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Session 154 Poster Abstracts
Atherosclerosis, Cardiovascular Risk and HIV Infection
Session Day and Time: Monday, 1-4 pm
Room: Hall B


952
Carotid Intima Media Thickness in HIV-infected Subjects and Community Controls
Marek Smieja*1, E Lonn1, F Smaill1, S Buracond1, S Smith1, S Anand1, K Gough2, J Gill3, S Trottier4, M Harris5, and The Canadian HIV Vascular Study Investigators
1McMaster Univ, Hamilton, Canada; 2St Michael`s Hosp, Toronto, Canada; 3Univ of Calgary, Canada; 4Univ Laval, Canada; and 5St Paul`s Hosp, Vancouver, Canada

 

 

 

 

Background:  Treatment greatly prolongs life expectancy of HIV-infected people, but causes lipid abnormalities that may predispose to cardiovascular disease. We measured carotid intima media thickness (IMT) to determine whether HIV-infected subjects had more subclinical vascular disease compared with population-based controls.

Methods:  This cross-sectional analysis of 594 subjects included 268 Caucasian HIV-infected subjects aged 35 years and older attending 5 academic HIV clinics in Canada; and compared them with 326 Caucasian population-based community controls from the Study of Health Assessment and Risk in Ethnic groups (SHARE). We used high-resolution B-mode ultrasonography to measure 12-segment mean maximal carotid IMT. Carotid IMT was read centrally by an experienced reader using dedicated computer software. Multiple linear regression was used to model the association between HIV status and carotid IMT, adjusting for Framingham risk factors.

Results:  HIV-infected adults had mean (SD) age of 46.9 (7.9) years, vs 51.3 (11.1) years for community controls (p <0.001), were more likely to smoke (37 vs 16%, p <0.001), and had higher total:HDL cholesterol ratios (5.3 vs. 4.7, p <0.001). Mean (SD) carotid IMT was 0.81 (0.23) and 0.77 (0.23), respectively, among HIV-infected subjects and controls. Carotid IMT was associated with HIV in unadjusted (b = 0.078, 95%CI 0.052 to 0.105, p <0.001) and covariate adjusted models (b = 0.069, 95%CI 0.045 to 0.092, p <0.001). HIV status was not significant after adjusting for exposure to the HIV drug stavudine, or to the drug class of protease inhibitors (b = –0.001, 95%CI –0.040 to 0.039, p = 0.39).

Conclusions:  HIV-infected subjects had a statistically significant and clinically important increase in carotid atherosclerosis compared with community controls, even after adjusting for cardiovascular risk factors. This risk is likely attributable to HIV medications, and not to HIV infection itself.