Cirrhotic cardiomyopathy: pathophysiology, assessment, and implications for liver transplantation

Cirrhotic cardiomyopathy (CCM) is a distinct form of cardiac dysfunction in patients with advanced chronic liver disease, defined by subclinical diastolic impairment and, less commonly, systolic dysfunction, in the absence of primary cardiac disease. The entity reflects a dynamic interplay between structural, functional, and biochemical alterations in the cirrhotic heart, compounded by the systemic effects of portal hypertension and inflammation. Recent advances in diagnostic criteria, most notably the 2020 CCM Consortium (CCC-2020) definitions, have refined diagnostics and aligned CCM with contemporary concepts of heart failure (HF). Nevertheless, conventional echocardiography provides only a static assessment, often underestimating cardiac vulnerability, whereas stress testing and novel imaging modalities highlight the central role of blunted cardiac reserve as a predictor of adverse outcomes. CCM is a stress-intolerant phenotype, with important implications in liver transplantation (LT), both peri- and post-operatively. Subclinical CCM is not considered a contraindication to LT, but accumulating evidence associates it with increased risk of post-LT HF and major adverse cardiac events, even though long-term survival is generally unaffected. Emerging data also challenge the long-held assumption of universal reversibility post-LT, suggesting variable trajectories of recovery that may extend over years. In the era of metabolic-associated steatotic liver disease, the intersection of persistent cardiac dysfunction with cardiometabolic multimorbidity further underscores the need for proactive surveillance post-LT and tailored management strategies. This review synthesizes current knowledge on CCM pathophysiology, assessment, and transplant implications, and highlights future research priorities, including risk prediction models, dynamic functional testing, and the potential role of HF therapies.