Human immunodeficiency virus (HIV)-positive patients are at increased risk of accelerated atherosclerosis and cardiovascular disease (CVD) progression. However, it remains unclear whether this is the result of antiretroviral therapy, CVD risk factors, viral infection, systemic inflammation, or a combination of these elements. This study evaluated the effects of untreated HIV on carotid intimal-medial thickening (cIMT) and serum levels of selected inflammatory markers (IMs), known measures of CVD progression.
A cross-sectional case-control study was performed in HIV-infected long-term nonprogressors (LTNPs), with a HIV-negative control group matched by age, race, and sex. Clinical data, lipid profile, CD4 cell counts, HIV-1 RNA levels, cIMT at 3 different locations, and serum levels of different IMs were recorded. Cardiovascular disease risk factors, cIMT, and IMs were statistically compared between the LTNP and HIV-negative groups.
Thirty-two subjects were enrolled (16 LTNP and 16 controls), and no significant difference in CVD risk factors was found. There was significantly increased cIMT at the carotid bulb for the LTNP group (P < 0.005). CD4 count, HIV-1 RNA levels, and duration of HIV infection were not significantly associated with cIMT. The only IM significantly higher in LTNPs was soluble tumor necrosis factor II (P = 0.002). Soluble vascular adhesion molecule-1 significantly correlated with bulb cIMT (r = 0.66; P = 0.014).
For the LTNPs, cIMT at the bulb and serum levels of soluble tumor necrosis factor II were significantly greater than the controls, and soluble vascular adhesion molecule-1 significantly correlated with bulb cIMT. This study emphasizes the role of viremia in promoting CVD among HIV-positive patients, likely through inducing systemic inflammation.