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EASL 2017: Curing Hepatitis C Reduces Cardiovascular Risk


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

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Presenting the findings, Patrice Cacoub from Hôpital Pitié-Salpêtrière in Paris stressed the importance of thinking of hepatitis C as a systemic disease that affects the heart, kidneys, blood vessels, 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.

Hepatitis C infection increases the risk of cardiovascular disease -- events such as heart attack, stroke, peripheral artery disease, and heart failure -- especially in older people and those with diabetes or high blood pressure. Hepatitis C virus (HCV) infection may promote heart disease by causing metabolic problems, but it may also do so by causing inflammation. What is less clear is whether hepatitis C treatment and sustained virological response after therapy affect the risk of cardiovascular disease.

The study population consisted of people with hepatitis C and cirrhosis without symptomatic liver disease (Child Pugh A stage) who had detectable HCV at baseline. Participants were enrolled in the ANRS CirVir cohort between 2006 and 2012 and followed for at least 5 years. The cohort was recruited originally to assess different methods of detecting hepatocellular carcinoma (HCC), a type of liver cancer, in people with hepatitis C. Participants were seen every 6 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 with HIV or hepatitis B coinfection. 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, 7 of them 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 virological response (SVR) to HCV 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).

This difference in risk began to become apparent after 3 years of follow-up, and was very pronounced after 6 years. Whereas 2.3% of those who achieved SVR had a cardiovascular event after 6 years of follow up, 8.7% of those who 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 increased cardiovascular risk. 

Multivariate analysis showed that hypertension was a significant predictor of a cardiovascular event (HR 3.24), as was current smoking (HR 4.20) and low serum albumin (HR 2.78).

However, the strongest predictor of cardiovascular was ethnicity. People of East Asian origin were 9 times more likely to experience a cardiovascular event (HR 9.20). Cacoub offered no explanation for why the risk might be so much higher in people of East Asian origin.

Cacoub said that the study findings "reinforce the systemic nature of HCV infection," adding 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.



P Cacoub, P Nahon, R Layese, et al. HCV eradication reduces the occurrence of major adverse cardiovascular events in hepatitis C cirrhotic patients: data from the prospective ANRS CO12 CirVir cohort. EASL International Liver Congress. Amsterdam, April 19-23, 2017. Abstract PS-032.