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, 45+/-8 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 0.91+/-0.33 mm in HIV patients and 0.74+/-0.17 mm in control subjects (P=0.0001). Multivariable predictors of baseline IMT in HIV patients were age (P<0.001), LDL cholesterol (P<0.001), cigarette pack-years (P=0.005), Latino race (P=0.062), and hypertension (P=0.074). When the control group was added to the analysis, HIV infection was an independent predictor of IMT (P=0.001). The rate of progression among the 121 HIV patients with a repeated IMT measurement at 1 year was 0.074+/-0.13 mm, compared with -0.006+/-0.05 mm in 27 control subjects (P=0.002). Age (P<0.001), Latino race (P=0.02), and nadir CD4 count < or =200 (P=0.082) 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 < or =200, suggesting that immunodeficiency and traditional coronary risk factors may contribute to atherosclerosis.
BACKGROUND:HIV-infectedpatients may be at increased risk for coronary events. The purpose of this study was to identify predictors of carotid intima-media thickness (IMT) in HIVpatients 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, 45+/-8 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 0.91+/-0.33 mm in HIVpatients and 0.74+/-0.17 mm in control subjects (P=0.0001). Multivariable predictors of baseline IMT in HIVpatients were age (P<0.001), LDL cholesterol (P<0.001), cigarette pack-years (P=0.005), Latino race (P=0.062), and hypertension (P=0.074). When the control group was added to the analysis, HIV infection was an independent predictor of IMT (P=0.001). The rate of progression among the 121 HIVpatients with a repeated IMT measurement at 1 year was 0.074+/-0.13 mm, compared with -0.006+/-0.05 mm in 27 control subjects (P=0.002). Age (P<0.001), Latino race (P=0.02), and nadir CD4 count < or =200 (P=0.082) were multivariable predictors of IMT progression. CONCLUSIONS: Carotid IMT is higher in HIVpatients than in age-matched control subjects and progresses much more rapidly than previously reported rates in non-HIV cohorts. In HIVpatients, carotid IMT is associated with classic coronary risk factors and with nadir CD4 count < or =200, suggesting that immunodeficiency and traditional coronary risk factors may contribute to atherosclerosis.
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