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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Apr 8, 2015; 7(4): 662-672
Published online Apr 8, 2015. doi: 10.4254/wjh.v7.i4.662
Arrhythmia risk in liver cirrhosis
Ioana Mozos, Department of Functional Sciences, “Victor Babes” University of Medicine and Pharmacy, 300173 Timisoara, Romania
Author contributions: Mozos I reviewed the literature and wrote the manuscript.
Conflict-of-interest: No potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Ioana Mozos, MD, PhD, Associate Professor, Department of Functional Sciences, “Victor Babes” University of Medicine and Pharmacy, T. Vladimirescu Street 14, 300173 Timisoara, Romania.
Telephone: +40-745-610004 Fax: +40-256-490626
Received: August 23, 2014
Peer-review started: August 24, 2014
First decision: October 14, 2014
Revised: December 4, 2014
Accepted: January 15, 2015
Article in press: January 19, 2015
Published online: April 8, 2015


Interactions between the functioning of the heart and the liver have been described, with heart diseases affecting the liver, liver diseases affecting the heart, and conditions that simultaneously affect both. The heart is one of the most adversely affected organs in patients with liver cirrhosis. For example, arrhythmias and electrocardiographic changes are observed in patients with liver cirrhosis. The risk for arrhythmia is influenced by factors such as cirrhotic cardiomyopathy, cardiac ion channel remodeling, electrolyte imbalances, impaired autonomic function, hepatorenal syndrome, metabolic abnormalities, advanced age, inflammatory syndrome, stressful events, impaired drug metabolism and comorbidities. Close monitoring of cirrhotic patients is needed for arrhythmias, particularly when QT interval-prolonging drugs are given, or if electrolyte imbalances or hepatorenal syndrome appear. Arrhythmia risk may persist after liver transplantation due to possible QT interval prolongation, persistence of the parasympathetic impairment, post-transplant reperfusion and chronic immunosuppression, as well as consideration of the fact that the transplant itself is a stressful event for the cardiovascular system. The aims of the present article were to provide a review of the most important data regarding the epidemiology, pathophysiology, and biomarkers of arrhythmia risk in patients with liver cirrhosis, to elucidate the association with long-term outcome, and to propose future research directions.

Key Words: Arrhythmia, Atrial fibrillation, Cirrhotic cardiomyopathy, Electrocardiography, Liver cirrhosis, Liver transplantation, Sudden cardiac death, Tpeak-Tend interval, Ventricular tachycardia, Long-QT syndrome

Core tip: Arrhythmias and electrocardiographic changes occur in several non-cardiac diseases, including liver cirrhosis. Supraventricular and ventricular arrhythmias, including atrial fibrillation and flutter, and premature atrial and ventricular contractions, have been reported in cirrhotic patients. It is questionable whether the prevalence of atrial fibrillation and flutter is high in patients with liver cirrhosis, or if liver cirrhosis protects against supraventricular arrhythmias.


Interactions between the functioning of the heart and the liver have been described, with heart diseases affecting the liver, liver diseases affecting the heart, and conditions that simultaneously affect both[1,2]. Thus, it is important for both hepatologists and cardiologists to understand the relationship between the liver and the heart. Indeed, involvement of the cardiovascular system in end-stage liver disease is well recognized, and there are reports of cardiovascular symptoms in patients with liver cirrhosis, including chronotropic incompetence, cardiomyopathy, prolonged QT intervals, hyperdynamic circulation with an increased cardiac output and decreased peripheral vascular resistance, and impaired ventricular contractility in response to physiologic and pharmacologic stimuli[3,4].

Liver cirrhosis is a fatal condition, and is most often caused by harmful alcohol consumption, metabolic syndrome related to being overweight or obese, or hepatitis B or C virus infection[5,6]. Arrhythmias and electrocardiographic changes can occur with liver cirrhosis, for which cases of atrial fibrillation and flutter, premature atrial and ventricular contractions, and ventricular arrhythmias have been reported[7]. The most important risk factors for arrhythmias in patients with cirrhosis include cirrhotic cardiomyopathy, cardiac ion channel remodeling, electrolyte imbalances, impaired autonomic function, hepatorenal syndrome, metabolic abnormalities, advanced age, inflammatory syndrome, and comorbidities. The aims of the present article were to provide a review of the most important data regarding the epidemiology, pathophysiology and biomarkers of arrhythmia risk in patients with liver cirrhosis, to elucidate the association with long-term outcome, and to propose future research directions.


The heart is one of the most adversely affected organs in patients with liver cirrhosis[8]. Cirrhotic cardiomyopathy can appear in all forms of cirrhosis due to physical or pharmacologic stress, and includes increased cardiac output, decreased response to physiologic and pharmacologic stimuli, systolic and diastolic dysfunction, and electrophysiologic abnormalities in the absence of any known cardiac disease[1,9-11]. Cirrhotic cardiomyopathy involves changes affecting the cardiomyocyte plasma membrane, attenuated stimulatory pathways, and increased activities of inhibitory systems[3]. In order to differentiate between cardiomyopathy resulting from cirrhosis with cardiomyopathy due to the underlying cause of cirrhosis, Zaky et al[8] prefer the term “cirrhosis-associated cardiomyopathy”.

Diastolic dysfunction at rest is present in most cirrhotic patients, is more prevalent in those with ascites[12], and precedes the development of systolic dysfunction[9]. Although severe heart failure due to cirrhotic cardiomyopathy is rare, its prevalence is unknown, considering that the disease is latent, and becomes apparent when the patient is subjected to a stressful event, including exercise, drugs, hemorrhage, infections, and surgery[9,13]. At least one feature of cardiomyopathy is present in the majority of patients with severe or moderate liver failure, though the association between liver disease severity and cardiac dysfunction is controversial[9,12]. Cirrhotic cardiomyopathy is reversible after liver transplantation[14] and may contribute to the pathogenesis of hepatorenal syndrome[9].

Structural and histologic changes in cardiac chambers and subsequent structural myocardial heterogeneity may contribute to electrical instability. Increased left ventricular wall thickness was described as a supportive criterion in patients with cirrhotic cardiomyopathy[15], and it is known to impair myocardial oxygen demand. Myocardial hypertrophy (left ventricular hypertrophy and increased interventricular septum) and fibrosis cause diastolic dysfunction and contribute to structural heterogeneity and arrhythmia risk[2]. Autopsy studies have described subendocardial and myocyte edema and patchy fibrosis, in addition to myocardial hypertrophy[16]. However, further studies are needed to confirm the relationship between cardiac structural heterogeneity and arrhythmic events in cirrhotic patients.


Multiple electrophysiologic abnormalities have been described in liver cirrhosis, including prolonged QT intervals, increased QT dispersion, chronotropic incompetence, and electromechanical uncoupling. These signs occur in the absence of known cardiovascular disease, and are related to autonomic dysfunction, severe portal hypertension, liver dysfunction, cytokines and endotoxins, and are independent of the cause of cirrhosis[1,7,17-19].

The QT interval varies from daytime to nighttime due to the diurnal variations in autonomic tone, circulatory status and oxygen demands[18,20]; the minimum value of the corrected QT (QTc), rather than the maximum value, shows a significant diurnal variation[20]. The Bazett formula incompletely corrects the QT interval for heart rate, and the Fridericia method is therefore suggested to be the most reliable and valid[7]. Chronotropic incompetence refers to lack of heart rate response to physiologic and pharmacologic demands, including exercise, head tilt, inotropes, and increased norepinephrine concentrations[8], which limits exercise capacity. Electromechanical uncoupling leads to the dyssynchrony between electrical and mechanical systole[8].

Long QT intervals

A prolonged QT interval, found incidentally by Kowalski et al[21], is the electrophysiologic hallmark of cirrhotic cardiomyopathy. It represents the most common electrocardiographic finding in patients with liver cirrhosis, appearing in half of cirrhotic patients[4,10,22,23], with a higher incidence than in patients with mild chronic active hepatitis[24]. Prolongation of the QT interval predisposes the patients to a potentially fatal polymorphic ventricular tachycardia called torsade de pointes, which can degenerate into ventricular fibrillation and cause sudden cardiac death[25]. Delayed repolarization of cardiomyocytes due to potassium channel abnormalities and sympathoadrenergic hyperactivity may contribute to QT interval prolongation[17,18,26]. The main factors associated with QT interval prolongation in cirrhotic patients are reviewed in Table 1. Gender difference in the QTc interval is abolished in cirrhosis, which is not influenced by gonadal hormones nor restored after liver transplantation[27].

Table 1 Factors associated with QT prolongation in liver cirrhosis.
Autonomic neuropathyPlasma norepinephrine, diurnal variations
Liver dysfunctionChild-Pugh class, portal hypertension, pediatric end-stage liver disease score
Serum markersElectrolytes, serum uric acid, serum bile salts, creatinine, plasma renin activity, aldosterone, atrial natriuretic factor, gonadal hormones, norepinephrine
Volume overloadLeft ventricular end diastolic dimensions
Coronary heart diseaseRisk factors: older age, male gender, smoking, arterial hypertension, diabetes mellitus
Left ventricular hypertrophy-
Stressful eventsAcute gastrointestinal bleeding
Drugs: excessive accumulation, impaired metabolization, distribution, or excretionErythromycin, fluoroquinolones, telipressin, sevoflurane

QT prolongation in liver pathology was first described in alcoholic liver diseases[28], and has since been associated with alcoholic etiology in patients with liver cirrhosis[10,19,29]. Chronic, heavy alcohol consumption affects both the heart and the liver, increases the mass and impairs the function of the left ventricle[1,30], and causes subclinical heart muscle injury, patchy delays in conduction and cardiac arrhythmias[31]. Delays in intraventricular conduction and nonuniform myocardial involvement have been described in alcoholic cardiomyopathy[30], and life-threatening ventricular arrhythmias are found in alcoholics without heart disease[32]. Alcohol alters the resting membrane potential due to inhibition of sodium-potassium-ATPase, delays calcium binding and transport by the cardiac sarcoplasmic reticulum, and impairs calcium channels[33]. Acute alcoholic states, including binge drinking and the “holiday heart syndrome,” are also associated with an increased prevalence of cardiac arrhythmias and sudden cardiac death[34]. The amount and duration of alcohol intake is related to life-threatening arrhythmias, though small quantities can be significant in susceptible individuals[35]. On the other hand, a protective effect of moderate alcohol consumption against sudden cardiac death has also been demonstrated[36,37], likely related to polyphenols, increased concentrations of high-density lipoprotein cholesterol, fibrinolysis, and polyunsaturated fatty acids, decreased platelet aggregation and coagulation factors, with beneficial effects on endothelial function and inflammation[38]. Arrhythmogenesis may be attributed to the hyperadrenergic state of drinking and withdrawal, electrolyte imbalances, impaired vagal heart rate control, repolarization abnormalities with prolonged QT intervals, worsening of myocardial ischemia, or sleep apnea[31].

Prolonged QT intervals have been reported in patients with primary biliary cirrhosis and other chronic non-alcoholic liver diseases, and were shown to be associated with the severity of autonomic neuropathy and increased cardiovascular risk[39], as well as with the pathophysiology of cirrhosis and liver dysfunction[17,40,41]. A prolonged QT interval is common in children with chronic liver disease[42], where it is related to the pediatric end-stage liver disease score, portal hypertension, and high mortality[43]. QT interval prolongation is proportional to the Child-Pugh class[10,17,16], and is related to the presence of portal hypertension, including mild portal hypertension[18,22,44,43], liver dysfunction[44], hepatic venous pressure gradient[22], and markers of hyperdynamic circulation[40]. Furthermore, plasma calcium level[22], serum uric acid[10], serum bile salts, electrolytes, creatinine, plasma renin activity, aldosterone, atrial natriuretic factor, and gonadal hormones are associated with prolonged QT intervals in patients with liver cirrhosis[17,45]. QT interval is also related to cardiac serum markers, but not to vasodilator (endothelin-3, calcitonin gene-related peptide) or vasoconstrictor (endothelin-1) markers[46]. A multivariate analysis showed that plasma norepinephrine was independently correlated with QTc duration, demonstrating that sympathoadrenergic hyperactivity is a risk factor for QT prolongation[17,47]. Disturbances of excitation-contraction coupling have been reported in cirrhotic patients with QT interval prolongation, attributable to defective potassium channel function in ventricular cardiomyocytes[18,40]. Moaref et al[13] showed a positive correlation between QT prolongation and left ventricular end diastolic dimensions in cirrhotic patients, indicating a direct relationship between electrophysiologic changes and the severity of volume overload. Volume overload is related to the progression of liver cirrhosis and prolongation of the repolarization time by the stretching of myofibers, and volume control is recommended in cirrhotic patients to prevent decompensation[13].

Prolonged QTc is related to an increased mortality rate in patients with chronic liver diseases[48]. Among these, patients with a QTc longer than 440 ms have a significantly lower survival rate than those with normal QTc[17]. The clinical significance of QT prolongation in liver cirrhosis is unclear, considering that sudden cardiac death and torsade de pointes are rare[9]. However, acute gastrointestinal bleeding further prolongs QTc in patients with liver cirrhosis, which predicts bleeding-induced mortality[49]. QT prolongation and electromechanical dyssynchrony have not been observed in septic cardiodepression, the inflammatory phenotype of cardiac dysfunction that is mediated through cytokines[15].

Drug-induced QT prolongation

Child-Pugh and model for end-stage liver disease scores correlate with drug clearance[50]. As a result, patients with liver disease often require dosage adjustments in order to prevent adverse effects caused by excessive drug or metabolite accumulation[51]. Accumulation results from altered activity of drug-metabolizing enzymes and drug distribution, as well as from impaired renal excretion. For example, the activity of cytochrome P450 3A, the most abundant hepatic drug-metabolizing enzyme, is reduced in liver cirrhosis[51,52]. The activity of this enzyme varies according to the etiology and severity of liver disease[51,53]. Patients with transjugular intrahepatic portosystemic shunts are at increased risk for abnormal QT prolongation when exposed to oral cytochrome P450 substrates with QT-prolonging effects[54].

Drugs affecting the QT interval should be avoided in patients with liver cirrhosis, or used with caution under close ECG monitoring[2]. For example, the use of fluoroquinolones as secondary prophylaxis for spontaneous bacterial peritonitis in cirrhotic patients can predict QT prolongation[19]. Drug administration should be critically reviewed, with consideration of indications, interactions and adverse reactions, to prevent drug-induced torsade de pointes[55] and QT prolongation, particularly in patients with hepatic failure[56,57]. Werner et al[55] described a case of secondary torsade de pointes tachycardia in a 50-year-old patient with alcoholic liver cirrhosis who was admitted for hematemesis and melena after administration of QT-active drugs. Chung et al[58] reported a case of torsade de pointes after induction of anesthesia for liver transplantation with QT prolonging drugs: sevoflurane (to maintain anesthesia) and palonosetron (for postoperative nausea and vomiting). Faigel et al[45] also reported prolonged QT intervals and torsade de pointes in three cirrhotic patients with bleeding esophageal varices who received endoscopic sclerotherapy, vasopressin and neuroleptics. Lehmann et al[59] presented a patient with newly diagnosed cirrhosis and kidney failure who underwent cardiopulmonary resuscitation twice after terlipressin, an analogue of vasopressin.

Ventricular repolarization

The Tpe corresponds to the transmural dispersion of repolarization, and is a predictor of ventricular arrhythmias and sudden cardiac death[60-62]. The Tpe/QT ratio is also used as an index of ventricular arrhythmogenesis[63]. A prolonged Tpe interval and Tpe/QT interval ratio have been reported in patients with chronic hepatitis B infection, indicating an increased ventricular repolarization heterogeneity[64]. Liver cirrhosis affects ventricular repolarization via electrolyte imbalances, impaired autonomic function, subclinical cardiomyopathy, reduced β-adrenergic receptor function, post-receptor pathway defects, altered physical properties of myocyte plasma membranes, elevated levels of cardiotoxins, ion channel remodeling, portosystemic shunting, and systemic circulatory disturbances[10,16,22,44,65,66].

Late ventricular potentials

Chronic alcoholics exhibit late ventricular potentials, low-amplitude and high-frequency waveforms appearing in the terminal part of the ECG QRS complex, which are predictors of re-entry ventricular tachycardia and sudden cardiac death[35,67]. Late ventricular potentials are associated with histologically significant fatty liver caused by chronic alcohol intake, revealing preclinical myocardial lesions and identifying alcoholic patients at risk of lethal arrhythmias[68].

Ion channel remodeling

Cardiac ion channel remodeling, particularly of potassium channels, occurs in patients with liver cirrhosis[26]. Moreover, reduced transient outward and delayed rectifier potassium currents have been detected in ventricular myocytes from cirrhotic animals[26], which prolong the action potential and the QT interval[7]. Ionic channels, as well β-adrenergic receptors and G proteins, are altered by endotoxins and increased biliary acids in patients with cholestasis[16].


Patients with liver cirrhosis show impaired autonomic cardiovascular reflexes, with the parasympathetic system more commonly affected than the sympathetic system[7]. The escape of systemic and intestinal vasodilators from degraded, diseased liver and the formation of new blood vessels in the gut explain arteriolar vasodilation of the systemic and splanchnic circulations[8]. The reduction in circulating blood volume and hyperdynamic circulation enhances the activities of the sympathetic nervous and renin-angiotensin-aldosterone systems. The resulting increased cardiac output and reduced systemic vascular resistance may induce myocardial remodeling and left ventricular hypertrophy, causing systolic and diastolic dysfunction and cardiomyopathy[7,8]. Sympathetic overactivity is associated with an increase in inflammatory cytokines, such as interleukin-1b, -6 and -8, tumor necrosis factor (TNF)-α, and transforming growth factor-β[8], which is a profibrogenic and proapoptotic stimulant[18]. Cardiovascular autonomic dysfunction has also been described in chronic alcoholic liver disease and chronic hepatitis B and C virus infections[64].


Palpitations, dyspnea, angina chest discomfort, electrocardiographic changes, tachycardia and bradycardia have all been described in patients with viral hepatitis[69], myocarditis, acute pericarditis and cardiomyopathy[70-72]. Sinus tachycardia occurs in most patients and is related to the febrile response[72]. Myocarditis may be a serious extrahepatic complication, and hepatitis B virus antigens have been detected in small intramyocardial vessels[71]. The cardiac abnormalities may be caused by viral infection, hyperbilirubinemia, hemorrhage in the myocardium and pericardium, or by immune mechanisms[69,71]. Chronic hepatitis B infection triggers autoimmune disorders and several extrahepatic disorders may appear, including of the ganglia and the heart[73]. Endothelial progenitor cells may serve as a virus carrier, enabling transinfection in injured endothelial cells to cause hepatitis B virus-associated myocarditis[73]. Hayashi et al[69] reported a case of fulminant hepatitis complicated with myocarditis, with myocardial infarction-like electrocardiographic changes. Hepatitis C virus infection has been detected often in patients with dilated and hypertrophic cardiomyopathy, and may be an important causal agent in the pathogenesis of the disease and cause arrhythmias[72,74]. Interferon, successfully used to treat patients with chronic hepatitis C infections, may induce several cardiovascular complications, such as tachycardia, myocardial infarction and congestive heart failure[75].


Cell death is a central mechanism involved in liver damage, for which several promising noninvasive biomarkers have been associated with QT prolongation, including soluble cytokeratin 18, TNF and TNF-related apoptosis-inducing ligand receptors and their ligands, various isoforms of high mobility group box-1, small non-coding RNAs (microRNAs) and microparticles (extracellular vesicles)[76]. These biomarkers could be utilized in future studies to assess arrhythmia risk in liver cirrhosis. Fibrosis serum markers, such as hyaluronic acid and laminin[77], may also be indicators of electrophysiologic abnormalities in cirrhotic patients.

Natriuretic peptides are produced by the cardiac atrial and ventricular myocytes[78], and are higher in myocardial ischemia, heart failure and left ventricular tachycardia, as well as in liver cirrhosis and renal failure[79]. Plasma levels of N-terminal pro-brain natriuretic peptide (BNP) are useful markers of increased cardiovascular risk, cardiac subclinical dysfunction, atrial volume, and early decompensation of cirrhosis, and are increased proportionate to the stage of chronic liver disease[78]. Elevated levels of BNP are related to interventricular septal thickness and the impairment of diastolic function in asymptomatic patients with cirrhosis, and may be a marker of the presence of cirrhotic cardiomyopathy[80]. Henriksen et al[81] also reported that circulating pro-BNP and BNP are related to severity of liver disease (Child-Pugh score, serum albumin, coagulation factors and hepatic venous pressure gradient) and markers of cardiac dysfunction (QT interval, heart rate and plasma volume), but not to indicators of hyperdynamic circulation.


Cirrhotic patients also have an increased risk and prevalence of coronary heart disease, which is also a cause of QT prolongation[1,82,83]. Risk factors for coronary heart disease, such as older age, male gender, smoking and arterial hypertension[82,84], are independent predictors of several electrocardiographic abnormalities in cirrhotic patients[19]. Moreover, liver disease severity is associated with many electrocardiographic features of coronary heart disease[19]. Considering low serum cholesterol, low blood pressure values and higher levels of circulating estrogens, cirrhosis should protect against coronary atherosclerosis[82]. However, recent reports have demonstrated an increased prevalence of major risk factors for atherosclerosis and cardiovascular disease in liver cirrhosis, especially in nonalcoholic steatohepatitis-cirrhosis[19,85]. Hypercholesterolemia in patients with primary biliary cirrhosis should be considered a cardiovascular risk factor, and further studies are needed to confirm if arrhythmias are related to it.

Arrhythmias are also associated with hypoxia and orthodeoxia due to hepatopulmonary syndrome. Hepatorenal syndrome may be another important contributor, influenced by systolic dysfunction and insufficient ventricular contractile reserve[2,86]. Ventricular arrhythmia risk and sudden cardiac death are increased in patients with renal failure, and even mild reductions in kidney function can alter the electrophysiologic properties of the myocardium[87]. Arrhythmia risk is related not only to renal function, but also to electrolyte imbalances, sympathetic activity, and levels of parathyroid hormone, hemoglobin, hematocrit and inflammatory markers[87].

Accumulation of bile acids in the liver due to obstructed ducts results in high circulating concentrations[88], with immunosuppressive effects[89]. In addition to the concentration, the composition of bile acids is important for arrhythmogenesis[90]. Taurocholic acid, a conjugated primary bile acid, has a negative inotropic effect and reduces the duration of the action potentials in the ventricular myocytes by reducing inward sodium and calcium and increasing outward potassium currents[88]. The increased level of non-ursodeoxycholic acids in patients with arrhythmias suggests that ursodeoxycholic acids provide cardioprotective and hepatoprotective effects[90]. Although the exact intracellular effects of bile salts are not clear, they may act on muscarinic or cell-surface bile acid receptors involved in the regulation of macrophage functions[89] or directly damage cardiac calcium channels due to the detergent-like properties[91].


Atrial fibrillation and flutter are arrhythmias that are more frequently diagnosed in cirrhotic patients, and are significantly associated with arteriosclerosis, hypercholesterolemia and diabetes mellitus[92]. Atrial fibrillation after septic shock and sinus bradycardia with cardiac arrest were reported after living-donor liver transplantation in a 58-year-old man diagnosed with hepatocellular carcinoma and liver cirrhosis, which required resuscitation and temporary pacing[93]. Josefsson et al[19] reported several supraventricular arrhythmias in cirrhotic patients, such as atrial and junctional premature beats, atrial flutter or fibrillation, sinus tachycardia or bradycardia. Pre-transplant evaluation of cirrhotic patients also revealed atrioventricular-conduction defects, such as complete or incomplete right or left bundle branch block and intraventricular blocks.

Inflammation may promote cardiac and arrhythmogenic complications in non-alcoholic fatty liver disease[94]. Patients with liver fibrosis have elevated plasma levels of inflammatory markers, and several studies have indicated that inflammation plays a significant role in the generation, maintenance, and perpetuation of atrial fibrillation[95]. However, Zamirian et al[96] suggested that liver cirrhosis has a protective effect against atrial fibrillation, despite significant metabolic abnormalities, inflammatory syndrome and enlarged left atria. The low prevalence of atrial fibrillation observed in their study may be the result of the accumulation of anti-arrhythmic or anti-inflammatory substances that are normally metabolized by an intact functioning liver; this would explain the development of atrial fibrillation after liver transplantation[96]. However, no data concerning the influence of inflammation in the relationship of arrhythmias and liver cirrhosis have been reported, which should be the aim of future studies.

The low prevalence atrial fibrillation in cirrhotic patients reported by Zamirian et al[96] may also have been related to the low prevalence of systemic hypertension in their patients or the administration of medications (spironolactone and beta-blockers) that reduce atrial excitability. Spironolactone reduces myocardial fibrosis of dilated atria and P-wave duration, producing an antifibrotic effect in the ventricles and reducing QT interval duration[97,98]. Beta-blockers are given as prophylaxis for variceal bleeding, such as for large esophageal varices, resulting in vasoconstriction in the splanchnic compartment, which increases preload and improves diastolic function[78]. Beta-blocker therapy may also prevent bleeding from portal hypertensive gastropathy and the development of spontaneous bacterial peritonitis. However, recent studies have warned about their use in decompensated cirrhosis, as they are associated with poor survival[99,100]. Beta-blockers decrease chronotropy and depress atrioventricular conduction, resulting in bradycardia or high-grade heart block[100].

Myocardial fibrosis is dysrhythmogenic[98], and atrial interstitial fibrosis is associated with changes in the electrical properties of the atria, including depressed excitability, increased refractoriness and conduction slowing or block[96,101]. Angiotensin-converting enzyme (ACE) inhibitors protect against myocardial fibrosis and prevent cardiac remodeling[102] and atrial fibrillation[103]. Drugs that interfere with the renin-angiotensin system, such as angiotensin II-receptor blockers, also prevent atrial remodeling[103]. However, ACE inhibitors and other afterload-reducing drugs should be used with caution considering the risk for aggravating the vasodilatory state[2].

Statins are known for their pleiotropic and anti-hypertrophic effects, suppressing arrhythmogenesis and improving endothelial function[104]. Desensitization of cardiac myocytes to catecholamines due to downregulation of beta-adrenergic receptors in the myocardium of cirrhotic patients could also be a protective mechanism against occurrence of tachyarrhythmia and atrial fibrillation[96].

The main mechanisms explaining the influence of cirrhosis on the higher prevalence or the protection against atrial fibrillation are reviewed in Table 2.

Table 2 Atrial fibrillation in patients with liver cirrhosis.
Higher prevalence due toLower prevalence due to
Enlarged left atria (cirrhotic cardiomyopathy)Accumulation of antiarrhythmic and anti-inflammatory substances
Electrolyte imbalancesLow prevalence of hypertension
Hepatorenal syndromeMedication: diuretics, beta-blockers, ACE-inhibitors, statins
Serum bile acid concentrationDownregulation of beta-adrenergic receptors in the myocardium
Metabolic abnormalities
Inflammatory syndrome
Atrial interstitial fibrosis

No specific therapy can be recommended for cirrhotic patients with heart conditions, but it should be supportive and directed against heart failure and pulmonary stasis[1,15]. Surgical stress, including transjugular intrahepatic portosystemic shunt insertion, surgical portosystemic shunting and liver transplantation can facilitate heart failure[15,103]. However, severe heart failure can be prevented by vasodilated peripheral circulation, which unloads the heart, and a compensatory decrease of some negatively inotropic regulatory mechanisms[15]. Aldosterone antagonists may reduce left ventricular dilatation and wall thickness, and improve diastolic function[15]. QT interval prolongation may be improved by beta-blockers, which also lower portal pressure and reduce the hyperdynamic load, but their effect on contractile dysfunction and mortality should be the focus of further studies[15,105].

Liver transplantation is currently the only proven treatment for patients with cirrhotic cardiomyopathy[11] and can improve cardiac hypertrophy, diastolic and systolic function, and autonomic dysfunction[1,2,14,15,29,41,106,107]. The prolonged QT interval reverses in approximately half of the patients after liver transplantation, likely a consequence of diminished portosystemic shunting, but can also be prolonged[27,108]. Total cardiac events after liver transplantation, particularly arrhythmias, and post-transplant mortality are associated with prolonged QTc and the presence of a Q wave[19]. A prolonged QTc interval also predicts post-transplant atrial arrhythmias[19] and peri-transplant heart failure[109]. However, liver transplantation is a stressful event for the cardiovascular system of the patients with advanced liver disease, considering also the advanced age and comorbidities[110]. Furthermore, liver transplantation highlights the limitation of the cardiac reserve, even in patients with no previous history of cardiac disease[15]. Although autonomic dysfunction, measured by heart rate variability, is partially corrected 2-6 years after liver transplantation, parasympathetic impairment is not improved[107].

Considering the high prevalence of cirrhotic cardiomyopathy and coronary heart disease and the high perioperative mortality, a careful cardiac evaluation of patients with liver cirrhosis is required before liver transplantation, including electrocardiography, cardiopulmonary exercise testing, dobutamine stress echocardiography, coronary angiography and myocardial perfusion imaging, and coronary multidetector computed tomography angiography[1,105,111]. Post-transplant reperfusion may result in cardiac death due to arrhythmias, acute heart failure, and myocardial infarction[15,110,112]. Risk factors for arrhythmia occurring during reperfusion of the graft are severe hydroelectrolytic and acid-base imbalances and hypothermia[112]. The most important risk factors for arrhythmias after liver transplantation are included in Table 3. Zaballos et al[112] reported the case of a man with severe hemodynamic alterations who developed atrioventricular re-entry tachycardia related to dual nodal conduction during liver transplantation. Kobayashi et al[93] reported complete atrioventricular block and cardiac arrest with diffuse myocardial abscesses after liver transplantation in a woman with liver cirrhosis and hepatocellular carcinoma, which required resuscitation and temporary cardiac pacing. Chin et al[113] described a case of torsade de pointes and a prolonged QTc after liver transplantation in a 39-year-old male patient with hepatitis B-related cirrhosis, which was due to low hematocrit and a low arterial blood pressure, demonstrating the importance of an optimal coronary perfusion to prevent sudden cardiac death. Cardiovascular disease also contributes to late mortality after transplantation, due to the secondary development of hypertension, hyperlipidemia, diabetes and obesity from chronic immunosuppression[82].

Table 3 Risk factors for arrhythmias after liver transplantation.
Risk factor
Stress of major surgery
Advanced age
Comorbidities: low blood pressure, anemia, limitation of the cardiac reserve
Hydroelectrolytic and acid-base imbalances
Secondary development of hypertension, diabetes mellitus, obesity

The latency of cirrhotic cardiomyopathy requires careful assessment of arrhythmia risk in cirrhotic patients. To evaluate the predictive value of ventricular repolarization indices in liver cirrhosis, further follow-up studies are needed. In particular, future studies should focus on the relationships between arrhythmia risk and structural heterogeneity of the cirrhotic heart, markers of inflammation, fibrosis and immunologic syndromes, and biomarkers of liver cell death and active infection. Close monitoring of cirrhotic patients is needed for arrhythmias, particularly when QT interval-prolonging drugs are given, or if electrolyte imbalances or hepatorenal syndrome appear. Arrhythmia risk may persist after liver transplantation due to possible QT interval prolongation, persistence of the parasympathetic impairment, post-transplant reperfusion and chronic immunosuppression, as well as consideration of the fact that the transplant itself is a stressful event for the cardiovascular system.


P- Reviewer: Sirin G, Sunami Y, Xiong XJ, Wang CX S- Editor: Qi Y L- Editor: A E- Editor: Liu SQ

1.  Møller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J. 2013;34:2804-2811.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 259]  [Cited by in F6Publishing: 271]  [Article Influence: 24.6]  [Reference Citation Analysis (0)]
2.  Fouad YM, Yehia R. Hepato-cardiac disorders. World J Hepatol. 2014;6:41-54.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 89]  [Cited by in F6Publishing: 78]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
3.  Al Hamoudi W, Lee SS. Cirrhotic cardiomyopathy. Ann Hepatol. 2006;5:132-139.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Mozos I. Ventricular arrhythmia risk in noncardiac diseases. Cardiac arrhythmias. Mechanisms, pathophysiology and treatment. Croatia: In Tech 2014; 89-109.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  Wiegand J, Berg T. The etiology, diagnosis and prevention of liver cirrhosis: part 1 of a series on liver cirrhosis. Dtsch Arztebl Int. 2013;110:85-91.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 23]  [Cited by in F6Publishing: 73]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
6.  Blachier M, Leleu H, Peck-Radosavljevic M, Valla DC, Roudot-Thoraval F. The burden of liver disease in Europe: a review of available epidemiological data. J Hepatol. 2013;58:593-608.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 879]  [Cited by in F6Publishing: 868]  [Article Influence: 78.9]  [Reference Citation Analysis (0)]
7.  Boyer TD, Manns MP, Sanyal AJ.  Zakim and Boyerʼs Hepatology. A Textbook of Liver Disease. Philadelphia: Elsevier, Saunders 2012; .  [PubMed]  [DOI]  [Cited in This Article: ]
8.  Zaky A, Lang JD. Cirrhosis-associated cardiomyopathy. J Anesth Clin Res. 2012;3:266.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 5]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
9.  Baik SK, Fouad TR, Lee SS. Cirrhotic cardiomyopathy. Orphanet J Rare Dis. 2007;2:15.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 75]  [Cited by in F6Publishing: 78]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
10.  Mozos I, Costea C, Serban C, Susan L. Factors associated with a prolonged QT interval in liver cirrhosis patients. J Electrocardiol. 2011;44:105-108.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 21]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
11.  Wiese S, Hove JD, Bendtsen F, Møller S. Cirrhotic cardiomyopathy: pathogenesis and clinical relevance. Nat Rev Gastroenterol Hepatol. 2014;11:177-186.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 155]  [Cited by in F6Publishing: 159]  [Article Influence: 15.9]  [Reference Citation Analysis (0)]
12.  Merli M, Calicchia A, Ruffa A, Pellicori P, Riggio O, Giusto M, Gaudio C, Torromeo C. Cardiac dysfunction in cirrhosis is not associated with the severity of liver disease. Eur J Intern Med. 2013;24:172-176.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 49]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
13.  Moaref A, Zamirian M, Yazdani M, Salehi O, Sayadi M, Aghasadeghi K. The Correlation between Echocardiographic Findings and QT Interval in Cirrhotic Patients. Int Cardiovasc Res J. 2014;8:39-43.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Huffman C, Wagman G, Fudim M, Zolty R, Vittorio T. Reversible cardiomyopathies--a review. Transplant Proc. 2010;42:3673-3678.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 23]  [Cited by in F6Publishing: 26]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
15.  Yang YY, Lin HC. The heart: pathophysiology and clinical implications of cirrhotic cardiomyopathy. J Chin Med Assoc. 2012;75:619-623.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 20]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
16.  Wong F. Cirrhotic cardiomyopathy. Hepatol Int. 2009;3:294-304.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 129]  [Cited by in F6Publishing: 124]  [Article Influence: 7.8]  [Reference Citation Analysis (0)]
17.  Bernardi M, Calandra S, Colantoni A, Trevisani F, Raimondo ML, Sica G, Schepis F, Mandini M, Simoni P, Contin M. Q-T interval prolongation in cirrhosis: prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors. Hepatology. 1998;27:28-34.  [PubMed]  [DOI]  [Cited in This Article: ]
18.  Zardi EM, Abbate A, Zardi DM, Dobrina A, Margiotta D, Van Tassell BW, Afeltra A, Sanyal AJ. Cirrhotic cardiomyopathy. J Am Coll Cardiol. 2010;56:539-549.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 214]  [Cited by in F6Publishing: 214]  [Article Influence: 15.3]  [Reference Citation Analysis (0)]
19.  Josefsson A, Fu M, Björnsson E, Kalaitzakis E. Prevalence of pre-transplant electrocardiographic abnormalities and post-transplant cardiac events in patients with liver cirrhosis. BMC Gastroenterol. 2014;14:65.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 31]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
20.  Hansen S, Møller S, Bendtsen F, Jensen G, Henriksen JH. Diurnal variation and dispersion in QT interval in cirrhosis: relation to haemodynamic changes. J Hepatol. 2007;47:373-380.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 38]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
21.  Kowalski HJ, Abelmann WH. The cardiac output at rest in Laennec’s cirrhosis. J Clin Invest. 1953;32:1025-1033.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 410]  [Cited by in F6Publishing: 444]  [Article Influence: 6.3]  [Reference Citation Analysis (0)]
22.  Genovesi S, Prata Pizzala DM, Pozzi M, Ratti L, Milanese M, Pieruzzi F, Vincenti A, Stella A, Mancia G, Stramba-Badiale M. QT interval prolongation and decreased heart rate variability in cirrhotic patients: relevance of hepatic venous pressure gradient and serum calcium. Clin Sci (Lond). 2009;116:851-859.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 73]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
23.  Bernardi M, Maggioli C, Dibra V, Zaccherini G. QT interval prolongation in liver cirrhosis: innocent bystander or serious threat? Expert Rev Gastroenterol Hepatol. 2012;6:57-66.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 66]  [Cited by in F6Publishing: 61]  [Article Influence: 5.1]  [Reference Citation Analysis (0)]
24.  Akiyama T, Batchelder J, Worsman J, Moses HW, Jedlinski M. Hypocalcemic Torsades de Pointes. J Electrocardiol. 1989;22:89-92.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Del Rosario ME, Weachter R, Flaker GC. Drug-induced QT prolongation and sudden death. Mo Med. 2010;107:53-58.  [PubMed]  [DOI]  [Cited in This Article: ]
26.  Ward CA, Ma Z, Lee SS, Giles WR. Potassium currents in atrial and ventricular myocytes from a rat model of cirrhosis. Am J Physiol. 1997;273:G537-G544.  [PubMed]  [DOI]  [Cited in This Article: ]
27.  Adigun AQ, Pinto AG, Flockhart DA, Gorski JC, Li L, Hall SD, Chalasani N. Effect of cirrhosis and liver transplantation on the gender difference in QT interval. Am J Cardiol. 2005;95:691-694.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 39]  [Cited by in F6Publishing: 39]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
28.  Day CP, James OF, Butler TJ, Campbell RW. QT prolongation and sudden cardiac death in patients with alcoholic liver disease. Lancet. 1993;341:1423-1428.  [PubMed]  [DOI]  [Cited in This Article: ]
29.  Finucci G, Lunardi F, Sacerdoti D, Volpin R, Bortoluzzi A, Bombonato G, Angeli P, Gatta A. Q-T interval prolongation in liver cirrhosis. Reversibility after orthotopic liver transplantation. Jpn Heart J. 1998;39:321-329.  [PubMed]  [DOI]  [Cited in This Article: ]
30.  Luca C. Electrophysiological properties of right heart and atrioventricular conducting system in patients with alcoholic cardiomyopathy. Br Heart J. 1979;42:274-281.  [PubMed]  [DOI]  [Cited in This Article: ]
31.  Kupari M, Koskinen P. Alcohol, cardiac arrhythmias and sudden death. Novartis Found Symp. 1998;216:68-79; discussion 79-85.  [PubMed]  [DOI]  [Cited in This Article: ]
32.  Moushmoush B, Abi-Mansour P. Alcohol and the heart. The long-term effects of alcohol on the cardiovascular system. Arch Intern Med. 1991;151:36-42.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 29]  [Cited by in F6Publishing: 27]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
33.  Lorsheyd A, de Lange DW, Hijmering ML, Cramer MJ, van de Wiel A. PR and OTc interval prolongation on the electrocardiogram after binge drinking in healthy individuals. Neth J Med. 2005;63:59-63.  [PubMed]  [DOI]  [Cited in This Article: ]
34.  Mozos I, Serban C, Mihaescu R. Late ventricular potentials in cardiac and extracardiac diseases. Cardiac arrhythmias-New considerations, Croatia: In Tech 2012; 227-256.  [PubMed]  [DOI]  [Cited in This Article: ]
35.  Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death) developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Europace. 2006;8:746-837.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 372]  [Cited by in F6Publishing: 357]  [Article Influence: 19.8]  [Reference Citation Analysis (0)]
36.  Priori SG, Aliot E, Blomstrom-Lundqvist C, Bossaert L, Breithardt G, Brugada P, Camm AJ, Cappato R, Cobbe SM, Di Mario C. Task Force on Sudden Cardiac Death of the European Society of Cardiology. Eur Heart J. 2001;22:1374-1450.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 540]  [Cited by in F6Publishing: 563]  [Article Influence: 24.5]  [Reference Citation Analysis (0)]
37.  de Vreede-Swagemakers JJ, Gorgels AP, Weijenberg MP, Dubois-Arbouw WI, Golombeck B, van Ree JW, Knottnerus A, Wellens HJ. Risk indicators for out-of-hospital cardiac arrest in patients with coronary artery disease. J Clin Epidemiol. 1999;52:601-607.  [PubMed]  [DOI]  [Cited in This Article: ]
38.  di Giuseppe R, de Lorgeril M, Salen P, Laporte F, Di Castelnuovo A, Krogh V, Siani A, Arnout J, Cappuccio FP, van Dongen M. Alcohol consumption and n-3 polyunsaturated fatty acids in healthy men and women from 3 European populations. Am J Clin Nutr. 2009;89:354-362.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 76]  [Cited by in F6Publishing: 79]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
39.  Kempler P, Szalay F, Váradi A, Keresztes K, Kádár E, Tánczos E, Petrik J. Prolongation of the QTc-interval reflects the severity of autonomic neuropathy in primary biliary cirrhosis and in other non-alcoholic liver diseases. Z Gastroenterol. 1993;31 Suppl 2:96-98.  [PubMed]  [DOI]  [Cited in This Article: ]
40.  Henriksen JH, Fuglsang S, Bendtsen F, Christensen E, Møller S. Dyssynchronous electrical and mechanical systole in patients with cirrhosis. J Hepatol. 2002;36:513-520.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 85]  [Cited by in F6Publishing: 76]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
41.  Zamirian M, Tavassoli M, Aghasadeghi K. Corrected QT interval and QT dispersion in cirrhotic patients before and after liver transplantation. Arch Iran Med. 2012;15:375-377.  [PubMed]  [DOI]  [Cited in This Article: ]
42.  Fishberger SB, Pittman NS, Rossi AF. Prolongation of the QT interval in children with liver failure. Clin Cardiol. 1999;22:658-660.  [PubMed]  [DOI]  [Cited in This Article: ]
43.  Arikan C, Kilic M, Tumgor G, Levent E, Yuksekkaya HA, Yagci RV, Aydogdu S. Impact of liver transplantation on rate-corrected QT interval and myocardial function in children with chronic liver disease*. Pediatr Transplant. 2009;13:300-306.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 22]  [Cited by in F6Publishing: 21]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
44.  Ytting H, Henriksen JH, Fuglsang S, Bendtsen F, Møller S. Prolonged Q-T(c) interval in mild portal hypertensive cirrhosis. J Hepatol. 2005;43:637-644.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 40]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
45.  Faigel DO, Metz DC, Kochman ML. Torsade de pointes complicating the treatment of bleeding esophageal varices: association with neuroleptics, vasopressin, and electrolyte imbalance. Am J Gastroenterol. 1995;90:822-824.  [PubMed]  [DOI]  [Cited in This Article: ]
46.  Henriksen JH, Gülberg V, Fuglsang S, Schifter S, Bendtsen F, Gerbes AL, Møller S. Q-T interval (QT(C)) in patients with cirrhosis: relation to vasoactive peptides and heart rate. Scand J Clin Lab Invest. 2007;67:643-653.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 18]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]
47.  Camm AJ, Yap YG, Malik M.  Acquired long QT syndrome. 2007;.  [PubMed]  [DOI]  [Cited in This Article: ]
48.  Kosar F, Ates F, Sahin I, Karincaoglu M, Yildirim B. QT interval analysis in patients with chronic liver disease: a prospective study. Angiology. 2007;58:218-224.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 25]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
49.  Trevisani F, Di Micoli A, Zambruni A, Biselli M, Santi V, Erroi V, Lenzi B, Caraceni P, Domenicali M, Cavazza M. QT interval prolongation by acute gastrointestinal bleeding in patients with cirrhosis. Liver Int. 2012;32:1510-1515.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 38]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
50.  Albarmawi A, Czock D, Gauss A, Ehehalt R, Lorenzo Bermejo J, Burhenne J, Ganten TM, Sauer P, Haefeli WE. CYP3A activity in severe liver cirrhosis correlates with Child-Pugh and model for end-stage liver disease (MELD) scores. Br J Clin Pharmacol. 2014;77:160-169.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 44]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
51.  Vuppalanchi R, Liang T, Goswami CP, Nalamasu R, Li L, Jones D, Wei R, Liu W, Sarasani V, Janga SC. Relationship between differential hepatic microRNA expression and decreased hepatic cytochrome P450 3A activity in cirrhosis. PLoS One. 2013;8:e74471.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 33]  [Cited by in F6Publishing: 33]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
52.  Chalasani N, Gorski JC, Patel NH, Hall SD, Galinsky RE. Hepatic and intestinal cytochrome P450 3A activity in cirrhosis: effects of transjugular intrahepatic portosystemic shunts. Hepatology. 2001;34:1103-1108.  [PubMed]  [DOI]  [Cited in This Article: ]
53.  Frye RF, Zgheib NK, Matzke GR, Chaves-Gnecco D, Rabinovitz M, Shaikh OS, Branch RA. Liver disease selectively modulates cytochrome P450--mediated metabolism. Clin Pharmacol Ther. 2006;80:235-245.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 172]  [Cited by in F6Publishing: 176]  [Article Influence: 9.8]  [Reference Citation Analysis (0)]
54.  Vuppalanchi R, Juluri R, Ghabril M, Kim S, Thong N, Gorski JC, Chalasani N, Hall SD. Drug-induced QT prolongation in cirrhotic patients with transjugular intrahepatic portosystemic shunt. J Clin Gastroenterol. 2011;45:638-642.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 8]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
55.  Werner CR, Riessen R, Gregor M, Bitzer M. [Unexpected complication following esophageal variceal hemorrhage - Case 2/2011]. Dtsch Med Wochenschr. 2011;136:217.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 2]  [Article Influence: 0.2]  [Reference Citation Analysis (0)]
56.  Stanek EJ, Simko RJ, DeNofrio D, Pavri BB. Prolonged quinidine half-life with associated toxicity in a patient with hepatic failure. Pharmacotherapy. 1997;17:622-625.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 2]  [Reference Citation Analysis (0)]
57.  Barre J, Mallat A, Rosenbaum J, Deforges L, Houin G, Dhumeaux D, Tillement JP. Pharmacokinetics of erythromycin in patients with severe cirrhosis. Respective influence of decreased serum binding and impaired liver metabolic capacity. Br J Clin Pharmacol. 1987;23:753-757.  [PubMed]  [DOI]  [Cited in This Article: ]
58.  Chung EJ, Jeon YS, Kim HJ, Lee KH, Lee JW, Han KA, Jung SH. Torsade de pointes in liver transplantation recipient after induction of general anesthesia: a case report. Korean J Anesthesiol. 2014;66:80-84.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 9]  [Article Influence: 0.9]  [Reference Citation Analysis (0)]
59.  Lehmann M, Bruns T, Herrmann A, Fritzenwanger M, Stallmach A. [54-year-old male with hepatic cirrhosis and therapy-associated torsade de pointes tachycardia]. Internist (Berl). 2011;52:445-48, 450.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 5]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
60.  Castro Hevia J, Antzelevitch C, Tornés Bárzaga F, Dorantes Sánchez M, Dorticós Balea F, Zayas Molina R, Quiñones Pérez MA, Fayad Rodríguez Y. Tpeak-Tend and Tpeak-Tend dispersion as risk factors for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome. J Am Coll Cardiol. 2006;47:1828-1834.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 361]  [Cited by in F6Publishing: 350]  [Article Influence: 19.4]  [Reference Citation Analysis (0)]
61.  Antzelevitch C, Sicouri S, Di Diego JM, Burashnikov A, Viskin S, Shimizu W, Yan GX, Kowey P, Zhang L. Does Tpeak-Tend provide an index of transmural dispersion of repolarization? Heart Rhythm. 2007;4:1114-1116; author reply 1116-1119.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 182]  [Cited by in F6Publishing: 206]  [Article Influence: 12.1]  [Reference Citation Analysis (0)]
62.  Arteyeva NV, Goshka SL, Sedova KA, Bernikova OG, Azarov JE. What does the T(peak)-T(end) interval reflect? An experimental and model study. J Electrocardiol. 2013;46:296.e1-296.e8.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 39]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
63.  Kilicaslan F, Tokatli A, Ozdag F, Uzun M, Uz O, Isilak Z, Yiginer O, Yalcin M, Guney MS, Cebeci BS. Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio are prolonged in patients with moderate and severe obstructive sleep apnea. Pacing Clin Electrophysiol. 2012;35:966-972.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 48]  [Cited by in F6Publishing: 55]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
64.  Demir C, Demir M. Evaluation of Tp-e interval and Tp-e/QT ratio in patients with chronic hepatitis B. Prague Med Rep. 2013;114:239-245.  [PubMed]  [DOI]  [Cited in This Article: ]
65.  Zambruni A, Trevisani F, Caraceni P, Bernardi M. Cardiac electrophysiological abnormalities in patients with cirrhosis. J Hepatol. 2006;44:994-1002.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 118]  [Cited by in F6Publishing: 123]  [Article Influence: 6.8]  [Reference Citation Analysis (0)]
66.  Møller S, Hove JD, Dixen U, Bendtsen F. New insights into cirrhotic cardiomyopathy. Int J Cardiol. 2013;167:1101-1108.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 71]  [Cited by in F6Publishing: 78]  [Article Influence: 7.1]  [Reference Citation Analysis (0)]
67.  Benchimol Barbosa PR, Sousa MO, Barbosa EC, Bomfim Ade S, Ginefra P, Nadal J. Analysis of the prevalence of ventricular late potentials in the late phase of myocardial infarction based on the site of infarction. Arq Bras Cardiol. 2002;78:352-363.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 6]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
68.  Pochmalicki G, Genest M, Jibril H. Late ventricular potentials and heavy drinking. Heart. 1997;78:163-165.  [PubMed]  [DOI]  [Cited in This Article: ]
69.  Hayashi J, Kashiwagi S, Okeda T, Okamura H, Ishibashi H, Hiramatsu Y, Fujino T. Electrocardiographic changes related to hypersecretion of catecholamine in a patient with fulminant hepatitis. Jpn J Med. 1988;27:187-190.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 3]  [Article Influence: 0.1]  [Reference Citation Analysis (0)]
70.  Adler R, Takahashi M, Wright HT. Acute pericarditis associated with hepatitis B infection. Pediatrics. 1978;61:716-719.  [PubMed]  [DOI]  [Cited in This Article: ]
71.  Ursell PC, Habib A, Sharma P, Mesa-Tejada R, Lefkowitch JH, Fenoglio JJ. Hepatitis B virus and myocarditis. Hum Pathol. 1984;15:481-484.  [PubMed]  [DOI]  [Cited in This Article: ]
72.  Matsumori A, Sasayama S. Newer aspects of pathogenesis of heart failure: hepatitis C virus infection in myocarditis and cardiomyopathy. J Card Fail. 1996;2:S187-S194.  [PubMed]  [DOI]  [Cited in This Article: ]
73.  Rong Q, Huang J, Su E, Li J, Li J, Zhang L, Cao K. Infection of hepatitis B virus in extrahepatic endothelial tissues mediated by endothelial progenitor cells. Virol J. 2007;4:36.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 22]  [Cited by in F6Publishing: 23]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
74.  Matsumori A, Ohashi N, Hasegawa K, Sasayama S, Eto T, Imaizumi T, Izumi T, Kawamura K, Kawana M, Kimura A. Hepatitis C virus infection and heart diseases: a multicenter study in Japan. Jpn Circ J. 1998;62:389-391.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 42]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
75.  Matsumori A, Matoba Y, Sasayama S. Dilated cardiomyopathy associated with hepatitis C virus infection. Circulation. 1995;92:2519-2525.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 125]  [Cited by in F6Publishing: 105]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
76.  Eguchi A, Wree A, Feldstein AE. Biomarkers of liver cell death. J Hepatol. 2014;60:1063-1074.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 135]  [Cited by in F6Publishing: 140]  [Article Influence: 14.0]  [Reference Citation Analysis (0)]
77.  Li F, Zhu CL, Zhang H, Huang H, Wei Q, Zhu X, Cheng XY. Role of hyaluronic acid and laminin as serum markers for predicting significant fibrosis in patients with chronic hepatitis B. Braz J Infect Dis. 2012;16:9-14.  [PubMed]  [DOI]  [Cited in This Article: ]
78.  Licata A, Corrao S, Petta S, Genco C, Cardillo M, Calvaruso V, Cabibbo G, Massenti F, Cammà C, Licata G. NT pro BNP plasma level and atrial volume are linked to the severity of liver cirrhosis. PLoS One. 2013;8:e68364.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 23]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
79.  Panagopoulou V, Deftereos S, Kossyvakis C, Raisakis K, Giannopoulos G, Bouras G, Pyrgakis V, Cleman MW. NTproBNP: an important biomarker in cardiac diseases. Curr Top Med Chem. 2013;13:82-94.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 69]  [Cited by in F6Publishing: 74]  [Article Influence: 6.7]  [Reference Citation Analysis (0)]
80.  Wong F, Siu S, Liu P, Blendis LM. Brain natriuretic peptide: is it a predictor of cardiomyopathy in cirrhosis? Clin Sci (Lond). 2001;101:621-628.  [PubMed]  [DOI]  [Cited in This Article: ]
81.  Henriksen JH, Gøtze JP, Fuglsang S, Christensen E, Bendtsen F, Møller S. Increased circulating pro-brain natriuretic peptide (proBNP) and brain natriuretic peptide (BNP) in patients with cirrhosis: relation to cardiovascular dysfunction and severity of disease. Gut. 2003;52:1511-1517.  [PubMed]  [DOI]  [Cited in This Article: ]
82.  Garg A, Armstrong WF. Echocardiography in liver transplant candidates. JACC Cardiovasc Imaging. 2013;6:105-119.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 44]  [Cited by in F6Publishing: 36]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
83.  Keeffe BG, Valantine H, Keeffe EB. Detection and treatment of coronary artery disease in liver transplant candidates. Liver Transpl. 2001;7:755-761.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 68]  [Cited by in F6Publishing: 61]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
84.  Kalaitzakis E, Rosengren A, Skommevik T, Björnsson E. Coronary artery disease in patients with liver cirrhosis. Dig Dis Sci. 2010;55:467-475.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 64]  [Cited by in F6Publishing: 57]  [Article Influence: 4.1]  [Reference Citation Analysis (1)]
85.  Kadayifci A, Tan V, Ursell PC, Merriman RB, Bass NM. Clinical and pathologic risk factors for atherosclerosis in cirrhosis: a comparison between NASH-related cirrhosis and cirrhosis due to other aetiologies. J Hepatol. 2008;49:595-599.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 82]  [Cited by in F6Publishing: 81]  [Article Influence: 5.1]  [Reference Citation Analysis (0)]
86.  Ruiz-del-Arbol L, Monescillo A, Arocena C, Valer P, Ginès P, Moreira V, Milicua JM, Jiménez W, Arroyo V. Circulatory function and hepatorenal syndrome in cirrhosis. Hepatology. 2005;42:439-447.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 412]  [Cited by in F6Publishing: 364]  [Article Influence: 19.2]  [Reference Citation Analysis (0)]
87.  Mozos I. Laboratory markers of ventricular arrhythmia risk in renal failure. Biomed Res Int. 2014;2014:509204.  [PubMed]  [DOI]  [Cited in This Article: ]
88.  Binah O, Rubinstein I, Bomzon A, Better OS. Effects of bile acids on ventricular muscle contraction and electrophysiological properties: studies in rat papillary muscle and isolated ventricular myocytes. Naunyn Schmiedebergs Arch Pharmacol. 1987;335:160-165.  [PubMed]  [DOI]  [Cited in This Article: ]
89.  Kawamata Y, Fujii R, Hosoya M, Harada M, Yoshida H, Miwa M, Fukusumi S, Habata Y, Itoh T, Shintani Y. A G protein-coupled receptor responsive to bile acids. J Biol Chem. 2003;278:9435-9440.  [PubMed]  [DOI]  [Cited in This Article: ]
90.  Desai MS, Penny DJ. Bile acids induce arrhythmias: old metabolite, new tricks. Heart. 2013;99:1629-1630.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 20]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
91.  Rainer PP, Primessnig U, Harenkamp S, Doleschal B, Wallner M, Fauler G, Stojakovic T, Wachter R, Yates A, Groschner K. Bile acids induce arrhythmias in human atrial myocardium--implications for altered serum bile acid composition in patients with atrial fibrillation. Heart. 2013;99:1685-1692.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 54]  [Cited by in F6Publishing: 64]  [Article Influence: 5.8]  [Reference Citation Analysis (0)]
92.  Gundling F, Schmidtler F, Zelihic E, Seidl H, Haller B, Ronel J, Löffler N, Schepp W. [Frequency of cardiac arrhythmia in patients with liver cirrhoses and evaluation of associated factors]. Z Gastroenterol. 2012;50:1149-1155.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 8]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
93.  Kobayashi T, Sato Y, Yamamoto S, Oya H, Takeishi T, Kokai H, Hatakeyama K. Temporary cardiac pacing for fatal arrhythmia in living-donor liver transplantation: three case reports. Transplant Proc. 2008;40:2818-2820.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 4]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
94.  Ballestri S, Lonardo A, Bonapace S, Byrne CD, Loria P, Targher G. Risk of cardiovascular, cardiac and arrhythmic complications in patients with non-alcoholic fatty liver disease. World J Gastroenterol. 2014;20:1724-1745.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 184]  [Cited by in F6Publishing: 177]  [Article Influence: 17.7]  [Reference Citation Analysis (1)]
95.  Yap YG. Inflammation and atrial fibrillation: cause or para-phenomenon? Europace. 2009;11:980-981.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 9]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
96.  Zamirian M, Sarmadi T, Aghasadeghi K, Kazemi MB. Liver cirrhosis prevents atrial fibrillation: A reality or just an illusion? J Cardiovasc Dis Res. 2012;3:109-112.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 19]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
97.  Milliez P, Deangelis N, Rucker-Martin C, Leenhardt A, Vicaut E, Robidel E, Beaufils P, Delcayre C, Hatem SN. Spironolactone reduces fibrosis of dilated atria during heart failure in rats with myocardial infarction. Eur Heart J. 2005;26:2193-2199.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 143]  [Cited by in F6Publishing: 151]  [Article Influence: 7.9]  [Reference Citation Analysis (0)]
98.  Wong KY, Wong SY, McSwiggan S, Ogston SA, Sze KY, MacWalter RS, Struthers AD. Myocardial fibrosis and QTc are reduced following treatment with spironolactone or amiloride in stroke survivors: a randomised placebo-controlled cross-over trial. Int J Cardiol. 2013;168:5229-5233.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 13]  [Article Influence: 1.2]  [Reference Citation Analysis (0)]
99.  Sersté T, Melot C, Francoz C, Durand F, Rautou PE, Valla D, Moreau R, Lebrec D. Deleterious effects of beta-blockers on survival in patients with cirrhosis and refractory ascites. Hepatology. 2010;52:1017-1022.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 372]  [Cited by in F6Publishing: 348]  [Article Influence: 24.9]  [Reference Citation Analysis (1)]
100.  Ge PS, Runyon BA. The changing role of beta-blocker therapy in patients with cirrhosis. J Hepatol. 2014;60:643-653.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 90]  [Cited by in F6Publishing: 92]  [Article Influence: 9.2]  [Reference Citation Analysis (0)]
101.  Sanders P, Morton JB, Davidson NC, Spence SJ, Vohra JK, Sparks PB, Kalman JM. Electrical remodeling of the atria in congestive heart failure: electrophysiological and electroanatomic mapping in humans. Circulation. 2003;108:1461-1468.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 475]  [Cited by in F6Publishing: 465]  [Article Influence: 22.1]  [Reference Citation Analysis (0)]
102.  Yu M, Zheng Y, Sun HX, Yu DJ. Inhibitory effects of enalaprilat on rat cardiac fibroblast proliferation via ROS/P38MAPK/TGF-β1 signaling pathway. Molecules. 2012;17:2738-2751.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 33]  [Cited by in F6Publishing: 34]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
103.  Schaer BA, Schneider C, Jick SS, Conen D, Osswald S, Meier CR. Risk for incident atrial fibrillation in patients who receive antihypertensive drugs: a nested case-control study. Ann Intern Med. 2010;152:78-84.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 72]  [Cited by in F6Publishing: 75]  [Article Influence: 5.4]  [Reference Citation Analysis (0)]
104.  Tousoulis D, Oikonomou E, Siasos G, Stefanadis C. Statins in heart failure--With preserved and reduced ejection fraction. An update. Pharmacol Ther. 2014;141:79-91.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 18]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
105.  Møller S, Dümcke CW, Krag A. The heart and the liver. Expert Rev Gastroenterol Hepatol. 2009;3:51-64.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 38]  [Cited by in F6Publishing: 40]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
106.  Bal JS, Thuluvath PJ. Prolongation of QTc interval: relationship with etiology and severity of liver disease, mortality and liver transplantation. Liver Int. 2003;23:243-248.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 119]  [Cited by in F6Publishing: 123]  [Article Influence: 5.9]  [Reference Citation Analysis (1)]
107.  Baratta L, Tubani L, Merli M, Labbadia F, Facchini D, De Marco R, Rossi M, Attili AF, Berloco P, Ginanni Corradini S. Long-term effect of liver transplantation on cirrhotic autonomic cardiac dysfunction. Dig Liver Dis. 2010;42:131-136.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 10]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
108.  Carey EJ, Gautam M, Ingall T, Douglas DD. The effect of liver transplantation on autonomic dysfunction in patients with end-stage liver disease. Liver Transpl. 2008;14:235-239.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 18]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]
109.  Josefsson A, Fu M, Allayhari P, Björnsson E, Castedal M, Olausson M, Kalaitzakis E. Impact of peri-transplant heart failure & amp; left-ventricular diastolic dysfunction on outcomes following liver transplantation. Liver Int. 2012;32:1262-1269.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 24]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
110.  Rugină M, Predescu L, Sălăgean M, Gheorghe L, Gheorghe C, Tulbure D, Popescu I, Bubenek-Turconi S. Pre-liver transplantation, cardiac assessment. Chirurgia (Bucur). 2012;107:283-290.  [PubMed]  [DOI]  [Cited in This Article: ]
111.  Keeling AN, Flaherty JD, Davarpanah AH, Ambrosy A, Farrelly CT, Harinstein ME, Flamm SL, Abecassis MI, Skaro AI, Carr JC. Coronary multidetector computed tomographic angiography to evaluate coronary artery disease in liver transplant candidates: methods, feasibility and initial experience. J Cardiovasc Med (Hagerstown). 2011;12:460-468.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 38]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
112.  Zaballos M, Jimeno C, Jiménez C, Fraile JR, Almendral E. [Dual atrioventricular nodal conduction and arrhythmia with severe hemodynamic alterations during liver retransplantation]. Rev Esp Anestesiol Reanim. 2005;52:355-358.  [PubMed]  [DOI]  [Cited in This Article: ]
113.  Chin JH, Park JY, Kim YK, Kim SH, Kong YG, Park PH, Hwang GS. Torsades de pointes triggered by severe diastolic hypotension with low hematocrit in the neohepatic stage of liver transplantation: a case report. Transplant Proc. 2010;42:1959-1962.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 15]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]