Abstract
Background. Hepatitis C virus (HCV) infection may increase the risk of cardiovascular disease (CVD). We evaluated the association of chronic HCV infection and coronary atherosclerosis among participants in the Multicenter AIDS Cohort Study. Methods. We assessed 994 men with or without human immunodeficiency virus (HIV) infection (87 of whom had chronic HCV infection) for coronary plaque, using noncontrast coronary computed tomography (CT); 755 also underwent CT angiography. We then evaluated the associations of chronic HCV infection and HIV infection with measures of plaque prevalence, extent, and stenosis. Results. After adjustment for demographic characteristics, HIV serostatus, behaviors, and CVD risk factors, chronic HCV infection was significantly associated with a higher prevalence of coronary artery calcium (prevalence ratio, 1.29; 95% confidence interval [CI], 1.02-1.63), any plaque (prevalence ratio, 1.26; 95% CI, 1.09-1.45), and noncalcified plaque (prevalence ratio, 1.42; 95% CI, 1.16-1.75). Chronic HCV infection and HIV infection were independently associated with the prevalence of any plaque and of noncalcified plaque, but there was no evidence of a synergistic effect due to HIV/HCV coinfection. The prevalences of coronary artery calcium, any plaque, noncalcified plaque, a mixture of noncalcified and calcified plaque, and calcified plaque were significantly higher among men with an HCV RNA load of ≥2 × 106 IU/mL, compared with findings among men without chronic HCV infection. Conclusions. Chronic HCV infection is associated with subclinical CVD, suggesting that vigilant assessments of cardiovascular risk are warranted for HCV-infected individuals. Future research should determine whether HCV infection duration or HCV treatment influence coronary plaque development.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 257-265 |
| Number of pages | 9 |
| Journal | Journal of Infectious Diseases |
| Volume | 213 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jan 15 2016 |
Funding
Data in this article were collected by the MACS, with centers ( principal investigators) at the Johns Hopkins Bloomberg School of Public Health (Joseph B. Margolick), the Northwestern University Feinberg School of Medicine and the Cook County Bureau of Health Services (Steven M. Wolinsky), the University of California–Los Angeles (Roger Detels), and the University of Pittsburgh (Charles R. Rinaldo) and the data center at the Johns Hopkins Bloomberg School of Public Health (Lisa P. Jacobson). The MACS Web site is available at: http://www.statepi. jhsph.edu/macs/macs.html. Accessed 14 August 2015. This work was supported by the National Heart Lung and Blood Institute (RO1 HL095129 to W. S. P.); the National Center for Advancing Translational Sciences (UL1 TR001079), a component of the National Institutes of Health and National Institutes of Health Roadmap for Medical Research; the University of Washington’s CVD and Metabolic Complications of HIV/AIDS Data Coordinating Center (5R01 HL095126); the American Heart Association ( predoctoral fellowship award 13PRE16970094 to R. M.); and Johns Hopkins University (predoctoral research program award to R. M.). The MACS is funded by the National Center for Research Resources, the National Institute of Allergy and Infectious Diseases, and the National Cancer Institute (UO1-AI-35042, UM1-AI-35043, UO1-AI-35039, UO1-AI-35040, and UO1-AI-35041).
Keywords
- atherosclerosis
- cardiovascular disease
- hepatitis C virus infection
- human immunodeficiency virus type 1
- plaque
ASJC Scopus subject areas
- Infectious Diseases
- Immunology and Allergy
