Curing hepatitis C reduces the risk of cardiovascular events
in people with compensated cirrhosis, a large French study presented this week
at the International Liver Congress in Amsterdam shows.

Presenting the findings, Patrice Cacoub of Hôpital
Pitié-Salpêtrière, Paris, stressed the importance of thinking of hepatitis C as
a systemic disease that affects the heart, the kidneys, blood vessels, the
brain and glucose metabolism through mechanisms that are still to be fully
understood. Hepatitis C is also associated with an increased risk of
non-hepatic cancers, especially non-Hodgkin lymphoma.

C infection increases the risk of cardiovascular disease
– events such as
heart attack, stroke, peripheral artery disease and heart failure – especially
in people with older people and those with diabetes or high blood pressure. Hepatitis
C may promote heart disease by causing metabolic problems, but may also do so
by causing inflammation.

What is less clear is whether hepatitis C treatment and
sustained virologic response after treatment affect the risk of cardiovascular

The study population consisted of people with hepatitis C
and cirrhosis without symptomatic liver disease (Child Pugh A stage) who had
detectable HCV virus at baseline. Participants were enrolled in the ANRS CirVir
cohort between 2006 and 2012 and followed for at least five years. The cohort
was recruited originally to assess different methods of detecting
hepatocellular carcinoma (liver cancer) in people with hepatitis C.
Participants were seen every six months and information about all
cardiovascular events was included in their medical records.

This analysis included 878 people from the cohort, who were
followed for a median of 57.5 months. The study excluded people coinfected with
HIV or hepatitis B. The study evaluated the incidence of stroke, heart attack,
angina, peripheral artery disease, heart failure or cardiac arrest.

During the follow up period 79 major cardiovascular events
occurred in 62 members of the cohort population and 15 people died, seven due
to a cardiovascular event. The most common event was heart failure (23 reported
cases) followed by stroke (16 people). Heart attack and cardiac arrest were
less common.

Having a sustained virologic response to treatment during
the follow-up period reduced the risk of a cardiovascular event by 65%, although
confidence in the precision of this estimate of risk reduction was low (hazard
ratio 0.35, 95% CI 0.09-0.97). This difference in risk began to become apparent
after three years of follow-up, and was very pronounced after six years:
whereas 2.3% of those who achieved SVR had a cardiovascular event after six
years of follow up, 8.7% of those were not cured had experienced a
cardiovascular event by this stage.

Among this population
of people with early-stage cirrhosis, those with markers of poorer liver function
had a higher risk of cardiovascular events. High total bilirubin
(17µmol/L), low serum albumin (35 g/L) and very low platelet count were
each independently associated with an increased risk. 

Multivariate analysis showed that
hypertension was a significant predictor of a cardiovascular event (HR 3.24,
95% CI 1.78-5.91 p0.001) as did current smoking (HR 4.20, 95% CI 2.11-8.64,
p0.001) and low serum albumin (HR 2.78, 95% CI 1.3-5.5).

However, the strongest predictor
of cardiovascular was ethnicity. People of East Asian origin were nine times
more likely to experience a cardiovascular event (HR 9.20, 95% CI 2.46-24.95,
p=0.03). Professor Cacoub offered no explanation for why the risk might be so
much higher in people of East Asian origin.

Professor Cacoub said that the
study findings “reinforce the systemic nature of HCV infection”, and that the
effect of curing hepatitis C on cardiovascular risk should be taken into
account when considering who is eligible for direct-acting antiviral treatment.