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Carotid Intimal Medial Thickness in Human Immunodeficiency Virus-Infected Women: Effects of Protease Inhibitor Use, Cardiac Risk Factors, and the Metabolic Syndrome

Program in Nutritional Metabolism (S.J., S.E.D., K.V.F., J.R.K., S.G.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114; Massachusetts General Hospital Biostatistical Center (H.L.), Boston Heart Foundation (L.C.H., J.M.C., R.S.L.), Massachusetts General Hospital, Boston, Massachusetts 02114; and Department of Infectious Diseases (S.J.), Skejby Hospital, DK-8200 Aarhus, Denmark

Address all correspondence and requests for reprints to: Steven Grinspoon, M.D., Program in Nutritional Metabolism, Massachusetts General Hospital, Boston, Massachusetts 02114. E-mail: Sgrinspoon{at}partners.org.

Context: Little is known regarding carotid intimal medial thickness (IMT) in HIV-infected women and the risk factors for subclinical atherosclerosis in this population, including antiretroviral therapy and the metabolic syndrome.

Objective: Our objective was to assess carotid IMT in relationship to HIV status and antiretroviral therapy in HIV-infected women in comparison with healthy age- and body mass index (BMI)-matched control subjects.

Setting and Subjects: The study took place at an academic medical center and included 97 HIV-infected women compared with 86 age- and BMI-matched healthy control subjects.

Main Outcome Measures: We assessed carotid IMT, metabolic syndrome, and risk factors for increased IMT.

Results: Carotid IMT was not increased in HIV-infected women [0.62 mm (0.57–0.68); median (IQR)] compared with non-HIV-infected women [0.61 mm (0.55–0.68)] matched for age and BMI (P = 0.07) but was increased significantly among HIV patients receiving a protease inhibitor (PI) [0.65 (0.59–0.71) mm] vs. non-PI-treated patients [0.61 (0.57–0.66) mm] (P < 0.05) and vs. control subjects [0.61 (0.55–0.68) mm] (P < 0.05). The prevalence of metabolic syndrome was significantly increased among the HIV-infected women compared with control subjects and particularly in PI- vs. non-PI-treated HIV patients (45 vs. 19%, P = 0.001). Metabolic syndrome score correlated with IMT among non-HIV patients but not among the HIV group. Individual risk factors most strongly associated with IMT in multivariate regression modeling in the control group were age and waist-to-hip ratio, and among the HIV group age and waist circumference.

Conclusions: These data demonstrate increased carotid IMT in HIV-infected women receiving PI therapy, which may be due to associated metabolic abnormalities related to PI therapy or more direct effects of this medication class on the vasculature. Additional studies of the mechanisms by which PI uses results in subclinical atherosclerosis are needed.

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