Cirrhotic Cardiomyopathy

Zardi, Enrico Maria; Abbate, Antonio; Zardi, Domenico Maria; Dobrina, Aldo; Margiotta, Domenico Paolo Emanuele; Tassel, Benjamin W. Van; Afeltra, Antonella; Sanyal, Arun J.

doi:10.1016/j.jacc.2009.12.075

Cited by 314 publications

(318 citation statements)

References 88 publications

(109 reference statements)

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“…Therefore, the clinical significance J Gastrointestin Liver Dis, September 2014 Vol. 23 No 3 of QT prolongation in cirrhosis still remains to be clarified [42]. Prolongation of the QT interval may also worsen after TIPS insertion both in cirrhotic and non-cirrhotic portal hypertensive patients.…”

Section: Qt Interval and Dispersionmentioning

confidence: 99%

“…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]. In CCM, left and right ventricular contractile function may decrease resulting in an altered responsiveness to physical, physiological and pharmacological activity, leading to the characteristic symptoms of heart failure [4].…”

Section: Introductionmentioning

confidence: 99%

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Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Páll¹,

Czifra²,

Vitális³

et al. 2014

JGLD

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Hyperdynamic circulation, systolic and diastolic left ventricular dysfunction and certain electrophysiological abnormalities have been associated with cirrhosis and known for a long time. These clinical features have been introduced as cirrhotic cardiomyopathy (CCM), which is characterized by blunted myocardial contractile responsiveness to physical, physiological and pharmacological stress. Importantly, cardiac dysfunction can be reversible and can improve due to effective medical treatment and also after liver transplantation. Echocardiography and electrocardiography are essential tools for recognizing the characteristic changes in the myocardial function and also the alterations in the electrophysiological properties of the heart. Laboratory markers are auxiliary modalities further aiding the establishment of the correct diagnosis. In this review, we aimed to collect the pathophysiological background and clinical characteristics of CCM with the intention of summarizing the current possibilities for the diagnosis establishment and treatment of this cardio-hepatic disorder.Abbreviations: A: late diastolic transmitral peak flow velocity; ACE: angiotensin converting enzyme; ANP: atrial natriuretic peptide; ARB: angiotensin receptor blocker; BNP: brain natriuretic peptide; cAMP: cyclic adenosine monophosphate; CCM: cirrhotic cardiomyopathy; CGRP: calcitonin gene-related peptide; CO: carbon monoxide; DD: diastolic dysfunction; DT: deceleration time; E: early diastolic transmitral peak flow velocity; Ea: early diastolic velocity of the septal mitral annulus; EF: ejection fraction; MUGA: Multi Gated Acquisition Scan; NO: nitric oxide; NSBB: non-selective beta-blocker; pro-BNP: pro-brain natriuretic peptide; QTc: corrected QT interval; RAAS: renin-angiotensin aldosterone system; RALES: Randomized Aldactone Evaluation Study; suPAR: urokinase-type plasminogen activator receptor; TDI: Tissue Doppler Imaging; TIPS: transjugular intrahepatic portosystemic shunt; TNF-alpha: tumor necrosis factor-alpha.

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Section: Qt Interval and Dispersionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Páll¹,

Czifra²,

Vitális³

et al. 2014

JGLD

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“…This condition is independent of the etiology of cirrhosis and has been linked to an impairment of myocardial structure and function [77]. However, several studies have reported a wide spectrum of cardiovascular changes in cirrhotic patients, ranging from the sub-clinical stage of compensated liver disease to the typical hyperkinetic state of HS in decompensated disease [78,79].…”

Section: Cirrhotic Cardiomyopathymentioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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“…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]. Cirrhotic cardiomyopathy is characterized by blunted contractile responsiveness to stress and/or altered diastolic relaxation with electrophysiological abnormalities in the absence of any other known cardiac disease, in patients with liver cirrhosis [6]. The pathogenetic mechanisms of cirrhotic cardiomyopathy include abnormalities in the beta-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects [1,7].…”

mentioning

confidence: 99%

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

Cichoż‐Lach¹,

Tomaszewski²,

Kowalik³

et al. 2015

Adv Clin Exp Med

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Background. Liver cirrhosis is associated with functional abnormalities of the cardiovascular system with coexisting electrocardiographic (ECG) abnormalities. Objectives.The aim was to analyze ECG changes in patients with cirrhosis, to evaluate whether alcoholic etiology of cirrhosis and ascites has an impact on ECG changes. Material and Methods. The study involved 81 patients with previously untreated alcoholic cirrhosis (64 patients with ascites, classes B and C according to the Child-Pugh classification; and 17 without ascites, categorized as class A); 41 patients with previously untreated cirrhosis due to chronic hepatitis C (HCV -30 patients with ascites, classes B and C; and 11 without ascites, class A); 42 with alcoholic steatohepatitis and 46 with alcoholic steatosis. The control group consisted of 32 healthy volunteers. Twelve-lead ECG recordings were performed and selected parameters were measured. Results. Significantly longer QT and QTc intervals and lower QRS voltage were found in patients with alcoholic and HCV cirrhosis compared to the controls. Significantly lower QRS voltage was found in subjects with ascites than in those without ascites. Removal of ascites significantly increased QRS voltage. Conclusions. In cirrhosis, irrespective of etiology, ECG changes involved prolonged QT and QTc intervals and reduced QRS voltage. Prolonged QT and QTc intervals were not related to the severity of cirrhosis or to the presence of ascites. However, low QRS voltage was associated with the presence of ascites. Removal of ascites reverses low QRS voltage (Adv Clin Exp Med 2015, 24, 4, 615-622).

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Cirrhotic Cardiomyopathy

Cited by 314 publications

References 88 publications

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Clinical implications of the hyperdynamic syndrome in cirrhosis

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

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