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HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal
Márton Kolossváry1,2, David Celentano3, Gary Gerstenblith4
1Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Pathology #301, Baltimore, MD, 21287, USA.
Insights
Human immunodeficiency virus (HIV) infection does not directly worsen coronary artery disease (CAD) progression. However, traditional risk factors may accelerate CAD more significantly in HIV-infected individuals.
Area of Science:
- Cardiology
- Infectious Diseases
- Epidemiology
Background:
- Coronary artery disease (CAD) is a significant concern, and its progression in human immunodeficiency virus (HIV)-infected individuals requires careful evaluation.
- Understanding the direct and indirect effects of HIV on CAD is crucial for patient management and risk stratification.
Purpose of the Study:
- To determine if HIV infection directly or indirectly accelerates the clinical progression of coronary artery disease (CAD).
- To investigate the association between HIV status, traditional cardiovascular risk factors, and CAD progression markers.
Main Methods:
- A prospective epidemiological study included 300 African Americans with asymptomatic CAD (226 HIV-infected).
- Coronary CT angiography was performed at two time points to assess Agatston scores, plaque counts, and segment stenosis score (SSS).
- Linear mixed models analyzed the impact of HIV infection, ASCVD risk, and cocaine use on CAD progression.
Main Results:
- No significant differences in annual progression rates of Agatston scores, plaque counts, or SSS were observed between HIV-infected and HIV-uninfected groups.
- Multivariate analysis showed HIV infection was not directly associated with CAD outcomes.
- ASCVD risk scores and cocaine use duration significantly increased CAD progression in HIV-infected individuals, but not in HIV-uninfected individuals.
Conclusions:
- HIV infection is not directly linked to accelerated coronary artery disease progression.
- Traditional risk factors, such as ASCVD risk and cocaine use, play a more significant role in accelerating CAD in HIV-infected patients.
- HIV-infected individuals are not inherently destined for worse CAD profiles, highlighting the importance of managing conventional risk factors.
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.
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