Abstract / Summary
Cardiocirculatory dysfunction in cirrhosis encompasses impaired cardiac reserve, diastolic dysfunction, systemic vasodilation, neurohormonal activation, and progressive reliance on compensatory cardiac activity.This systematic review evaluated how pharmacological interventions affecting cardiac function, vascular tone, effective circulating volume, or natriuretic signaling influence cardiovascular, renal, and clinical outcomes in adults with cirrhosis.MEDLINE via PubMed, Scopus, Web of Science Core Collection, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched for clinical studies published from August 1, 2016, through July 31, 2026.Eligibility was structured according to the Population, Intervention, Comparator, and Outcomes (PICO) framework, and study selection followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 (PRISMA 2020) guidelines.Five studies involving 465 participants were included in a narrative synthesis.Metoprolol did not restore impaired cardiac reserve or improve cardiac morphology in established cirrhotic cardiomyopathy.In refractory ascites, propranolol suppressed sympathetic support of systolic function, reduced renal perfusion pressure, and impaired renal function.Conversely, carvedilol-based targeted heart-rate reduction, with ivabradine added when required, improved left ventricular diastolic function and was associated with fewer episodes of acute kidney injury and hepatic encephalopathy, although mortality was not significantly reduced in the randomized comparison.Ularitide caused clinically important reductions in blood pressure, decreased urine output, and increased adverse reactions, while targeted albumin therapy did not improve cardiovascular biomarkers, renal dysfunction, or survival.The four randomized study results raised some concerns about bias, while the nonrandomized study had moderate risk of bias.These findings indicate that cardiovascular interventions in cirrhosis cannot be characterized as uniformly beneficial or harmful.Their effects may depend on disease severity, cardiac phenotype, and the extent to which sympathetic and hemodynamic compensation is required to preserve systemic and renal perfusion.Prospective, phenotype-stratified trials integrating cardiac, systemic, and renal endpoints are needed before individualized treatment strategies can be recommended.