Background:  HIV⁺ patients are at increased risk of cardiovascular disease (CVD). Chronic inflammation and endothelial dysfunction may play a key role. Carotid intima media thickness (IMT) is an established marker for subclinical atherosclerosis. We assessed inflammatory markers and endothelial activation in HIV, and their relationship to carotid IMT.

Methods:  We enrolled 62 HIV⁺ patients and 32 HIV^– healthy controls. We measured carotid IMT and reported internal carotid artery (ICA) and common carotid artery (CCA) thickness for both left and right sides. We measured fasting lipids, insulin, tumor necrosis factor (TNF) -a, soluble TNF receptors (sTNFRI and II), interleukin (IL) -6, high sensitivity C-reactive protein (hsCRP), the established CVD marker myeloperoxidase (MPO); as well as 3 endothelial markers:  soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and von Willebrand factor (vWF). Wilcoxon rank sum tests and Spearman Rank correlation coefficients were used.

Results:  Of the patients, 40% were white and 60% male. Median age and body mass index were higher in the HIV⁺ group (age 44 vs 38 years, p = 0.03; body mass index 26 vs 25 kg/m², p = 0.02). Triglycerides (TG) and insulin were higher and HDL cholesterol (CHOL) lower in the HIV⁺ group (all p <0.0001). All carotid IMT measurements were higher in the HIV⁺ vs HIV^– group (ICA p £0.02; CCA p £0.04). MPO, hsCRP, sICAM-1, IL-6, and TNF-a were higher in the HIV⁺ than the HIV^– group (MPO 54.6 vs 37.9 pg/mL, p = 0.005; hsCRP 56.5 vs 34.6 pg/mL, p <0.001; sICAM-1 53 vs 40.7 pg/mL, p = 0.037; IL-6 51.6 vs 39.9 pg/mL, p = 0.048; TNF-a 51.9 vs 41.1 pg/mL, p = 0.58); sTNFRI, vWF, and sVCAM-1 were similar between the groups; sTNFRII was higher in the HIV^– group (58.4 vs 42.8 pg/mL, p = 0.008). In the HIV⁺ group, R CCA positively correlated with TNF-a (p = 0.02) and IL-6 (p = 0.02). In the HIV^– group, both R and L CCA positively correlated with TNF-a (p £0.015) and R CCA with hsCRP (p = 0.03). None of the endothelial markers correlated with IMT in either group. In both groups, sVCAM-1 correlated with sTNFRII (p <0.001) and MPO (p <0.001); both sICAM-1 and vWF correlated with IL-6 and hsCRP (sVCAM-1/hsCRP, p<0.001). TG and total (but not HDL) CHOL correlated with IMT measurements in both groups, while insulin did not.

Conclusions: This study shows enhanced endothelial activation, increased inflammatory cytokines, and higher IMT in HIV⁺ patients. Inflammation markers correlated with carotid IMT and with endothelial activation, which support a role for inflammation in endothelial activation and CVD in HIV.