Congestion and remodeling biomarker profiles in cirrhotic cardiomyopathy

Background

Cirrhotic cardiomyopathy constitutes a HFpEF-like syndrome marked by diastolic dysfunction and congestion, where reliance on echocardiography alone may underestimate clinically meaningful heart failure phenotypes. Biomarkers reflecting distinct pathophysiological pathways may help identify clinically relevant heart failure phenotypes in cirrhotic patients.

Methods

We studied 43 patients with non-alcoholic liver cirrhosis without known cardiovascular disease and 40 healthy controls undergoing clinical evaluation, transthoracic echocardiography, and biomarker assessment. NT-proBNP and soluble suppression of tumorigenicity 2 (sST2) were analyzed in relation to diastolic function, echocardiographic markers of congestion, and cirrhosis severity.

Results

Cirrhotic patients had significantly higher NT-proBNP levels compared with controls (39.8 ± 146.5 vs. 18.7 ± 5.5 pg/mL, p < 0.001), with further elevation in patients presenting diastolic dysfunction (median 59.1 vs. 30.8 pg/mL, p = 0.0036) and marked increases in those with concomitant ascites (median 272 pg/mL). NT-proBNP correlated with left atrial volume index (r = 0.36, p = 0.022) and pulmonary artery systolic pressure (r = 0.48, p = 0.018).

sST2 concentrations were also higher in cirrhotic patients than in controls (5.3 ± 2.25 vs. 2.05 ± 0.99 ng/mL, p < 0.001) but showed no association with ascites, Child–Pugh class, or echocardiographic indices of congestion.

Conclusions

NT-proBNP identifies a congestion-driven heart failure phenotype in cirrhotic cardiomyopathy, strongly influenced by volume overload and hemodynamic stress, whereas sST2 appears dissociated from liver-related congestion, suggesting an association with myocardial remodeling. Distinct biomarker profiles may support HFpEF-oriented phenotyping and individualized management strategies in patients with cirrhosis.