Cardiac alterations in cirrhosis: reversibility after liver transplantation

Torregrosa, Miquel; Aguadé, Santi; Dos, Laura; Segura, Rosa; González, Antonio; Evangelista, Artur; Castell, Joan Martí i; Margarit, C; Esteban, Rafael; Guardia, J.; Genescà, Joan

doi:10.1016/j.jhep.2004.09.008

Cited by 280 publications

(228 citation statements)

References 28 publications

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“…Worsening of cardiac function after OLT, however, is brief and resolves within about 6 months, when the hyperdynamic circulation disappears. A normalization of cardiac function and amelioration of electrophysiological abnormalities are usually observed in these patients [78,85,86]. In conclusion, clinical understanding of CC in endstage liver disease is the best way to avoid life-threatening consequences in patients undergoing special procedures (TIPS or OLT).…”

Section: Cirrhotic Cardiomyopathymentioning

confidence: 91%

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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Section: Cirrhotic Cardiomyopathymentioning

confidence: 91%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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“…Interestingly, it seems to cure the associated cardiomyopathy as well [20]. Previously, amelioration of left ventricular hypertrophy, diastolic (lusitropic) dysfunction and normalization of the contractile function after transplantation have been reported [7]. Prolonged QTc has also been shown to be reversible by liver transplantation, despite remaining lengthened right after the surgery [94].…”

Section: Liver Transplantationmentioning

confidence: 98%

“…In the case of CCM, appearance of electrophysiological abnormalities may result in an increased risk for the development of both atrial and ventricular rhythm disturbances. Fortunately, these abnormalities may be reversible after liver transplantation [7]. Cardiac dysfunction is considered to be multifactorial in chronic liver diseases.…”

Section: Introductionmentioning

confidence: 99%

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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“…Diastolic dysfunction becomes more pronounced in the first 3 months posttransplant, possibly owing to increased ventricular hypertrophy [89]. When followed long-term for more than 1 year, there is complete reversal of cardiac changes in the posttransplant patients [90].…”

Section: Clinical Presentations and Consequences Of Cirrhotic Cardiommentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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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.

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Cardiac alterations in cirrhosis: reversibility after liver transplantation

Cited by 280 publications

References 28 publications

Clinical implications of the hyperdynamic syndrome in cirrhosis

Clinical implications of the hyperdynamic syndrome in cirrhosis

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Cirrhotic cardiomyopathy

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