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


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
30 11 2021
Historique:
received: 19 05 2021
accepted: 15 11 2021
entrez: 1 12 2021
pubmed: 2 12 2021
medline: 15 2 2022
Statut: epublish

Résumé

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.

Identifiants

pubmed: 34848791
doi: 10.1038/s41598-021-02556-w
pii: 10.1038/s41598-021-02556-w
pmc: PMC8632934
doi:

Substances chimiques

Cocaine I5Y540LHVR

Types de publication

Journal Article Observational Study Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

23110

Subventions

Organisme : NIDA NIH HHS
ID : R21 DA048780
Pays : United States
Organisme : NIDA NIH HHS
ID : U01 DA040325
Pays : United States

Informations de copyright

© 2021. The Author(s).

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Auteurs

Márton Kolossváry (M)

Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Pathology #301, Baltimore, MD, 21287, USA.
MTA-SE Cardiovascular Imaging Research Group, Heart and Vascular Center, Semmelweis University, 68 Városmajor str., Budapest, Hungary, 1122.

David Celentano (D)

Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, 614 Wolfe N Wolfe St, Baltimore, MD, 21205, USA.

Gary Gerstenblith (G)

Department of Medicine, Johns Hopkins University School of Medicine, 733 N Broadway, Baltimore, MD, 21205, USA.

David A Bluemke (DA)

School of Medicine and Public Health, University of Wisconsin, 750 Highland Ave, Madison, WI, 53726, USA.

Raul N Mandler (RN)

National Institute on Drug Abuse, National Institutes of Health, 10 Center Dr, Bethesda, MD, 20814, USA.

Elliot K Fishman (EK)

Department of Radiology, Johns Hopkins University School of Medicine, 601 N Caroline St, Baltimore, MD, 21205, USA.

Sandeepan Bhatia (S)

Institute of Human Virology, University of Maryland School of Medicine, 725 W Lombard St, Baltimore, MD, 21201, USA.

Shaoguang Chen (S)

Institute of Human Virology, University of Maryland School of Medicine, 725 W Lombard St, Baltimore, MD, 21201, USA.

Shenghan Lai (S)

Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Pathology #301, Baltimore, MD, 21287, USA. slai@jhmi.edu.
Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, 614 Wolfe N Wolfe St, Baltimore, MD, 21205, USA. slai@jhmi.edu.
Department of Medicine, Johns Hopkins University School of Medicine, 733 N Broadway, Baltimore, MD, 21205, USA. slai@jhmi.edu.
Department of Radiology, Johns Hopkins University School of Medicine, 601 N Caroline St, Baltimore, MD, 21205, USA. slai@jhmi.edu.
Institute of Human Virology, University of Maryland School of Medicine, 725 W Lombard St, Baltimore, MD, 21201, USA. slai@jhmi.edu.

Hong Lai (H)

Department of Radiology, Johns Hopkins University School of Medicine, 601 N Caroline St, Baltimore, MD, 21205, USA.
Institute of Human Virology, University of Maryland School of Medicine, 725 W Lombard St, Baltimore, MD, 21201, USA.

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