For many years, it has been known that impaired liver function and portal hypertension are associated with a pronounced splanchnic vasodilatation. This leads to important circulatory changes with displacement of the circulating blood volume resulting in central hypovolemia [1]. The combination of effective hypovolemia, arterial hypotension, and baroreceptor-activation of potent vasoconstricting systems such as the sympathetic nervous system leads to a hyperdynamic circulation and a multi-organ failure including impaired function of the heart [2]. In a patient with a full-blown decompensated state of cirrhosis, the heart rate and cardiac output are typically increased [1]. Both experimental and clinical studies have shown that the dimensions of the cirrhotic heart are augmented and the contractility and electromechanical function are impaired [3, 4]. This condition has been termed cirrhotic cardiomyopathy, which designates a cardiac dysfunction that includes impaired cardiac contractility with systolic and diastolic dysfunction and electromechanical abnormalities in the absence of other known causes of cardiac disease [4]. Cirrhotic cardiomyopathy can be demasked by physical or pharmacological stress, which may reveal in particular a systolic dysfunction, which seems to contribute to several cirrhotic complications such as the formation of ascites [5, 6] and the development of hepatic nephropathy [7, 8]. Additionally, cirrhotic cardiomyopathy seems associated with the development of heart failure in relation to invasive procedures such as shunt insertion and liver transplantation [9, 10]. Abnormal left ventricular diastolic function, caused by decreased left ventricular compliance and relaxation, implies an abnormal filling pattern of the ventricles. The transmitral blood flow is changed, with an increased atrial contribution to the late ventricular filling [4]. The pathophysiological background of the diastolic dysfunction in cirrhosis is an increased stiffness of the myocardial wall, most likely because of a combination of mild myocardial hypertrophy, fibrosis, and subendothelial edema [2, 3]. The increase in myocardial stiffness is also reflected by other parameters of diastolic dysfunction, such as a prolonged time for the ventricles to relax after diastolic filling at a specific end-diastolic volume, which reflects an increased resistance to the ventricular inflow [4]. Natriuretic peptides are regarded as markers of volume overload and impaired contractility, and are released by stretch of the atrial fibers such as in patients with ascites where the right atrium has been reported increased partly because of volume overload with expanded blood volume [1, 4]. However, the interpretation of increased natriuretic peptides in patients who from a functional point of view suffer from effective hypovolemia is complex. Activation of the renin–angiotensin–aldosterone system (RAAS) is associated with cardiac disease such as hypertrophy and heart failure, and seems to be related to diastolic dysfunction in both cirrhotic and non-cirrhotic patients with portal hypertension [11]. Furthermore, RAAS may induce fibrosis, and there is evidence of relationships between plasma aldosterone and E/A ratio; thus, RAAS may be both directly and indirectly involved in diastolic dysfunction [4]. Echocardiography is the method more frequently utilised for the detection of left ventricular diastolic dysfunction. Diastolic dysfunction is expressed as a decreased S. Moller (&) Department of Clinical Physiology and Nuclear Medicine 239, Faculty of Health Sciences, Hvidovre Hospital, Centre of Functional Imaging and Research, University of Copenhagen, 2650 Hvidovre, Denmark e-mail: soeren.moeller@regionh.dk
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May 23, 2016
Liv Andrés-Jensen + 9
Open Access