The clinical course of patients with advanced liver disease is complicated by progressive impairment in circulatory function characterised by low arterial pressure, high cardiac output, and decreased systemic vascular resistance.¹ Clinical and experimental investigations performed during the past two decades have shed light on the multiple mechanisms accounting for these disturbances. These studies have also established the pathogenic role of circulatory dysfunction in organ specific syndromes that commonly develop in cirrhotic patients, such as the hepatorenal and the hepatopulmonary syndromes.^2,3 The heart is another functionally compromised organ in cirrhotic patients. However, whether the hyperdynamic circulation, by overloading the heart, induces cirrhotic cardiomyopathy or whether this is a specific cardiac dysfunction of cirrhotic patients has been subject of extensive discussions.⁴

Cardiac function abnormalities in cirrhosis are clinically not apparent. However, when cardiac function is explored, a reduction in right ventricular volume, probably secondary to reduced venous return, and left ventricular dysfunction, characterised by left ventricular preload and volume, are observed.^5,6 Moreover, cardiac structural abnormalities, including hypertrophy of the myocardium and increased left ventricle thickness and hence diastolic dysfunction, have also been described.⁷ Cirrhotic cardiomyopathy is latent, probably because of the low peripheral vascular resistance presented by these patients, which reduces cardiac afterload. The existence of an abnormal ventricular behaviour can however be unveiled during exercise or following pharmacological stress. It has been demonstrated that left ventricular end diastolic pressure increases and stroke index and left ventricular ejection fraction decrease more …