Protease inhibitor exposure and HIV infection were not associated with increased carotid intima-media thickness (median 0.690 mm for PI users vs 0.712 mm for PI-naive and 0.698 mm for uninfected).
Cohort (n=134)
Yes
Does protease inhibitor exposure or HIV infection increase carotid artery intima-media thickness compared to unexposed or uninfected matched subjects?
Traditional cardiovascular risk factors, rather than HIV infection or protease inhibitor exposure, are the primary predictors of subclinical atherosclerosis as measured by carotid intima-media thickness.
Absolute Event Rate: 0.69% vs 0.712%
CONTEXT: The impact of HIV infection and exposure to antiretroviral therapy on the development of subclinical atherosclerosis is incompletely understood. OBJECTIVE: To compare intima-media thickness (IMT) of the carotid artery between HIV-infected subjects receiving protease inhibitor-containing regimens and subjects not receiving these regimens and to compare differences in the IMT of the carotid artery between HIV-infected subjects and HIV-uninfected subjects. METHODS: A prospective matched cohort study in university-based outpatient clinics. Groups of three individuals (triads) matched on the following characteristics were enrolled: age, sex, race/ethnicity, smoking status, blood pressure and menopausal status. Group 1, HIV-infected subjects with continuous use of protease inhibitor (PI) therapy for > or = 2 years; group 2, HIV-infected subjects without prior PI use; and group 3: HIV-uninfected. Ultrasonographers at six sites sent standardized ultrasound images to a central reading site for carotid IMT measurements. Carotid IMT was compared within the HIV-infected groups (1 and 2) and between the HIV-infected and uninfected groups in a matched analysis. RESULTS: One hundred and thirty-four individuals were enrolled in 45 triads. The median IMT in groups 1, 2 and 3 was 0.690, 0.712 and 0.698 mm, respectively. There were no statistically significant differences in IMT between groups 1 and 2, or in the combined HIV groups compared with the HIV uninfected group. Significant predictors of carotid IMT in a multivariate model included high-density lipoprotein (HDL) cholesterol, the interaction of HDL cholesterol and triglycerides, age and body mass index. CONCLUSIONS: We found no association between PI inhibitor exposure or HIV infection and carotid IMT.
Currier et al. (Thu,) conducted a cohort in HIV infection (n=134). Protease inhibitor (PI) therapy vs. HIV-infected without prior PI use and HIV-uninfected subjects was evaluated on Intima-media thickness (IMT) of the carotid artery. Protease inhibitor exposure and HIV infection were not associated with increased carotid intima-media thickness (median 0.690 mm for PI users vs 0.712 mm for PI-naive and 0.698 mm for uninfected).