Objective: Regression of fibrosis and portal hypertension is heterogeneous even after sustained virological response (SVR) achieved after therapy with direct-acting antivirals (DAAs). Clinically significant portal hypertension may persist in a relevant proportion of patients with cirrhosis. Cirrhosis is also associated with circulatory changes (hyperdynamic state) and subclinical cardiac dysfunction (cirrhotic cardiomyopathy), which may be relevant to fibrosis reversibility. The aim was to assess the association between baseline systemic haemodynamic and echocardiographic profiles and the improvment of liver stiffness/fibrosis in patients with chronic hepatitis C treated with DAAs who achieved SVR. Design and method: Longitudinal observational study including 145 patients with chronic hepatitis C. All patients underwent pre-treatment cardiovascular assessment in an Internal Medicine clinic, including systolic/diastolic blood pressure, heart rate, and haemodynamic/functional parameters: total peripheral resistance (TPR), estimated portal venous pressure (PVP), pulmonary systolic pressure (PSP), left ventricular isovolumetric relaxation time (IVRT/“TRIVE”), left ventricular mass index (LVMI), and diastolic function markers (E/A ratio E/A and E/e ratio E/e). Liver stiffness was quantified by transient elastography before initiation of DAAs and at follow-up after SVR. Fibrosis stages were defined using study-specific cut-offs and patients were divided into 4 groups: mild, moderate and severe fibrosis and cirrhosis. Improvment was defined as a reduction in fibrosis stage from severe fibrosis or cirrhosis to mild or moderate fibrosis. Statistical analysis was performed using SPSS v29.0, with significance set at p<0.05. Results: Patients who exhibited regression of fibrosis showed a profile consistent with lower activation of the hyperdynamic state and better diastolic performance: lower values of TPR, PVP, PSP, IVRT/“TRIVE”, LVMI and E/e and higher E/A ratios. The difference observed in the diastolic component reached statistical significance (p=0.023). Conclusions: These findings suggest that fibrosis reversibility after viral eradication may depend on the degree of circulatory dysfunction and cardiac remodeling/dysfunction associated with portal hypertension. Identifying patients with more favorable profiles—namely lower TPR/PVP, lower PSP, reduced IVRT, non-increased LVMI, and E/A and E/e ratios consistent with better diastolic function—helps clarify mechanisms of reversibility and guide more individualized post-SVR follow-up. Cardio-hepatological integration may support surveillance and referral/monitoring decisions within a precision medicine framework.
Alcântara et al. (Fri,) studied this question.