Cirrhotic Cardiomyopathy: Moving From Description to Intervention

Prevalent cardiovascular disease in liver transplant (LT) candidates is estimated at 15%–30% and is a leading cause of morbidity and mortality after transplant.1 Cardiac-specific mortality is the most common cause of death in patients with metabolic dysfunction-associated steatotic liver disease2 and the second most common indication for adult LT.3 Cirrhotic cardiomyopathy (CCM) is present in 30%–80% of LT candidates4 and is defined as subclinical myocardial dysfunction in the absence of primary heart disease in patients with cirrhosis.5 CCM is associated with hyperdynamic circulation, low systemic vascular resistance, and metabolic and inflammatory derangements seen in progressive liver cirrhosis. Post-LT manifestations of CCM range from early cardiogenic shock to late-onset congestive heart failure (HF) across a broad range of left ventricular ejection fractions (LVEFs). Extensive literature describes alterations in the renin-angiotensin-aldosterone and sympathetic pathways, with associated structural changes in the myocardium including monocyte/macrophage infiltration and decreased contractility and fibrosis. Clinical evidence for development of CCM can be found in subtle electrocardiogram changes, including prolonged QTc interval, and a blunted response to dobutamine used in cardiac stress testing. Cardiologists asked to risk-stratify these patients preoperatively or assist in the management of post-LT cardiogenic/mixed shock or less severe congestive HF, we review the preoperative prolonged QTc and the advanced echo images and then get to the business of deploying HF therapies, which sometimes includes temporary mechanical circulatory support. In 2020, the International Cirrhotic Cardiomyopathy Consortium (CCC-2020) updated its consensus diagnostic guidelines for CCM, which were originally established in 2005 by the Montreal World Congress of Gastroenterology. CCM by echocardiographic criteria is defined as systolic dysfunction; LVEF