Background-HIV-infected patients may be at increased risk for coronary events. The purpose of this study was to identify predictors of carotid intima-media thickness (IMT) in HIV patients at baseline and to measure IMT progression over 1 year. Methods and Results-We measured blood lipids, inflammatory markers, and IMT in 148 HIV-infected adults (mean age, 45Ϯ8 years) and in 63 age-and sex-matched HIV-uninfected control subjects. The mean duration of HIV infection was 11 years, and the median duration of protease inhibitor treatment was 3.3 years. Mean baseline IMT was 0.91Ϯ0.33 mm in HIV patients and 0.74Ϯ0.17 mm in control subjects (Pϭ0.0001). Multivariable predictors of baseline IMT in HIV patients were age (PϽ0.001), LDL cholesterol (PϽ0.001), cigarette pack-years (Pϭ0.005), Latino race (Pϭ0.062), and hypertension (Pϭ0.074). When the control group was added to the analysis, HIV infection was an independent predictor of IMT (Pϭ0.001). The rate of progression among the 121 HIV patients with a repeated IMT measurement at 1 year was 0.074Ϯ0.13 mm, compared with Ϫ0.006Ϯ0.05 mm in 27 control subjects (Pϭ0.002). Age (PϽ0.001), Latino race (Pϭ0.02), and nadir CD4 count Յ200 (Pϭ0.082) were multivariable predictors of IMT progression. Conclusions-Carotid IMT is higher in HIV patients than in age-matched control subjects and progresses much more rapidly than previously reported rates in non-HIV cohorts. In HIV patients, carotid IMT is associated with classic coronary risk factors and with nadir CD4 count Յ200, suggesting that immunodeficiency and traditional coronary risk factors may contribute to atherosclerosis.

HIV-infected subjects had thicker carotid IMT compared to controls. While HIV patients also had higher T-cell activation, hs-CRP levels, and CMV-specific T-cell responses, only CMV-specific T-cell responses were independently associated with IMT. Accelerated atherosclerosis in HIV patients may be mediated by heightened CMV-induced immune responses.