Objective: The aim of this article is to determine whether HIV-infected (HIV+) men have either higher incidence or more rapid progression of coronary artery calcium (CAC) compared with HIV-uninfected (HIV−) controls.
Design: Prospective observational study.
Setting: Multicenter study in four US academic research centers: University of Pittsburgh, Johns Hopkins University, University of California Los Angeles, and Northwestern University.
Participants: Eight hundred and twenty-five men (541 HIV+ and 284 HIV−) enrolled in the cardiovascular substudy of the Multicenter AIDS Cohort Study who underwent serial cardiac computed tomography (CT) imaging during a mean follow-up of 5 years (range, 2–8 years).
Main outcome measures: Incidence and progression of CAC assessed by cardiac CT.
Results: During follow-up, 21% of HIV+ men developed incident CAC compared with 16% of HIV− men. This association persisted after adjustment for traditional and HIV-associated risk factors: hazard ratio 1.64 (1.13–3.14). However, there was no association between HIV serostatus and CAC progression among men with CAC present at baseline. Current smoking and increased insulin resistance, both modifiable risk factors, were independently associated with increased incidence of CAC. No evidence supporting an elevated risk for either CAC progression or incidence was found for either dyslipidemia or long-term usage of antiretroviral therapy.
Conclusion: In this large study of HIV+ and HIV− men who underwent serial cardiac CT scan imaging, HIV+ men were at significantly higher risk for development of CAC: hazard ratio 1.64 (1.13–3.14). In addition, two important and modifiable risk factors were identified for increased incidence of CAC. Taken together, these findings underscore the potential importance for smoking cessation and interventions to improve insulin resistance among HIV+ men.
aDepartment of Infectious Diseases and Microbiology
bDepartment of Epidemiology, Graduate School of Public Health, University of Pittsburg, Pennsylvania
cJohns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
dLos Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California
eNorthwestern University, Chicago, Illinois
fSchool of Health Sciences, Duquesne University, Pittsburgh, Pennsylvania
gJohns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Correspondence to Dr Lawrence A. Kingsley, Department of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15213, USA. Tel: +1 412 624 5069; e-mail: Kingsley@pitt.edu
Lawrence A. Kingsley and Jennifer Deal contributed equally to the writing of this article.
Received 5 April, 2015
Revised 5 August, 2015
Accepted 7 August, 2015