Chronic hepatitis
C virus (HCV) infection is associated with an important early warning sign of
cardiovascular disease, investigators from the Multicenter AIDS Cohort Study
(MACS) report in the online edition of the Journal
of Infectious Diseases. Both HIV and HCV infections were independently
associated with hardening of the coronary artery, but there was no evidence
that HIV/HCV co-infection worsened atherosclerosis. After controlling for HIV
infection and other factors associated with heart disease, a consistent
relationship was present between chronic HCV infection and coronary artery
plaque formation.
“This is the
largest study to date to demonstrate that chronic HCV [CHC] infection is
associated with subclinical coronary atherosclerosis, an important predictor of
future cardiovascular disease [CVD],” write the authors. “The association of
CHC with plaque remained significant after adjustment for…recognized CVD risk
factors and was independent of HIV infection.”
Both HIV and HCV
can cause systemic inflammation and increased immune activation, risk factors
for hardening of the arteries. HIV infection has been associated with
subclinical arterial disease, but the relationship between HCV infection and
atherosclerosis is unclear.
Investigators from
the large, on-going MACS study therefore designed a cross-sectional
study to evaluate the association between HCV infection and the formation of
coronary plaques.
A total of 994
HIV-positive and HIV-negative men (87 with chronic HCV infection) aged between 40
and 70 years who received care before January 2010 were enrolled in the study. All
the patients had a coronary CT assessment and 755 also underwent CT
angiography. The investigators evaluated the association between chronic HCV
and HIV infection and measures of plaque prevalence, extent and stenosis
(narrowing of the arteries).
Men with HCV were
more likely than HCV-negative men to be HIV-positive (81% vs. 60%),
African-American, have low educational attainment, be current smokers, have a
history of injecting drug use and to be taking medication for hypertension or
diabetes (all differences significant, p < 0.05). Median HCV RNA among the
infected men was 2.0x106 iu/ml.
Overall prevalence
of coronary artery plaque was significantly higher among men with chronic HCV
infection compared to HCV-uninfected men (89% vs. 75%, p = 0.02). Prevalence of
non-calcified plaque was also elevated among those with HCV (77% vs. 58%, p
< 0.01). However, prevalence did not differ by HCV infection status for
coronary artery calcium (CAC) scores, mixed plaque, calcified plaque, or
narrowing of the coronary artery by 50% or more.
After taking into
account other potential risk factors for arterial disease, both chronic HCV
infection and HIV infection were independently associated with prevalence of
any plaque (adjusted prevalence ratio [aPR] = 1.26; 95% CI, 1.09-1.45 and 1.12;
95% CI, 1,03-1.22, respectively) and non-calcified plaque (aPR = 1.42; 95% CI,
1.16-1.75 and 1.27; 95% CI, 1.11-1.45, respectively).
Chronic HCV
infection (but not HIV) was associated with CAC scores. There was no evidence
of an interaction between HCV and HIV; in other words, co-infection did not
make prevalence and extent of subclinical coronary atherosclerosis worse.
A higher HCV load
was associated with more extensive plaque formation.
The authors’
findings remained robust after taking into account factors such as current
injecting drug use, the presence of fatty liver disease, fibrosis, CD4 cell
count, HIV load, and the exclusion of individuals with chronic hepatitis B
virus (HBV) infection.
“The elevated
prevalence of subclinical coronary atherosclerosis among men with chronic HCV
infection, especially men with the highest HCV RNA levels, provides further
evidence supporting a link between chronic HCV infection and cardiovascular
disease,” conclude the authors. “The presence of HCV infection may warrant
vigilant cardiovascular risk assessment in these patients.”