Isosorbide mononitrate and propranolol compared with propranolol alone for the prevention of variceal rebleeding

Gournay, Jérôme; Masliah, Claude; Martin, Thierry; Perrin, D.; Galmiche, Jean–Paul

doi:10.1053/jhep.2000.8106

Cited by 156 publications

(61 citation statements)

References 26 publications

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“…Only one study has performed a direct comparison between the combination of propranolol plus ISMN and propranolol alone in patients with prior variceal hemorrhage. 116 This study showed a benefit of combination therapy (33% vs. 41% rebleeding rate), but it was not statistically significant. Data collected from different randomized clinical trials show that the median rebleeding rate in patients treated with combined pharmacological therapy is around 33%-35%, 35,36 lower than that obtained with ␤-blockers alone.…”

Section: E Patients With Cirrhosis Who Have Recovered From Acute Varmentioning

confidence: 58%

“…Therefore, the pharmacological therapy of choice in the prevention of variceal rebleeding is probably the combination of a nonselective ␤-blocker and a nitrate. However, this combination has significantly greater side effects compared to ␤-blockers alone 35,116 and is poorly tolerated in clinical practice so that most patients end up taking ␤-blockers alone.…”

Section: E Patients With Cirrhosis Who Have Recovered From Acute Varmentioning

confidence: 99%

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Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

et al. 2007

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Section: E Patients With Cirrhosis Who Have Recovered From Acute Varmentioning

confidence: 58%

Section: E Patients With Cirrhosis Who Have Recovered From Acute Varmentioning

confidence: 99%

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

et al. 2007

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“…Pharmacologic therapy includes use of a nonselective β-blocker. 111,[119][120][121][122] Although it has been proposed, 123 combined treatment with isosorbide mononitrate and propranolol is not recommended.…”

Section: Secondary Prophylaxismentioning

confidence: 99%

Current management of the complications of portal hypertension: variceal bleeding and ascites

Dib

Oberti²,

Calès³

2006

Canadian Medical Association Journal

109

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Portal hypertension is one of the main consequences of cirrhosis. It can result in severe complications, including bleeding of esophagogastric varices as well as spontaneous bacterial peritonitis or hepatorenal syndrome as complications of ascites. We describe in brief the pathophysiology of portal hypertension and review the current management of its complications, with emphasis on variceal bleeding and ascites. Pathophysiologic background Portal hypertensionPortal hypertension is defined as an increase in blood pressure in the portal venous system. The portal pressure is estimated indirectly by the hepatic venous pressure gradientthe gradient between the wedged (or occluded) hepatic venous pressure and the free hepatic venous pressure. A normal hepatic venous pressure gradient is less than 5 mm Hg.In cirrhosis, portal hypertension results from the combination of increased intrahepatic vascular resistance and increased blood flow through the portal venous system (Fig. 1). According to Ohm's law, portal venous pressure (P) is the product of vascular resistance (R) and blood flow (Q) in the portal bed (P = Q × R). Intrahepatic resistance increases in 2 ways: mechanical and dynamic. The mechanical component stems from intrahepatic fibrosis development; various pathologic processes are thought to contribute to increased intrahepatic resistance at the level of the hepatic microcirculation (sinusoidal portal hypertension): architectural distortion of the liver due to fibrous tissue, 1 regenerative nodules, 1 and collagen deposition in the space of Disse.2 The dynamic component results from a vasoconstriction in portal venules secondary to active contraction of portal and septal myofibroblasts, to activated hepatic stellates cells and to vascular smoothmuscle cells.3-5 Intrahepatic vascular tone is modulated by endogenous vasoconstrictors (e.g., norepinephrine, endothelin-1, angiotensin II, leukotrienes and thromboxane A 2 ) and enhanced by vasodilators (e.g., nitric oxide). In cirrhosis, increased intrahepatic vascular resistance results also from an imbalance between vasodilators and vasoconstrictors. 6Portal hypertension is characterized by increased cardiac output and decreased systemic vascular resistance, 7 which results in a hyperdynamic circulatory state with splanchnic and systemic arterial vasodilation. Splanchnic arterial vasodilation leads to increased portal blood flow, which in turn leads to more severe portal hypertension. Splanchnic arterial vasodilation results from an excessive release of endogenous vasodilators such as nitric oxide, glucagon and vasointestinal active peptide.An increase in the portocaval pressure gradient leads to the formation of portosystemic venous collaterals in an attempt to decompress the portal venous system. Esophageal varices, drained predominantly by the azygos vein, are clinically the most important collaterals because of their propensity to bleed. Esophageal varices can develop when the hepatic venous pressure gradient rises above 10 mm Hg. 8-10All factors that increase ...

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“…13,14 Combined β-adrenergic blocker and 5-isosorbide mononitrate (BB + ISMN) was more effective than BBs alone in the prevention of esophageal variceal rebleeding. 15,16 It is still unknown whether drug therapy is superior to EBL for preventing variceal rebleeding. Several randomized controlled trials have shown different results.…”

Section: Introductionmentioning

confidence: 99%

Comparison of endoscopic variceal ligation and beta-blocker (carvedilol) plus nitrate for the primary prevention of variceal bleeding

et al. 2017

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Background: Esophageal variceal bleed is a major problem in patients with cirrhosis. Endoscopic sclerotherapy and variceal ligation are effective in stopping bleeding in up to 90% of patients. Beta-blocker (Carvedilol) + Isosorbide Mononitrate are promising alternative to other nonselective beta blocker or endoscopic band ligation for the prevention of first variceal bleeding of medium to large varices, which needs to be further explored.Methods: The present study was an observational study in 200 patients at LLR and Associated Hospitals PG Department of Medicine GSVM Medical College, Kanpur. After randomization 120 patients underwent for Endoscopic Variceal ligation and 80 patients were put on beta-blocker (Carvedilol) + Isosorbide Mononitrate therapy for the primary prevention of variceal bleeding.Results: Most common cause of portal hypertension was liver cirrhosis (in carvedilol plus isosorbide mononitrate group 70%, and it was 85%. in EVL group. Bleeding in patients of carvedilol plus isosorbide mononitrate was significantly lower (23.75%) than patients of EVL (60%) group. Reduction in bleeding was statistically highly significant (p value < 0.05). Mortality among patients receiving combination therapy with carvedilol plus isosorbide mononitrate was (12.5%) comparison to EVL (21.66%). Reduction in mortality was statistically not significant. (p value >0.05). Adverse effects were significantly lower among patients receiving combination therapy with carvedilol plus isosorbide mononitrate (38.75%) than patients of EVL (86.66%) group.Conclusions: Both EVL and beta-blockers may be considered first-line treatment to prevent first variceal bleeding, whereas beta-blockers (carvedilol) plus isosorbide mononitrate may be the best choice for the prevention of re-bleeding.

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Isosorbide mononitrate and propranolol compared with propranolol alone for the prevention of variceal rebleeding

Cited by 156 publications

References 26 publications

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis

Current management of the complications of portal hypertension: variceal bleeding and ascites

Comparison of endoscopic variceal ligation and beta-blocker (carvedilol) plus nitrate for the primary prevention of variceal bleeding

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