Background: Coronary artery calcium (CAC) score has been shown to predict incident coronary heart disease (CHD). Studies in the general population have linked inflammatory mediators including monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-α with burden of coronary atherosclerosis but this relationship is often lost following correction for traditional cardiovascular (CVD) risk factors.

Methods: Cross-sectional study comparing baseline data from Hawaii Aging with HIV Cardiovascular Study (HAHCS) with the Multi-Ethnic Study of Atherosclerosis (MESA) cohort. HAHCS is a longitudinal single-center study of the role of oxidative stress and inflammation in HIV CHD risk. HIV⁺ participants were aged >40 years and on stable ART >6 months. MESA is a prospective multi-center cohort study investigating the prevalence, correlates, and progression of subclinical CHD. HIV^– controls were derived from MESA. CHD risk profiles including the Framingham Risk Score (FRS), clinical profile, lipid panel, and CAC score were assessed in all participants. Multivariable regression models compared CAC prevalence in HIV and MESA controls. Plasma biomarker multiplexing was performed on HAHSCS subjects by Milliplex Human Cardiovascular Disease panels (EMD Millipore).

Results: Study compared 125 participants from HAHCS (mean age 54.0 years, 87% male, body mass index [BMI] 26.6, 64% current or former smokers, 9% with diabetes, 26% anti-hypertensive therapy [AHT], 87% HIV RNA <50 copies) with 5795 participants from MESA (mean age 59.5 years, 38% male, BMI 28.5, 51% current or former smokers, 12% with diabetes, 35% AHT). 57% HAHCS and 45% MESA had a positive CAC score. Among participants with a positive CAC, the mean CAC was 266.9 in HAHCS and 244.5 in MESA. Using relative risk (RR) regression, participants with HIV were predicted to be at greater risk (relative risk [RR] = 1.24, p <0.01) of having a positive CAC score than controls, adjusted for age, gender, race, and CVD risk factors. In the HAHCS group, univariate logistic regression models revealed that MCP-1, TNF-α, and vascular endothelial growth factor (VEGF) was associated with the presence of CAC at p <0.10. In multivariate logistic regression models, MCP-1 (odds ratio [OR] = 1.01, p = 0.02) and TNF-α (OR = 1.19, p = 0.04) each remained significantly associated with the presence of CAC after adjustments for age and FRS.

Conclusions: HIV was independently associated with a positive CAC score. Higher MCP-1 and TNF-α predict the presence of CAC independent of traditional CVD risk factors in HIV⁺ subjects on ART.