Cirrhotic cardiomyopathy is a form of myocardial dysfunction specific to patients with cirrhosis, consisting of normal systolic function at rest, systolic incompetence under conditions of stress, increased thickness of the left ventricle, associated with impaired relaxation during diastole, and electrophysiological abnormalities [1]. All these changes occur independently of the underlying etiology of cirrhosis and in the absence of any known causes of cardiac disease [2]. Although first thought to be an academic novelty, the condition is now increasingly recognized as an important issue in cirrhosis, contributing to many complications of cirrhosis and negatively impacting survival. For example, systolic incompetence in cirrhotic patients with ascites and spontaneous bacterial peritonitis has been implicated in the development of renal dysfunction [3], the presence of diastolic dysfunction is associated with slow clearance of ascites following the insertion of a transjugular intrahepatic portosystemic stent shunt for the treatment of refractory ascites [4], while increasing severity of diastolic dysfunction in cirrhosis is linked to worse survival [5].Of the various aspects of cirrhotic cardiomyopathy, diastolic dysfunction is the most commonly investigated entity, as it has a prevalence of up to 64 % [5][6][7], and it is present at rest in affected patients and can be diagnosed with well-defined diagnostic criteria [8] and fairly standardized techniques. Diastolic dysfunction is said to be present when there is a failure of the left ventricle to relax during diastole, thereby impeding the filling of the left ventricle. The first indication of diastolic dysfunction is demonstrated by a decreased early filling of the left ventricle (E wave), slower deceleration of the jet stream of blood as it enters the left ventricle, and a greater dependence on the atrial systole to contribute to the final filling of the left ventricle (A wave). The echocardiographic findings that correspond to these changes include a reduced E/A ratio of \1 and a prolonged deceleration time when pulsed Doppler analysis of the transmitral flow pattern is used. Supportive findings include a prolonged isovolumic relaxation time (the time interval in the cardiac cycle from the closure of the aortic valve, to onset of filling by opening of the mitral valve), and/or thickened myocardium. As the diastolic dysfunction progresses, left ventricular compliance is reduced, which increases left atrial pressure and, in turn, increases early left ventricular filling despite impaired relaxation. This paradoxical normalization of the E/A ratio is called pseudonormalization. Further reduction in left ventricular compliance will lead to a stiffer ventricle. Left atrial pressure is markedly elevated and compensates with vigorous early diastolic filling. This 'restrictive' filling pattern is associated with an abrupt deceleration of flow with little additional filling during mid-diastole and atrial contraction, thus providing a markedly elevated E/A ratio [9] (Fig...