HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study

Márton Kolossváry,Elliot K Fishman,Raul N Mandler,Hong Lai,Shaoguang Chen,Gary Gerstenblith,David Celentano,Shenghan Lai,Sandeepan Bhatia,David A Bluemke

doi:10.1038/s41598-021-02556-w

Abstract

Our objective was to assess whether human immunodeficiency virus (HIV)-infection directly or indirectly promotes the progression of clinical characteristics of coronary artery disease (CAD). 300 African Americans with asymptomatic CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV-infected) who underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years) were randomly selected from 1429 participants of a prospective epidemiological study between May 2004 and August 2015. We calculated Agatston-scores, number of coronary plaques and segment stenosis score (SSS). Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use on CAD. There was no significant difference in annual progression rates between HIV-infected and—uninfected regarding Agatston-scores (10.8 ± 25.1/year vs. 7.2 ± 17.8/year, p = 0.17), the number of plaques (0.2 ± 0.3/year vs. 0.3 ± 0.5/year, p = 0.11) or SSS (0.5 ± 0.8/year vs. 0.5 ± 1.3/year, p = 0.96). Multivariately, HIV-infection was not associated with Agatston-scores (8.3, CI: [− 37.2–53.7], p = 0.72), the number of coronary plaques (− 0.1, CI: [− 0.5–0.4], p = 0.73) or SSS (− 0.1, CI: [− 1.0–0.8], p = 0.84). ASCVD risk scores and years of cocaine-use significantly increased all CAD outcomes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-medications were associated with any of the CAD outcomes. HIV-infection is not directly associated with CAD and therefore HIV-infected are not destined to have worse CAD profiles. However, HIV-infection may indirectly promote CAD progression as risk factors may have a more prominent role in the acceleration of CAD in these patients.

Highlights

Our objective was to assess whether human immunodeficiency virus (HIV)-infection directly or indirectly promotes the progression of clinical characteristics of coronary artery disease (CAD). 300 African Americans with asymptomatic CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV-infected) who underwent coronary CT angiography at two time points were randomly selected from 1429 participants of a prospective epidemiological study between May 2004 and August 2015
The demographic and clinical characteristics of all participants and HIV‐related clinical factors of HIV‐infected participants are presented in Table 1.Of the 300 participants, 210 (70.0%) were men and the mean age was 48.0 ± 7.2 years and 226 (75.3%) were infected with HIV at baseline, among HIV-infected, the mean CD4 count and log viral load were 446 ± 283 cell/mm[3] and 2.4 ± 1.1 copies/mL, respectively
Detailed results are in supplemental Table 4. The findings of this investigation show that (1) overall, HIV-infection was not independently associated with changes in any CAD markers among the total study population, and (2) duration of cocaine use was significantly associated with increased coronary Agatston-scores, number of coronary plaques and stenosis score (SSS)

Summary

Introduction

Our objective was to assess whether human immunodeficiency virus (HIV)-infection directly or indirectly promotes the progression of clinical characteristics of coronary artery disease (CAD). 300 African Americans with asymptomatic CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV-infected) who underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years) were randomly selected from 1429 participants of a prospective epidemiological study between May 2004 and August 2015. Our objective was to assess whether human immunodeficiency virus (HIV)-infection directly or indirectly promotes the progression of clinical characteristics of coronary artery disease (CAD). While data on hard end-points (myocardial infarction and death) show clear associations with HIV-infection, information regarding sub-clinical stages of CAD are c ontradictory[3,4,5,6]. It is unclear whether discrepancies of previous results are due to the cross-sectional study design, or whether there may be other factors which promote CAD in PLWH, which were less investigated, such as illegal substance use. It is the number of plaques, but the extent of CAD and the degree of stenosis, which are important and which can be summarized by the segment stenosis score (SSS)[15]

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Results

Conclusion