Randomized, controlled trial of carvedilol versus nadolol plus isosorbide mononitrate for the prevention of variceal rebleeding

Lo, Gin‐Ho; Chen, Wen‐Chi; Wang, Huay-Min; Yu, Hsien‐Chung

doi:10.1111/j.1440-1746.2012.07244.x

Cited by 66 publications

(52 citation statements)

References 32 publications

(50 reference statements)

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“…Lo et al randomized 121 patients to treatment either with low dose carvedilol of 6.25-12.5 mg or with propranolol and ISMN. A rather high and equal number of rebleeding of 61 and 60 % occurred, respectively, and no difference in mortality was observed [ 21 ]. The high rebleeding rates are most likely due to the fact that the patients were not treated endoscopically with band ligation, which is contrary to international guidelines.…”

Section: Carvedilolcontrasting

confidence: 63%

Variceal Rebleeding: Drugs, Endoscopy or Both

Bendtsen

Möller

Krag

2014

Variceal Hemorrhage

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Section: Carvedilolcontrasting

confidence: 63%

Variceal Rebleeding: Drugs, Endoscopy or Both

Bendtsen

Möller

Krag

2014

Variceal Hemorrhage

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“…In the setting of prevention of recurrent VH, carvedilol has only been compared to EVL alone [19] or to NSBB + ISMN [20] but has not been compared to standard of care with the combination of NSBB + EVL. Therefore, carvedilol is not recommended in this setting [8] .…”

Section: Ascitesmentioning

confidence: 99%

Current Management of the Complications of Cirrhosis and Portal Hypertension: Variceal Hemorrhage, Ascites, and Spontaneous Bacterial Peritonitis

García–Tsao

2016

Dig Dis

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Cirrhosis is not a single entity but represents a disease progression across different prognostic stages, with the compensated and decompensated stages being the most important. Variceal hemorrhage (VH) and ascites are complications of cirrhosis that denote the presence of a decompensated stage. Spontaneous bacterial peritonitis (SBP) is a common bacterial infection unique to patients with cirrhosis that can precipitate the development of recurrent VH and hepatorenal syndrome (HRS), complications that denote the presence of a ‘further decompensated' stage of cirrhosis. Main current issues in the management of VH include identification of different prognostic stages that allow for individualized patient care. Management of VH cannot be performed in an isolated manner, and the presence of other complications of cirrhosis (ascites, encephalopathy) should be taken into account both in the management and in the design of clinical trials. Because management of ascites per se has not resulted in significant changes in mortality, main management issues consist of preventing further decompensating events by preventing factors that will lead to worsening vasodilatation and hemodynamic status (infections, vasodilators), preventing volume depletion (overdiuresis, GI hemorrhage) and preventing structural kidney injury (nephrotoxins). Prophylaxis of bacterial infections such as SBP currently consists of the administration of antibiotics. By preventing infections, there is evidence that recurrent VH and HRS can also be prevented. However, response to recommended empirical antibiotics in patients with suspected infection, such as SBP, is currently significantly lower than in the past because of an increase in infections secondary to multidrug resistant (MDR) organisms. One of the main predictors of the development of MDR organisms is antibiotic prophylaxis and unnecessary and prolonged use of antibiotics in hospital. Therefore, appropriate antibiotics should be used in patients with a high suspicion of infection, and antibiotic prophylaxis should be restricted to patients with the highest risk of infection.

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“…This study demonstrated that after a followup of 30 mo there was no significant difference in incidence of recurrent upper gastrointestinal bleeding between carvedilol and combination groups (62% vs 61%; P = 0.90). There was no significant difference between the Rate of recurrence of variceal bleeding between the carvedilol and combination groups (51% vs 43%; P = 0.46) [41] . Interim analysis of a multicentre randomised controlled study comparing carvedilol with endoscopic band ligation for secondary prevention of variceal bleeding, demonstrated no significant and mortality reduction in patients with cirrhosis in several randomised controlled trials.…”

Section: Secondary Prophylaxismentioning

confidence: 82%

Is it time to replace propranolol with carvedilol for portal hypertension?

Abid¹,

Ali²,

Baig³

et al. 2015

WJGE

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Beta-adrenergic receptor antagonists (β-blockers) have been well established for use in portal hypertension for more than three decades. Different Non-selective β-blockers like propranolol, nadolol, timolol, atenolol, metoprolol and carvedilol have been in clinical practice in patients with cirrhosis. Carvedilol has proven 2-4 times more potent than propranolol as a beta-receptor blocker in trials conducted testing its efficacy for heart failure. Whether the same effect extends to its potency in the reduction of portal venous pressures is a topic of on-going debate. The aim of this review is to compare the hemodynamic and clinical effects of carvedilol with propranolol, and attempt assess whether carvedilol can be used instead of propranolol in patients with cirrhosis. Carvedilol is a promising agent among the beta blockers of recent time that has shown significant effects in portal hypertension hemodynamics. It has also demonstrated an effective profile in its clinical application specifically for the prevention of variceal bleeding. Carvedilol has more potent desired physiological effects when compared to Propranolol. However, it is uncertain at the present juncture whether the improvement in hemodynamics also translates into a decreased rate of disease progression and complications when compared to propranolol. Currently Carvedilol shows promise as a therapy for portal hypertension but more clinical trials need to be carried out before we can consider it as a superior option and a replacement for propranolol. Core tip: Carvedilol is a promising agent among the beta blockers of recent time that has shown significant effects in portal hypertension hemodynamics. For primary prophylaxis of variceal bleeding, the effects of carvedilol were compared to band ligation in a few trials and showed some promise, but there has been no comparison with propranolol. Patients not responding to propranolol have shown clinical response to carvedilol, opening a new window of clinical application. For secondary prophylaxis of variceal bleeding, carvedilol has been shown to be effective. However no head-tohead trials comparing propranolol and carvedilol for variceal re-bleeding were found in literature.

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Randomized, controlled trial of carvedilol versus nadolol plus isosorbide mononitrate for the prevention of variceal rebleeding

Abstract: Carvedilol was as effective as nadolol plus isorsorbide-5 -mononitrate mononitrate in the prevention of gastroesophageal variceal rebleeding with fewer severe adverse events and similar survival.

Cited by 66 publications

References 32 publications

Variceal Rebleeding: Drugs, Endoscopy or Both

Variceal Rebleeding: Drugs, Endoscopy or Both

Current Management of the Complications of Cirrhosis and Portal Hypertension: Variceal Hemorrhage, Ascites, and Spontaneous Bacterial Peritonitis

Is it time to replace propranolol with carvedilol for portal hypertension?

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