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HIV May Accelerate Coronary Artery Disease Progression Through Promoting the Adverse Effects of Conventional Cardiovascular Risk Factors and Illicit Drugs

Background: Only the independent effect of human immunodeficiency virus (HIV)-infection on coronary artery disease (CAD) has been investigated in cross-section studies, while rather than directly, HIV-infection may accelerate CAD through promoting the effects of risk factors. Furthermore, there is no information on the potential effects of HIV-infection on coronary plaque volumes. Therefore, we investigated whether HIV-infection directly or indirectly promotes clinical and volumetric characteristics of CAD in a observational longitudinal study. 
 
Methods: 300 individuals without cardiovascular symptoms (210 male; age: 48·0±7·2 years; 226 HIV-infected) underwent coronary CT angiography at two time points (mean follow-up: 4·0±2·3 years). We quantified Agatston-score, number of coronary plaques, segment stenosis score, and also segmented the coronary plaques to enumerate total, noncalcified (-100–350HU) and calcified (≥351HU) plaque volumes. Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use and high-sensitivity C-reactive protein on CT markers of CAD. 
 
Findings: There was no significant difference in annual progression rates between HIV-infected and -uninfected (p>0·05 for all). Multivariately, HIV-infection was not associated with any CAD parameter (p>0·05 for all). However, among HIV-infected individuals, each year of cocaine use significantly increased all CAD parameters (p<0·05 for all), while ASCVD risk score was significantly associated with CAD parameters except for Agatston-score (p<0·05). However, these associations were only apparent among HIV-infected individuals. Importantly, none of the HIV-medications were associated with any of the CAD outcomes. 
 
Interpretation: HIV-infection is not directly associated with CAD and therefore HIV-infected are not destined to have worse CAD profiles as compared to uninfected individuals. However, more aggressive management of conventional cardiovascular risk factors and abstinence from illicit drugs may be needed to achieve similar CAD status. 
 
Funding Statement: Procedures and tests were funded by the National Institute on Drug Abuse, and the National Institutes of Health (NIH R01DA12777, R01DA15020, R01DA25524, R21DA048780 and U01DA040325). 
 
Declaration of Interests: None. 
 
Ethics Approval Statement: The Committee on Human Research at the Johns Hopkins School of Medicine (Baltimore, MD) approved the study protocol, and all study participants provided written informed consent. All procedures used in this study were in accordance with HIPAA, local and federal regulations, and the Declaration of Helsinki.