⁺ children may be at significant risk of premature atherosclerosis. Longitudinal follow-up is ongoing to determine whether rates of progression of carotid IMT is significantly higher in HIV⁺ children.