Márton Kolossváry1,2, Elliot K Fishman3, Gary Gerstenblith4, David A Bluemke5, Raul N Mandler6, David Celentano7, Thomas S Kickler1, Sarah Bazr1, Shaoguang Chen1,8, Shenghan Lai9,10,11,12,13,14, Hong Lai3,8,15. 1. Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD, 21287, USA. 2. MTA-SE Cardiovascular Imaging Research Group, Heart and Vascular Center, Semmelweis University, 68 Városmajor str, Budapest, 1122, Hungary. 3. Department of Radiology, Johns Hopkins University School of Medicine, 601 N Caroline St, Baltimore, MD, 21205, USA. 4. Department of Medicine, Johns Hopkins University School of Medicine, 733 N Broadway, Baltimore, MD, 21205, USA. 5. University of Wisconsin School of Medicine and Public Health, 750 Highland Ave, Madison, WI, 53726, USA. 6. National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland, 10 Center Dr, Bethesda, MD, 20814, USA. 7. Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, 614 Wolfe N Wolfe St, Baltimore, MD, 21205, USA. 8. Institute of Human Virology, University of Maryland School of Medicine, W Lombard Street, Baltimore, MD, 21201, USA. 9. Department of Pathology, Johns Hopkins University School of Medicine, 600 N Wolfe St, Baltimore, MD, 21287, USA. slai@ihv.umaryland.edu. 10. Department of Radiology, Johns Hopkins University School of Medicine, 601 N Caroline St, Baltimore, MD, 21205, USA. slai@ihv.umaryland.edu. 11. Department of Medicine, Johns Hopkins University School of Medicine, 733 N Broadway, Baltimore, MD, 21205, USA. slai@ihv.umaryland.edu. 12. Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, 614 Wolfe N Wolfe St, Baltimore, MD, 21205, USA. slai@ihv.umaryland.edu. 13. Institute of Human Virology, University of Maryland School of Medicine, W Lombard Street, Baltimore, MD, 21201, USA. slai@ihv.umaryland.edu. 14. Department of Epidemiology and Public Health, University of Maryland School of Medicine, 655 W Baltimore St, Baltimore, MD, 21201, USA. slai@ihv.umaryland.edu. 15. Department of Epidemiology and Public Health, University of Maryland School of Medicine, 655 W Baltimore St, Baltimore, MD, 21201, USA.
Abstract
OBJECTIVES: To assess whether HIV infection directly or indirectly promotes coronary artery disease (CAD) volume progression in a longitudinal study of African Americans. METHODS: We randomly selected 300 individuals with subclinical CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV infected, 174 cocaine users) from 1429 cardiovascularly asymptomatic participants of a prospective epidemiological study between May 2004 and August 2015. Individuals underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years). We quantified noncalcified (NCP: -100-350HU), low-attenuation noncalcified (LA-NCP: -100-30HU), and calcified (CP: ≥ 351 HU) plaque volumes. Linear mixed models were used to assess the effects of HIV infection, atherosclerotic cardiovascular disease (ASCVD) risk, and years of cocaine use on plaque volumes. RESULTS: There was no significant difference in annual progression rates between HIV-infected and HIV-uninfected regarding NCP (8.7 [IQR: 3.0-19.4] mm3/year vs. 4.9 [IQR: 1.5-18.3] mm3/year, p = 0.14), LA-NCP (0.2 [IQR: 0.0-1.6] mm3/year vs. 0.2 [IQR: 0.0-0.9] mm3/year, p = 0.07) or CP volumes (0.3 [IQR: 0.0-3.4] mm3/year vs. 0.1 [IQR: 0.0-3.2] mm3/year, p = 0.30). Multivariately, HIV infection was not associated with NCP (-6.9mm3, CI: [-32.8-19.0], p = 0.60), LA-NCP (-0.1mm3, CI: [-2.6-2.4], p = 0.92), or CP volumes (-0.3mm3, CI: [-9.3-8.6], p = 0.96). However, each percentage of ASCVD and each year of cocaine use significantly increased total, NCP, and CP volumes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-associated medications had any effect on plaque volumes (p > 0.05 for all). CONCLUSIONS: The more profound adverse effect of risk factors in HIV-infected individuals may explain the accelerated progression of CAD in these people, as HIV infection was not independently associated with any coronary plaque volume. KEY POINTS: • Human immunodeficiency virus-infected individuals may have similar subclinical coronary artery disease, as the infection is not independently associated with coronary plaque volumes. • However, cardiovascular risk factors and illicit drug use may have a more profound effect on atherosclerosis progression in those with human immunodeficiency virus infection, which may explain the accelerated progression of CAD in these people. • Nevertheless, through rigorous prevention and abstinence from illicit drugs, these individuals may experience similar cardiovascular outcomes as -uninfected individuals.
OBJECTIVES: To assess whether HIV infection directly or indirectly promotes coronary artery disease (CAD) volume progression in a longitudinal study of African Americans. METHODS: We randomly selected 300 individuals with subclinical CAD (210 male; age: 48.0 ± 7.2 years; 226 HIV infected, 174 cocaine users) from 1429 cardiovascularly asymptomatic participants of a prospective epidemiological study between May 2004 and August 2015. Individuals underwent coronary CT angiography at two time points (mean follow-up: 4.0 ± 2.3 years). We quantified noncalcified (NCP: -100-350HU), low-attenuation noncalcified (LA-NCP: -100-30HU), and calcified (CP: ≥ 351 HU) plaque volumes. Linear mixed models were used to assess the effects of HIV infection, atherosclerotic cardiovascular disease (ASCVD) risk, and years of cocaine use on plaque volumes. RESULTS: There was no significant difference in annual progression rates between HIV-infected and HIV-uninfected regarding NCP (8.7 [IQR: 3.0-19.4] mm3/year vs. 4.9 [IQR: 1.5-18.3] mm3/year, p = 0.14), LA-NCP (0.2 [IQR: 0.0-1.6] mm3/year vs. 0.2 [IQR: 0.0-0.9] mm3/year, p = 0.07) or CP volumes (0.3 [IQR: 0.0-3.4] mm3/year vs. 0.1 [IQR: 0.0-3.2] mm3/year, p = 0.30). Multivariately, HIV infection was not associated with NCP (-6.9mm3, CI: [-32.8-19.0], p = 0.60), LA-NCP (-0.1mm3, CI: [-2.6-2.4], p = 0.92), or CP volumes (-0.3mm3, CI: [-9.3-8.6], p = 0.96). However, each percentage of ASCVD and each year of cocaine use significantly increased total, NCP, and CP volumes among HIV-infected individuals, but not among HIV-uninfected. Importantly, none of the HIV-associated medications had any effect on plaque volumes (p > 0.05 for all). CONCLUSIONS: The more profound adverse effect of risk factors in HIV-infected individuals may explain the accelerated progression of CAD in these people, as HIV infection was not independently associated with any coronary plaque volume. KEY POINTS: • Human immunodeficiency virus-infected individuals may have similar subclinical coronary artery disease, as the infection is not independently associated with coronary plaque volumes. • However, cardiovascular risk factors and illicit drug use may have a more profound effect on atherosclerosis progression in those with human immunodeficiency virus infection, which may explain the accelerated progression of CAD in these people. • Nevertheless, through rigorous prevention and abstinence from illicit drugs, these individuals may experience similar cardiovascular outcomes as -uninfected individuals.
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