Protease inhibitor therapy in HIV-infected women was associated with significantly increased carotid intimal medial thickness compared to non-PI-treated patients (0.65 mm vs 0.61 mm; P<0.05).
Cross-Sectional (n=183)
No
Does protease inhibitor use increase carotid intimal medial thickness in HIV-infected women?
Protease inhibitor use in HIV-infected women is associated with increased carotid intimal medial thickness and a higher prevalence of metabolic syndrome, indicating a higher risk of subclinical atherosclerosis.
Absolute Event Rate: 0.65% vs 0.61%
p-value: p=<0.05
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.
Johnsen et al. (Tue,) conducted a cross-sectional in HIV infection (n=183). Protease inhibitor (PI) therapy vs. Non-PI-treated HIV patients was evaluated on Carotid intimal medial thickness (IMT) (p=<0.05). Protease inhibitor therapy in HIV-infected women was associated with significantly increased carotid intimal medial thickness compared to non-PI-treated patients (0.65 mm vs 0.61 mm; P<0.05).
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