Cirrhotic cardiomyopathy

Abstract

Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

Clinical implications of the hyperdynamic syndrome in cirrhosis

“…A number of studies have reported electrophysiological abnormalities as common findings of cardiac dysfunction in liver cirrhosis. Electrocardiographic abnormalities are an early manifestation of cardiac changes in patients with liver disease: a prolongation of the QT interval, which is the hallmark of the ECG alterations could be related to severity of liver disease [83,84]. Worsening of cardiac function after OLT, however, is brief and resolves within about 6 months, when the hyperdynamic circulation disappears.…”

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

“…The pathophysiological background of the diastolic dysfunction in cirrhosis is the increased stiffness of the myocardial wall, which is often caused by myocardial hypertrophy and fibrosis due to activation of the RAAS [29]. Subendothelial edema and increased interstitial collagen deposition play a further role in the decreased ability for relaxation [2,8]. Based on the severity of diastolic heart function, patients may be relatively asymptomatic.…”

“…The functional and structural changes of the myocardium have been referred as cirrhotic cardiomyopathy (CCM), a slow progression myocardial dysfunction associated with cirrhosis [1]. Most importantly, this condition should not be confused with alcoholic cardiomyopathy where the underlying mechanism responsible for the structural and functional cardiac abnormalities is well defined [2]. In contrast to alcoholic cardiac disease, in the case of CCM any well-defined underlying provoking factor(s) can be identified; however, sometimes iron overload or alcohol consumption may worsen the already hampered structural and functional condition of the myocardium [3].…”

QT Interval Prolongation and QRS Voltage Reduction in Patients with Liver Cirrhosis

“…Cirrhotic cardiomyopathy develops in about half of all cirrhotic patients and markedly affects the long-term morbidity and mortality of those patients [1][2][3]. Cirrhotic cardiomyopathy results from multifactorial organic myocardial changes and is defined as systolic and diastolic cardiac dysfunction with co-existing electrocardiographic (ECG) abnormalities or abnormal serologic markers (brain natriuretic peptide [BNP], troponin 1, adrenomedullin) in patients with cirrhosis in the absence of cardiac diseases [1,2,4]. Patients with decompensated cirrhosis have been demonstrated to have elevated levels of the N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and left ventricle (LV) diastolic dysfunction [5].…”