Cirrhotic Cardiomyopathy: Pathophysiology, Diagnosis, and Clinical Management

Cirrhotic cardiomyopathy (CCM) is a syndrome of cardiac structural, functional, and electrophysiologic abnormalities arising in the setting of cirrhosis in the absence of preexisting primary heart disease. Its defining feature is not overt resting heart failure but an impairment of cardiac reserve: resting left ventricular ejection fraction is typically preserved or supranormal owing to the low-afterload, hyperdynamic state driven by splanchnic vasodilation and portal hypertension, yet contractile and chronotropic responses to stress are blunted. Over the past 2 decades, conceptualization of CCM has broadened from a purely “stress-unmasked systolic dysfunction” paradigm to a multidomain phenotype encompassing subclinical systolic dysfunction detectable by speckle-tracking global longitudinal strain, diastolic dysfunction defined by contemporary multi-parameter echocardiographic algorithms, QTc prolongation and other repolarization disturbances, and chronotropic incompetence—all superimposed on a background of neurohormonal activation and systemic inflammation. Diagnostic frameworks have evolved from the 2005 World Congress of Gastroenterology “Montreal” proposal to the 2019 CCM Consortium criteria, which integrate modern diastolic algorithms and global longitudinal strain to improve detection and reproducibility. Pooled prevalence approaches 50% across cirrhotic populations, though estimates vary substantially by criteria set, disease severity, and testing modality.