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. 2021 Aug;28(8):1190-1199.
doi: 10.1111/jvh.13523. Epub 2021 May 7.

Liver and cardiovascular mortality after hepatitis C virus eradication by DAA: Data from RESIST-HCV cohort

Affiliations

Liver and cardiovascular mortality after hepatitis C virus eradication by DAA: Data from RESIST-HCV cohort

Vincenza Calvaruso et al. J Viral Hepat. 2021 Aug.

Abstract

Real-world evidence on the course of Hepatitis C Virus (HCV) chronic liver disease after Sustained Virologic Response (SVR) obtained with direct-acting antiviral drugs (DAAs) are still limited, and the effects on mortality remain unclear. We evaluated the post-treatment survival of 4307 patients in the RESIST-HCV cohort (mean age 66.3 ± 11.6 years, 56.9% males, 24.7% chronic hepatitis, 66.9% Child-Pugh A cirrhosis and 8.4% Child-Pugh B cirrhosis) treated with DAAs between March 2015 and December 2016 and followed for a median of 73 weeks (range 16-152). Proportional cause-specific hazard regression for competing risks was used to evaluate the survival and to assess the predictors of liver and cardiovascular death. Overall, 94.7% of patients achieved SVR while 5.3% were HCV RNA-positive at last follow-up. Sixty-three patients (1.4%) died during the observation period. SVR was associated with a decreased risk of liver mortality (hazard ratio,HR0.09, beta -2.37, p < .001). Also, platelet count (HR 0.99, beta-0.01, p = .007) and albumin value (HR 0.26, beta -1.36 p = .001) were associated with liver mortality by competing risk analysis. SVR was associated with a reduced risk of cardiovascular mortality regardless of presence of cirrhosis (HR 0.07, beta-2.67, p < .001). Presence of diabetes (HR 3.45, beta 1.24, p = .014) and chronic kidney disease class ≥3 (HR 3.60, beta 1.28, p = 0.016) were two factors independently associated with higher risk of cardiovascular mortality. Patients with SVR to a DAA therapy have a better liver and cardiovascular survival, and the effects of HCV eradication are most evident in patients with compensated liver disease.

Keywords: chronic hepatitis; cirrhosis; competing risks; survival.

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Conflict of interest statement

Vincenza Calvaruso served on the advisory board of Abbvie and Intercept, and served on the speaker's bureau of Gilead, Salvatore Petta served on the advisory board of Abbvie and Gilead, and served on the speaker's bureau of Gilead and Abbvie, Marco Distefano, Gaetano Scifo, Maurizio Russello served on the advisory board of Abbvie and served on the speaker's bureau of Gilead and Abbvie, Giuseppe Cabibbo served on the advisory board of Bayer. Vito Di Marco received research support from Abbvie, Gilead, Intercept and Merck/MSD and served on the advisory boards of Abbvie, Gilead and MSD/Merck. Antonio Craxì received research support from Abbvie, Gilead, Merck/MSD and Intercept and consulted for and served on the speaker's bureau and advisory boards of Abbvie, Intercept, Gilead, and MSD/Merck. Giovanni Raimondo served on the advisory boards of Abbvie, Gilead, and MSD/Merck. Calogero Cammà served on the advisory board of Bayer and MSD/Merck. The other authors have no disclosures to declare.

Figures

FIGURE 1
FIGURE 1
Flow‐chart of the RESIST—HCV cohort
FIGURE 2
FIGURE 2
Cumulative incidence functions for LR and CV mortality performed using the parameter estimates of the cause‐specific hazard model and considering the best patient profile for continuous variables (PLT, Albumin, INR and bilirubin) in subjects with CKD <3 and without diabetes
FIGURE 3
FIGURE 3
Cumulative incidence functions for LR and CV mortality performed using the parameter estimates of the cause‐specific hazard model and considering the worst patient profile for continuous variables (PLT, Albumin, INR and bilirubin) in subjects with CKD stage 3 and diabetes

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