Curing hepatitis C reduces cardiovascular risk

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.

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 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 diseases.

The study population consisted of people with hepatitis C and cirrhosis without symptomatic liver disease (Child Pugh A stage) who had detectable hepatitis C virus (HCV) 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 with HIV or hepatitis B co-infection. 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 (SVR) 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 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 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 p<0.001) as was current smoking (HR 4.20, 95% CI 2.11-8.64, p<0.001) 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.