HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study
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...
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2021
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oai:doaj.org-article:b6968ff26b8a430db404c836341132a12021-12-05T12:14:09ZHIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study10.1038/s41598-021-02556-w2045-2322https://doaj.org/article/b6968ff26b8a430db404c836341132a12021-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-02556-whttps://doaj.org/toc/2045-2322Abstract 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.Márton KolossváryDavid CelentanoGary GerstenblithDavid A. BluemkeRaul N. MandlerElliot K. FishmanSandeepan BhatiaShaoguang ChenShenghan LaiHong LaiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021) |
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Medicine R Science Q Márton Kolossváry David Celentano Gary Gerstenblith David A. Bluemke Raul N. Mandler Elliot K. Fishman Sandeepan Bhatia Shaoguang Chen Shenghan Lai Hong Lai HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
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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. |
format |
article |
author |
Márton Kolossváry David Celentano Gary Gerstenblith David A. Bluemke Raul N. Mandler Elliot K. Fishman Sandeepan Bhatia Shaoguang Chen Shenghan Lai Hong Lai |
author_facet |
Márton Kolossváry David Celentano Gary Gerstenblith David A. Bluemke Raul N. Mandler Elliot K. Fishman Sandeepan Bhatia Shaoguang Chen Shenghan Lai Hong Lai |
author_sort |
Márton Kolossváry |
title |
HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
title_short |
HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
title_full |
HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
title_fullStr |
HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
title_full_unstemmed |
HIV indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
title_sort |
hiv indirectly accelerates coronary artery disease by promoting the effects of risk factors: longitudinal observational study |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/b6968ff26b8a430db404c836341132a1 |
work_keys_str_mv |
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