Background:  Recent studies suggest that HIV-infected patients are at increased risk for cardiovascular disease. It remains unclear whether this is because of HIV infection itself, its treatment, or an excess of traditional cardiovascular risk factors. Recently, detection of coronary artery calcium (CAC) by computerized tomography (CT scan) in HIV-uninfected persons has been shown to be a strong predictor of coronary artery disease independent of traditional risk factors. We used this approach to investigate the role of HIV infection in coronary artery disease.

Methods:  We measured CAC using a 16-detector Philips CT scanner in 247 HIV-infected participants from the University of California–San Francisco SCOPE cohort and 45 HIV-uninfected adults. No subjects had symptoms of active coronary artery disease. CAC scoring was determined using the modified Agatston method. The independent role of HIV infection per se, HIV-related disease factors, and other traditional cardiovascular risk factors in influencing CAC was determined by multivariable regression. 

Results:  The median age was 49 years (IQR 43 to 54) for the HIV-infected subjects and 48 years (IQR 43 to 54) for the uninfected; 91% of the HIV-infected and 78% of the uninfected were men. The median duration of HIV infection was 16 years (IQR 11 to 19), and the median CD4 cell nadir was 174 (IQR 41 to 330); 73% were on HAART (median duration of 6.8 years). Among the HIV-infected, 38% had detectable CAC vs 29% of the uninfected (p = 0.022); 16% of the HIV-infected had a calcium score >100 compared to 4% of controls (p = 0.039). After adjusting for age, gender, race, smoking, hypertension, and diabetes mellitus, the HIV-infected subjects had a significantly higher prevalence of detectable CAC (OR = 2.7, 95%CI 1.06 to 6.7, p = 0.037). A similar effect was observed when restricting the HIV-infected to subjects who had never used HAART (OR 3.3, 95%CI 0.77 to 13.9; p = 0.11). Among HIV-infected subjects, neither duration of HAART or PI therapy, nor proportion of time with a detectable HIV RNA level was associated with the presence of detectable CAC. Among the HIV-infected, only age, gender, and race were associated with detectable CAC.

Conclusions:  HIV infection is independently associated with a higher prevalence of CAC and, thus, subclinical coronary artery disease. This effect was observed even among those who had never received ART, arguing for a treatment-independent effect of HIV infection.