Carvedilol or propranolol in portal hypertension? A randomized comparison (original) (raw)
Related papers
Hepatology, 2002
Short-term carvedilol administration is more powerful than propranolol in decreasing hepatic venous pressure gradient (HVPG) in cirrhotic patients, but induces arterial hypotension that may prevent its long-term use in portal hypertensive patients. This study compared the HVPG reduction and safety of long-term carvedilol and propranolol. Fifty-one cirrhotic patients were randomly assigned to receive carvedilol (n = 26) and propranolol (n = 25). Hemodynamic measurements and renal function were assessed at baseline and after 11.1 ± 4.1 weeks. Carvedilol caused a greater decrease in HVPG than popranolol (− 19 ± 2% vs. − 12 ± 2%; P < 0.001). The proportion of patients achieving an HVPG reduction ⩾20% or ⩽ 20 mm Hg was greater after carvedilol (54% vs. 23%; P < 0.05). Carvedilol, but not propranolol caused a significant decrease in mean arterial pressure (MAP) (– 11 ± 1% vs. – 5 ± 3%; P = 0.05) and a significant increase in plasma volume (PV) and body weight (11 ± 5% and 2 ± 1%, respectively; P < 0.05). Glomerular filtration rate (GFR) was unchanged with either drug, but the dose of diuretics was increased more frequently after carvedilol (27% vs. 8% P = 0.07). Adverse events requiring discontinuation of treatment occurred in 2 patients receiving carvedilol and in 3 receiving propranolol. In conclusion, carvedilol has a greater portal hypotensive effect than propranolol in patients with cirrhosis. However, its clinical applicability may be limited by its systemic hypotensive effects. Further trials are needed to confirm the therapeutic potential of carvedilol. (HEPATOLOGY2002;36:1367–1373).
Annals of hepatology
Carvedilol appears to be more effective than propranolol in the treatment of portal hypertension in cirrhotic patients. Aim. To compare the effects of carvedilol vs. propranolol on systemic and splanchnic haemodynamics and to evaluate the adverse events associated with these treatments. We performed a systematic review following the Cochrane and PRISMA recommendations. Randomised controlled trials comparing carvedilol versus propranolol, in the treatment of portal hypertension in cirrhotic patients with oesophageal varices, with or without bleeding history were included. The primary outcome measure was the haemodynamic response to treatment. Four randomised trials and 153 patients were included; 79 patients received carvedilol (6.25-50 mg/d) and 74 patients received propranolol (10-320 mg/d). The hepatic vein pressure gradient (HVPG) decreased more with carvedilol than with propranolol (MD -2.21; 95% CI: -2.83 to -1.60, I(2) = 0%, P < 0.00001). Carvedilol was superior to proprano...
Alimentary Pharmacology and Therapeutics, 2002
The haemodynamic effects of propranolol have been well studied. Lebrec et al. demonstrated a greater than 20% reduction in the hepatic venous pressure gradient (HVPG) following the acute administration of propranolol, 1 but up to one-third of patients do not exhibit a portal hypotensive response. 2 This may be explained by a portal hypertensive model demonstrating that a rise in the portocollateral resistance accompanies the reduc-tion in portal blood¯ow, thus reducing the overall portal hypotensive response to propranolol. 3 Current evidence suggests that the goal of pharmacotherapy in reducing the risk of variceal haemorrhage is to achieve a fall in the HVPG to £ 12 mmHg 4 or a 20% 5 reduction from baseline values. The role of non-selective b-blockers in the primary prevention of variceal haemorrhage has been extensively studied. 6±14 Meta-analysis of these trials has clearly shown the bene®t of these drugs when compared with placebo. 15 However, many patients are intolerant to drug side-effects. a 1 antagonism has been investigated in three haemodynamic studies. 16±18 Impressive reductions in the HVPG were achieved and these were comparable with SUMMARY Background: Carvedilol is a non-selective vasodilating b-blocker with weak a 1 receptor antagonism. Recent studies have demonstrated its potential as a portal hypotensive agent. Aim: To assess the haemodynamic effects and patient tolerability of the acute and chronic administration of low-dose carvedilol.
Digestive and Liver Disease, 2014
Background and aims: Newer studies suggest that carvedilol, a beta-blocker with a moderate antialpha-1 activity, is superior to propranolol in reducing the portal pressure and risk of variceal bleeding. The effect on arterial blood pressure is a matter of concern especially in decompensated patients. Aims: to assess potential differential effects of beta-blockers and beta-blockers with moderate anti-alpha-1 activity on selected haemodynamic, humoral, and respiratory characteristics in cirrhosis. Methods: Patients with cirrhosis and portal hypertension were randomised to receive carvedilol (n = 16) or propranolol (n = 13). Cardiac, systemic and splanchnic parameters along with oxygen saturation and plasma renin were measured at inclusion and after 3 months. Results: Arterial blood pressure, heart rate, and cardiac output decreased equally, central circulation time and systemic vascular resistance increased significantly but similarly. Central blood volume, plasma volume and arterial compliance were unaltered. The QT c interval and renin levels decreased in the carvedilol group, however not significantly different from the propranolol group. Arterial oxygen saturation and alveolar arterial oxygen gradient remained constant in both groups. Hepatic venous pressure gradient decreased equally in the carvedilol and propranolol groups (−17% and −20%, non significant). Conclusions: Systemic haemodynamics and pulmonary effects of carvedilol and propranolol are modest and this study could not demonstrate any significant difference between the two treatments.
Hemodynamic effect of propranolol on portal hypertension in patients with HB s Ag-positive cirrhosis
Digestive Diseases and Sciences, 1986
Wedged hepatic venous pressure, free hepatic venous pressure, and cardiac index were measured before and one hour after intravenous and one month after chronic oral administration of propranolol in nine patients with HBsAg-positive cirrhosis. The gradient between wedged hepatic venous pressure and free hepatic venous pressure was decreased 22.7% at one hour after intravenous administration of 5 mg propranolol, and a sustained decrease in hepatic venous pressure gradient was also demonstrated in five patients after one month of continuous oral administration of propranolol. Thus, we conclude that chronic oral administration of propranolol can reduce the hepatic venous pressure gradient in patients with compensated HBsAg-positive cirrhosis.
Alimentary Pharmacology & Therapeutics, 2010
Aliment Pharmacol Ther 2010; 32: 105–112Aliment Pharmacol Ther 2010; 32: 105–112SummaryBackground Cirrhosis with arterial hypertension is not uncommon. Haemodynamic alterations in these patients and the effects of beta-blocker on hepatic venous pressure gradient (HVPG) and systemic haemodynamics have not been evaluated.Aims To compare the systemic haemodynamic alterations in hypertensive and normotensive cirrhotics, and to investigate the effects of propranolol on these parameters.Methods A retrospective analysis of consecutive hypertensive cirrhotic patients (n = 33) who underwent haemodynamic assessment and paired HVPG measurement was done. Normotensive cirrhotics (n = 50) served as controls.Results Hypertensive patients had a significantly higher heart rate, systemic (SVRI), and pulmonary vascular resistance. There was a significant reduction in mean arterial pressure (MAP) in the hypertensive cirrhotic group from 112 (107–130) mmHg to 95 (77–114) mmHg (P < 0.01), but no change in the normotensives. SVRI remained the same in the hypertensive cirrhotic group, but it increased in the normotensives. There was no correlation between MAP reduction and HVPG reduction.Conclusions The frequency of HVPG response with propranolol treatment in hypertensive cirrhotics is similar to normotensive cirrhotics. Propranolol treatment reduces MAP significantly in hypertensive patients with cirrhosis. Treatment with a nonselective beta-blocker is a good strategy for hypertensive cirrhotic patients.Background Cirrhosis with arterial hypertension is not uncommon. Haemodynamic alterations in these patients and the effects of beta-blocker on hepatic venous pressure gradient (HVPG) and systemic haemodynamics have not been evaluated.Aims To compare the systemic haemodynamic alterations in hypertensive and normotensive cirrhotics, and to investigate the effects of propranolol on these parameters.Methods A retrospective analysis of consecutive hypertensive cirrhotic patients (n = 33) who underwent haemodynamic assessment and paired HVPG measurement was done. Normotensive cirrhotics (n = 50) served as controls.Results Hypertensive patients had a significantly higher heart rate, systemic (SVRI), and pulmonary vascular resistance. There was a significant reduction in mean arterial pressure (MAP) in the hypertensive cirrhotic group from 112 (107–130) mmHg to 95 (77–114) mmHg (P < 0.01), but no change in the normotensives. SVRI remained the same in the hypertensive cirrhotic group, but it increased in the normotensives. There was no correlation between MAP reduction and HVPG reduction.Conclusions The frequency of HVPG response with propranolol treatment in hypertensive cirrhotics is similar to normotensive cirrhotics. Propranolol treatment reduces MAP significantly in hypertensive patients with cirrhosis. Treatment with a nonselective beta-blocker is a good strategy for hypertensive cirrhotic patients.
Gastroenterology, 2002
Postprandial increases in portal pressure may influence esophageal variceal rupture. The effects of chronic propranolol and octreotide (100 and 200 g subcutaneously in a single dose) on postprandial hemodynamics were evaluated. Methods: First study: 36 cirrhotic patients were studied at baseline and 30 and 60 minutes after a standard meal and then treated with propranolol (139 ؎ 9 mg/d during 39 ؎ 2 days). Second study: After baseline measurements, patients were randomized into 3 groups: (1) placebo, (2) octreotide (100 g), or (3) octreotide (200 g) (n ؍ 12 for each group). Thirty minutes postinjection a new baseline was established and measurements were repeated 30 and 60 minutes after the meal. Results: First study: Baseline portal pressure was 18.1 ؎ 1.2 mm Hg, 30 and 60 minutes after the meal it was 21.5 ؎ 0.8 mm Hg and 20.5 ؎ 0.8 mm Hg, respectively (both P < 0.01 vs. baseline). Cardiac index (CI) was 4.5 ؎ 0.2, 4.8 ؎ 0.2, and 4.9 ؎ 0.2 L ⅐ min ؊1 ⅐ m ؊2 , respectively (both P < 0.05 vs. baseline). Peripheral vascular resistance was 1012 ؎ 56, 902 ؎ 51 (P ؍ NS), and 884 ؎ 49 dynes ⅐ sec ⅐ cm ؊5 (P < 0.05 vs. baseline), respectively. Second study: Propranolol and placebo did not blunt postprandial increase in portal pressure. Octreotide (100 g) partially ameliorated postprandial increase in portal pressure. Octreotide (200 g) significantly enhanced the portal hypotensive effect of propranolol and blunted the postprandial increase in portal pressure. Conclusions: Octreotide blunts postprandial increase in portal pressure not prevented by long-term propranolol administration.
Journal of Hepatology, 1997
Background/Aims: The portal pressure response to propranolol varies significantly in individual patients with cirrhosis. At present, propranolol responders can he identified only by measuring the hepatic venous pressure gradient. The aims of this study were: 1) to investigate whether the noninvasive monitoring of portal blood flow by pulsed Doppler ultrasound and forearm blood flow by strain-gauge plethysmography can predict the hepatic venous pressure gradient response to propranolol in patients with cirrhosis, and 2) to analyze the factors that may influence this response. Methods: Hemodynamic measurements were undertaken in 80 patients with cirrhosis before and after receiving propranolol (0.15 mg/kg i.v., n=60) or placebo (n=20). Results: No changes were observed in the placebo group. Propranolol lowered (p<O.Ol) hepatic venous pressure gradient from 17.6k3.8 to 14.723.8 mmHg, portal blood flow from 1122&363 to 8972332 mbmin and forearm blood flow from 7.5223.1 to 6.1222.3 ml/min%. Changes in hepatic venous pressure gradient were correlated (~~0.01) with those of portal