Abstract 28: HIV Infection Is Associated With Greater Risk of Carotid Artery Lesions Over Seven Years

Abstract

Background: We previously found that low CD4+ T-cell counts among HIV-infected (HIV+) women and men were associated with an increased prevalence of carotid artery lesions in a cross-sectional analysis. We now report on the association of HIV infection with progression of subclinical atherosclerosis in the same well-characterized population of HIV+ and HIV-uninfected (HIV-) women and men. We hypothesized that HIV infection would be associated with greater progression over seven years of follow-up. Methods: We examined data from a subset of participants without a history of coronary heart disease in the Women’s Interagency HIV Study (WIHS) and Multicenter AIDS Cohort Study (MACS) who underwent serial B-mode carotid artery ultrasound imaging between 2004 and 2012 (median follow-up: 7 years). We included individuals with at least two examinations during this period, with a median of 4 exams among women and 3 exams among men. We evaluated changes in common carotid artery intima-media thickness (cIMT, mm) and the development of carotid artery lesions (focal IMT >1.5 mm), defined as an increased number of lesions over the time period, based on regression models with generalized estimated equations to take into account clustering by individual, controlling for demographic factors and smoking status. Models combining women and men, as well as stratified by cohort, are presented. Results: We studied 1011 women (74% HIV+) and 811 men (65% HIV+). The median age was 41 years (IQR 35-47) in women and 49 (IQR 44-55) in men. The unadjusted mean cIMT increased during the period from 0.725 to 0.752 mm in women and from 0.757 to 0.790 mm in men. The prevalence of carotid artery lesions increased from 8% to 15% in women and from 25% to 34% in men during follow-up. In analyses controlling for sex, age, race/ethnicity, study site, and smoking status, progression of carotid artery lesions differed by HIV serostatus. HIV+ persons had a 1.9-fold higher adjusted risk of developing lesions during the follow-up period than HIV- persons (17% with increase in lesions among HIV+ vs. 10% in HIV-; 95% CI 1.29-2.72, p=0.001). This association persisted in models stratified by cohort (in women, adjusted relative risk 1.66, 95% CI 0.96-2.89, p=0.07; in men, 1.92, 95% CI 1.14-3.11, p=0.01), with no evidence of effect modification by cohort (p=0.58). We did not find significant differences in cIMT change over time by HIV serostatus, either in combined or cohort-specific analyses. Conclusion: HIV infection was associated with a greater increase in carotid artery lesions over a seven-year period in both women and men. HIV appears to play a role in focal cIMT thickening in atherosclerosis-prone carotid artery segments, but not a generalized increase in wall thickness in the common carotid artery.