Cardiovascular risk factors and illicit drug use may have a more profound effect on coronary atherosclerosis progression in people living with HIV

Objectives: To assess whether HIV infection directly or indirectly promotes coronary artery disease (CAD) volume progression in a longitudinal study of African Americans. Methods: We randomly selected 300 individuals with subclinical CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV infected, 174 cocaine users) from 1429 cardiovascularly asymptomatic participants of a prospective epidemiological study between May 2004 and August 2015. Individuals underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years). We quantified noncalcified (NCP: −100–350HU), low-attenuation noncalcified (LA-NCP: −100-30HU), and calcified (CP: ≥ 351 HU) plaque volumes. Linear mixed models were used to assess the effects of HIV infection, atherosclerotic cardiovascular disease (ASCVD) risk, and years of cocaine use on plaque volumes. Results: There was no significant difference in annual progression rates between HIV-infected and HIV-uninfected regarding NCP (8.7 [IQR: 3.0–19.4] mm³/year vs. 4.9 [IQR: 1.5–18.3] mm³/year, p = 0.14), LA-NCP (0.2 [IQR: 0.0–1.6] mm³/year vs. 0.2 [IQR: 0.0–0.9] mm³/year, p = 0.07) or CP volumes (0.3 [IQR: 0.0–3.4] mm³/year vs. 0.1 [IQR: 0.0–3.2] mm³/year, p = 0.30). Multivariately, HIV infection was not associated with NCP (−6.9mm³, CI: [−32.8–19.0], p = 0.60), LA-NCP (−0.1mm³, CI: [−2.6–2.4], p = 0.92), or CP volumes (−0.3mm³, CI: [−9.3–8.6], p = 0.96). However, each percentage of ASCVD and each year of cocaine use significantly increased total, NCP, and CP volumes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-associated medications had any effect on plaque volumes (p > 0.05 for all). Conclusions: The more profound adverse effect of risk factors in HIV-infected individuals may explain the accelerated progression of CAD in these people, as HIV infection was not independently associated with any coronary plaque volume. Key Points: • Human immunodeficiency virus–infected individuals may have similar subclinical coronary artery disease, as the infection is not independently associated with coronary plaque volumes. • However, cardiovascular risk factors and illicit drug use may have a more profound effect on atherosclerosis progression in those with human immunodeficiency virus infection, which may explain the accelerated progression of CAD in these people. • Nevertheless, through rigorous prevention and abstinence from illicit drugs, these individuals may experience similar cardiovascular outcomes as -uninfected individuals.