Effect of chronic β-blockade on QT interval in patients with liver cirrhosis

Zambruni, Andrea; Trevisani, Franco; Micoli, Antonio Di; Savelli, Francesco; Berzigotti, Annalisa; Bracci, E.; Caraceni, Paolo; Domenicali, Marco; Felline, Palmiro; Zoli, Marco; Bernardi, Mauro

doi:10.1016/j.jhep.2007.11.012

Cited by 83 publications

(63 citation statements)

References 38 publications

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“…A Danish study did not demonstrate any correlation between a prolonged QT interval and the severity of portal hypertension in patients with cirrhosis; the QTc intervals were comparable in patients with mild (HVPG < 12 mm Hg) and severe (HVPG ≥ 12 mm Hg) portal hypertension, [22]. Similar results were presented by Zambruni et al [23].…”

Section: Discussionsupporting

confidence: 73%

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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Section: Discussionsupporting

confidence: 73%

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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“…In patients with normal baseline values, the QT interval was not found to be changed by β-blockade. Accordingly, the exact role of chronic β-adrenoceptor blockade in the arrhythmogenesis in cirrhotic patients is not fully elucidated and needs further investigation [52].…”

Section: Qt Interval and Dispersionmentioning

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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“…Zambruni and colleagues [93] assessed the effects of chronic administration of a nonselective b-blocker on QT intervals in a cohort of cirrhotic patients with varying degrees of decompensation. This was effective in reducing the QT interval only in patients with a baseline prolonged QT interval, but it lengthened the QT interval in those with normal baseline QT intervals.…”

Section: Treatment Of Cirrhotic Cardiomyopathymentioning

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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Effect of chronic β-blockade on QT interval in patients with liver cirrhosis

Cited by 83 publications

References 38 publications

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

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

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Cirrhotic cardiomyopathy

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