Background:  Inflammation and hemostasis perturbation may be involved in vascular complications of HIV infection. We examined atherogenic biomarkers and subclinical atherosclerosis in HIV⁺ adults before and after beginning HAART.

Methods:  In the Women’s Interagency HIV Study (WIHS), 127 HIV⁺ women studied pre- and post-HAART were propensity score-matched to HIV^– controls. We obtained 6 semi-annual measurements of soluble CD14, tumor necrosis factor (TNF)-a, soluble interleukin (IL)-2 receptor, IL-6, IL-10, monocyte chemoattractant protein (MCP)-1, D-dimer, and fibrinogen. Carotid artery intima-media thickness (cIMT) was measured by B-mode ultrasound.

Results:  Relative to HIV^– controls, HAART-naïve HIV⁺ women had elevated levels of soluble CD14 (1945 vs 1662 ng/mL, Wilcoxon signed rank p <0.0001), TNF-a (6.3 vs 3.4 pg/mL, p <0.0001), soluble IL-2 receptor (1587 vs 949 pg/mL, p <0.0001), IL-10 (3.3 vs 1.9 pg/mL, p <0.0001), MCP-1 (190 vs 163 pg/mL, p <0.0001), and D-dimer (0.43 vs 0.31 µg/mL, p <0.01). Elevated biomarker levels declined after HAART. While most biomarkers normalized to HIV-uninfected levels, in women on effective HAART, TNF-a levels remained elevated compared to HIV^– women (+0.8 pg/mL, p = 0.0002). Higher post-HAART levels of soluble IL-2 receptor (p = 0.02), IL-6 (p = 0.05), and D-dimer (p = 0.03) were associated with increased cIMT.

Conclusions:  Untreated HIV infection is associated with abnormal hemostasis (e.g., D-dimer), and pro-atherogenic (e.g., TNF-a) and anti-atherogenic (e.g., IL-10) inflammatory markers. HAART reduces most inflammatory mediators to levels found in HIV^– women. Increased inflammation and hemostasis are associated with subclinical atherosclerosis in recently treated women. These findings have potential implications for long-term risk of cardiovascular disease in HIV⁺ patients, even with effective therapy.