From the Journals

Viremic suppression linked to decreased MACE rate in patients with HCV-cirrhosis


 

FROM AMERICAN HEART JOURNAL

Hepatitis C viremic suppression was associated with a lower rate of cardiovascular events in patients with compensated HCV-related cirrhosis, compared with control patients who did not achieve a sustained virological response. In addition, predictive factors for major adverse cardiovascular events (MACEs) in compensated HCV-related cirrhosis were Asian ethnic origin, hypertension, smoking, and low serum albumin, according to a report in American Heart Journal.

A total of 878 patients with HCV-related cirrhosis were enrolled at 35 French centers. Upon enrollment, all patients received HCV treatment and were followed for MACEs, including stroke, myocardial infarction, ischemic heart disease, heart failure, peripheral arterial disease, cardiac arrest, and cardiovascular-related death, according to Patrice Cacoub, MD, of Sorbonne Universités, Paris, and his colleagues.

Hepatitis C Courtesy U.S. Department of Veterans Affairs
In multivariate analysis, Asian ethnic origin (P = .003), arterial hypertension (P less than .001), current smoking (P less than .001), and low serum albumin level (P less than .009) were positive predictors of MACE occurrence, while sustained virological response (P = .044) was a negative predictor.

Five-year survival for patients presenting with a MACE was 60% vs. 88% in patients who did not have an event.

“[Our] results strengthen the systemic nature of HCV infection, a chronic disease in which cardiovascular risk must be carefully assessed. The decreased rate of MACEs after [sustained virological response] in this population should be taken into account to enable wider access to new [direct-acting antivirals]. Further studies are warranted to evaluate whether a similar benefit can be obtained in less severe patients, such as noncirrhotic HCV-infected patients,” the researchers concluded.

The authors reported having no conflicts of interest.

SOURCE: Cacoub, P et al. Am Heart J. 2018;198:4-17.

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