Wendy S. Post, MD, MS; Matthew Budoff, MD; Lawrence Kingsley, PhD; Frank J. Palella Jr., MD; Mallory D. Witt, MD; Xiuhong Li, MS; Richard T. George, MD; Todd T. Brown, MD, PhD; Lisa P. Jacobson, ScD
Note: Dr. Post had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Data were collected by the MACS centers at the Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland (principal investigator, Joseph B. Margolick); Feinberg School of Medicine, Northwestern University, and Cook County Bureau of Health Services, Chicago, Illinois (principal investigator, Steven M. Wolinsky); University of California, Los Angeles, Los Angeles, California (principal investigator, Roger Detels); and University of Pittsburgh, Pittsburgh, Pennsylvania (principal investigator, Charles R. Rinaldo), as well as the data center at the Johns Hopkins Bloomberg School of Public Health (principal investigator, Lisa P. Jacobson).
Acknowledgment: The authors thank Andrea Stronski for administrative support for this study and Adrian Dobs, MD, MHS; Joseph Margolick, MD; and A. Richey Sharrett, MD, PhD, for their reviews of the manuscript draft and contributions to this study.
Grant Support: This study is funded by the National Heart, Lung, and Blood Institute (grant RO1 HL095129 to Dr. Post), with additional support from the National Center for Advancing Translational Sciences, a component of the National Institutes of Health and National Institutes of Health Roadmap for Medical Research (grant UL1 RR 025005). The MACS is funded by the National Institute of Allergy and Infectious Diseases, with additional supplemental funding from the National Cancer Institute (grants UO1-AI-35042, UL1-RR025005, UM1-AI-35043, UO1-AI-35039, UO1-AI-35040, and UO1-AI-35041).
Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M13-1754.
Reproducible Research Statement: Study protocol and statistical code: Data collection forms used as part of the core MACS visit are available on the MACS Web site (www.statepi.jhsph.edu/macs/macs.html). The study protocol and the computer code used to generate results reported in this article are available on request. Data set: Individual-level MACS data are available from Dr. Post (e-mail, email@example.com) after review of a concept sheet by the MACS executive committee.
Requests for Single Reprints: Wendy S. Post, MD, MS, Johns Hopkins University School of Medicine, Ciccarone Center for the Prevention of Heart Disease, Division of Cardiology, Carnegie 568, 600 North Wolfe Street, Baltimore, MD 21287; e-mail, firstname.lastname@example.org.
Current Author Addresses: Dr. Post: Johns Hopkins University School of Medicine, Ciccarone Center for the Prevention of Heart Disease, Division of Cardiology, Carnegie 568, 600 North Wolfe Street, Baltimore, MD 21287.
Dr. Budoff: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502.
Dr. Kingsley: University of Pittsburgh, Graduate School of Public Health, 418 Parran Hall, Fifth Avenue and Desoto Street, Pittsburgh, PA 15261.
Dr. Palella: Northwestern University, 645 North Michigan Avenue, Suite 900, Chicago, IL 60611.
Dr. Witt: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Chronic Disease Clinical Research Center, 1124 West Carson Street, Torrance, CA 90502.
Ms. Li: Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Room E7003, Baltimore, MD 21205.
Dr. George: Johns Hopkins University School of Medicine, 600 North Wolfe Street, Blalock 524D2, Baltimore, MD 21111.
Dr. Brown: Johns Hopkins University, Division of Endocrinology, Diabetes, and Metabolism, 1830 East Monument Street, Suite 333, Baltimore, MD 21287.
Dr. Jacobson: Johns Hopkins Bloomberg School of Public Health, Department of Epidemiology, 615 North Wolfe Street, Room E7646, Baltimore, MD 21205.
Author Contributions: Conception and design: W.S. Post, M. Budoff, L. Kingsley, R.T George, L.P. Jacobson.
Analysis and interpretation of the data: W.S. Post, L. Kingsley, F.J. Palella, X. Li, R.T George, T. Brown, L.P. Jacobson.
Drafting of the article: W.S. Post, L. Kingsley, F.J. Palella, R.T George, L.P. Jacobson.
Critical revision of the article for important intellectual content: W.S. Post, M. Budoff, L. Kingsley, F.J. Palella, M.D. Witt, X. Li, R.T George, T. Brown, L.P. Jacobson.
Final approval of the article: W.S. Post, M. Budoff, L. Kingsley, F.J. Palella, M.D. Witt, X. Li, R.T George, T. Brown, L.P. Jacobson.
Provision of study materials or patients: W.S. Post, M. Budoff, L. Kingsley, M.D. Witt, R.T George.
Statistical expertise: X. Li, L.P. Jacobson.
Obtaining of funding: W.S. Post, L. Kingsley, R.T George, L.P. Jacobson.
Administrative, technical, or logistic support: M. Budoff, L. Kingsley.
Collection and assembly of data: W.S. Post, M. Budoff, L. Kingsley, M.D. Witt, R.T George, L.P. Jacobson.
Coronary artery disease (CAD) has been associated with HIV infection, but data are not consistent.
To determine whether HIV-infected men have more coronary atherosclerosis than uninfected men.
Multicenter AIDS Cohort Study.
HIV-infected (n = 618) and uninfected (n = 383) men who have sex with men who were aged 40 to 70 years, weighed less than 136 kg (200 lb), and had no history of coronary revascularization.
Presence and extent of coronary artery calcium (CAC) on noncontrast cardiac computed tomography (CT) and of any plaque; noncalcified, mixed, or calcified plaque; or stenosis on coronary CT angiography.
1001 men had noncontrast CT, of whom 759 had coronary CT angiography. After adjustment for age, race, CT scanning center, and cohort, HIV-infected men had a greater prevalence of CAC (prevalence ratio [PR], 1.21 [95% CI, 1.08 to 1.35]; P = 0.001) and any plaque (PR, 1.14 [CI, 1.05 to 1.24]; P = 0.001), including noncalcified (PR, 1.28 [CI, 1.13 to 1.45]; P < 0.001) and mixed (PR, 1.35 [CI, 1.10 to 1.65]; P = 0.004) plaque, than uninfected men. Associations between HIV infection and any plaque or noncalcified plaque remained significant (P < 0.005) after CAD risk factor adjustment. HIV-infected men had a greater extent of noncalcified plaque after CAD risk factor adjustment (P = 0.026). They also had a greater prevalence of coronary artery stenosis greater than 50% (PR, 1.48 [CI, 1.06 to 2.07]; P = 0.020), but not after CAD risk factor adjustment. Longer duration of highly active antiretroviral therapy (PR, 1.09 [CI, 1.02 to 1.17]; P = 0.007) and lower nadir CD4+ T-cell count (PR, 0.80 [CI, 0.69 to 0.94]; P = 0.005) were associated with coronary stenosis greater than 50%.
Cross-sectional observational study design and inclusion of only men.
Coronary artery plaque, especially noncalcified plaque, is more prevalent and extensive in HIV-infected men, independent of CAD risk factors.
National Heart, Lung, and Blood Institute and National Institute of Allergy and Infectious Diseases.
Post WS, Budoff M, Kingsley L, Palella FJ, Witt MD, Li X, et al. Associations Between HIV Infection and Subclinical Coronary Atherosclerosis. Ann Intern Med. 2014;160:458–467. doi: 10.7326/M13-1754
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Published: Ann Intern Med. 2014;160(7):458-467.
Cardiology, Coronary Heart Disease, HIV, Infectious Disease.
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