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Hepatitis C and HIV Each Linked to Artery Plaque Buildup in Gay Men

February 19, 2016

Hepatitis C (HCV) and HIV infection were independently associated with markers of subclinical atherosclerosis -- including plaque and coronary artery calcium -- in a study of 994 men who have sex with men (MSM) in the Multicenter AIDS Cohort Study (MACS). The MACS investigators believe their findings suggest that "vigilant assessments of cardiovascular disease are warranted for HCV-infected individuals."

Ample research shows that HCV or HIV infection may boost the risk of cardiovascular disease by increasing immune activation and inflammation, which drive atherosclerosis progression. MACS researchers conducted this study to determine whether HCV promotes subclinical atherosclerosis in MSM with or without HIV and to learn whether HCV and HIV have a synergistic impact on subclinical atherosclerosis in men infected with both viruses.

The MACS is an ongoing prospective study of MSM with and at risk for HIV infection in four U.S. urban areas. Men make twice-yearly study visits. Starting in January 2010, men 40 to 70 years old without a history of cardiac surgery or percutaneous coronary intervention could undergo noncontrast computed tomography (CT) as part of a cardiovascular study. A subset of men underwent coronary CT angiography (CCTA). The MACS team used these scans to measure (1) coronary artery calcium; (2) presence, size and composition of plaque and (3) degree of stenosis. In the months before CT, the researchers collected serologic, clinical, demographic and behavioral data for each man.

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Of the 994 men who underwent CT, 755 also underwent CCTA, 87 had HCV infection, 613 had HIV infection, and 70 had HCV and HIV infection. Overall median age stood at 53 years, 58% of men were white, 31% black, and 11% were Hispanic or another race or ethnicity. Among men with HIV, 82% had an undetectable viral load and median CD4+ count measured 599 cells/mm3. Compared with HCV-negative men, those with HCV had a higher prevalence of any plaque on CCTA (89.3% versus 75.4%, P = .02) or of rupture-prone noncalcified plaque (76.8% versus 57.5%, P < .01). Prevalence of stenosis ≥50% did not differ by HCV status.

Regression analysis adjusted for cardiovascular risk factors determined that HCV infection was independently associated with prevalence of any plaque on CCTA (adjusted prevalence ratio [aPR] 1.26, 95% confidence interval [CI] 1.09 to 1.45), as was HIV infection (aPR 1.12, 95% CI 1.03 to 1.22). Both HCV and HIV were also independently associated with prevalence of noncalcified plaque (HCV aPR 1.42, 95% CI 1.16 to 1.75; HIV aPR 1.27, 95% CI 1.11 to 1.45). Chronic HCV, but not HIV, was associated with higher coronary artery calcium prevalence (aPR 1.29, 95% CI 1.02 to 1.63). Statistical modeling found no evidence of HCV/HIV synergy in any plaque outcome.

Compared with HCV-negative men, men with an HCV RNA load ≥2 x 106 IU/mL (but not below that level) had significantly elevated coronary artery calcium (aPR 1.53, 95% CI 1.20 to 1.97). Men with HCV RNA ≥2 x 106 IU/mL also had significantly elevated prevalence of any plaque and noncalcified plaque.

This MACS analysis is the largest study to date linking chronic HCV infection to subclinical coronary atherosclerosis, an established predictor of cardiovascular events. The association between chronic HCV and plaque remained significant after adjustment for black race, less education, current smoking, injection drug use and other cardiovascular risk factors. The impact of HCV on subclinical atherosclerosis was also independent of HIV infection. The MACS researchers believe their novel finding linking higher HCV RNA to subclinical atherosclerosis underlines the need for more study of whether HCV infection duration or curative therapy affects coronary plaque progression.

Mark Mascolini writes about HIV infection.


Copyright © 2016 Remedy Health Media, LLC. All rights reserved.


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