Association between human immunodeficiency virus infection and stiffness of the common carotid artery.

BACKGROUND AND PURPOSE Individuals with human immunodeficiency virus (HIV) who use highly active antiretroviral therapy (HAART) may have an increased risk for cardiovascular-related events, although the underlying mechanism remains unclear. We tested the hypothesis that carotid arterial stiffness was higher among persons using HAART compared to HAART-naïve and HIV-uninfected persons. METHODS Between 2004 and 2006, we performed high-resolution B-mode ultrasound on 2789 HIV-infected and HIV-uninfected participants of the Women's Interagency HIV Study (1865 women) and the Multicenter AIDS Cohort Study (924 men) and determined carotid arterial distensibility, which is a direct measure of carotid arterial stiffness. We used generalized estimating equations to evaluate the association between distensibility and HIV infection, CD4(+) cell count, and exposure to HAART adjusted for demographic, behavioral, and clinical characteristics. RESULTS In multivariable analysis, distensibility was 4.3% lower (95% confidence interval, -7.4% to -1.1%) among HIV-infected vs uninfected participants. Among HIV-infected participants with <200 CD4(+) cells, distensibility was 10.5% lower (95% confidence interval, -14.5% to -6.2%) than that among HIV-uninfected participants, and this effect did not differ significantly by cohort or race. Concurrent HAART use was independently associated with lower distensibility among Multicenter AIDS Cohort Study participants but not among Women's Interagency HIV Study participants. CONCLUSIONS Our finding that advanced HIV-related immunosuppression was associated with increased carotid arterial stiffness independent from the effects of traditional atherosclerosis risk factors suggests that the etiologic mechanism underlying reports of an increased cardiovascular disease risk among HIV-infected individuals might involve HIV-related immunosuppression leading to vascular dysfunction and arterial stiffening.