***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: BACKGROUND / AIMS A total of 213 patients with compensated cirrhosis , portal hypertension and no varices were included in a trial evaluating beta-blockers in preventing varices . Predictors of the development of hepatocellular carcinoma ( HCC ) , including hepatic venous pressure gradient ( HVPG ) were analyzed . METHODS Baseline laboratory tests , ultrasound and HVPG measurements were performed . Patients were followed prospect ively every three months until development of varices or variceal bleeding or end of the study in 09/02 . The endpoint was HCC development according to st and ard diagnostic criteria . Univariate and multivariate Cox regression models were developed to identify predictors of HCC . RESULTS In a median follow-up of 58 months 26/213 ( 12.2 % ) patients developed HCC . Eight patients were transplanted and 28 patients died without HCC . Twenty-one ( 84 % ) HCC developed in patients with HCV . On multivariate analysis HVPG ( HR 1.18 ; 95%CI 1.08 - 1.29 ) , albumin ( HR 0.34 ; 95%CI 0.14 - 0.83 ) and viral etiology ( HR 4.59 ; 95%CI 1.51 - 13.92 ) were independent predictors of HCC development . ROC curves identified 10 mmHg of HVPG as the best cut-off ; those who had an HVPG above this value had a 6-fold increase in the HCC incidence . CONCLUSIONS Portal hypertension is an independent predictor of HCC development . An HVPG > 10 mmHg is associated with a 6-fold increase of HCC risk Objective Non-selective β-blockers or endoscopic b and ligation ( EBL ) are recommended for primary prophylaxis of variceal bleeding in patients with oesophageal varices . Additional α-adrenergic blockade ( as by carvedilol ) may increase the number of patients with haemodynamic response ( reduction in hepatic venous pressure gradient ( HVPG ) of ≥20 % or to values < 12 mm Hg ) . Design Patients with oesophageal varices undergoing measurement of HVPG before and under propranolol treatment ( 80–160 mg/day ) were included . HVPG responders were kept on propranolol ( PROP group ) , while non-responders were placed on carvedilol ( 6.25–50 mg/day ) . Carvedilol responders continued treatment ( CARV group ) , while non-responders to carvedilol underwent EBL . The primary aim was to assess haemodynamic response rates  to carvedilol in propranolol non-responders . Results 36 % ( 37/104 ) of patients showed a HVPG response  to propranolol . Among the propranolol non-responders 56 % ( 38/67 ) eventually achieved a haemodynamic response  with carvedilol , while 44 % ( 29/67 ) patients were finally treated with EBL . The decrease in HVPG was significantly greater with carvedilol ( median 12.5 mg/day ) than with propranolol ( median 100 mg/day ) : −19±10 % versus −12±11 % ( p<0.001 ) . During a 2 year follow-up bleeding rates for PROP were 11 % versus CARV 5 % versus EBL 25 % ( p=0.0429 ) . Fewer episodes of hepatic decompensation  ( PROP 38%/CARV 26 % vs EBL 55 % ; p=0.0789 ) and significantly lower mortality ( PROP 14%/CARV 11 % vs EBL 31 % ; p=0.0455 ) were observed in haemodynamic responders compared to the EBL group . Conclusions Carvedilol leads to a significantly greater decrease in HVPG  than propranolol . Using carvedilol for primary prophylaxis a substantial proportion of non-responders to propranolol can achieve a haemodynamic response , which is associated with improved outcome with regard to prevention of variceal bleeding , hepatic decompensation and death UNLABELLED Current therapy for preventing the first variceal bleed includes beta-blocker and variceal b and ligation ( VBL ) . VBL has lower bleeding rates , with no differences in survival , whereas beta-blocker therapy can be limited by side effects . Carvedilol , a non-cardioselective vasodilating beta-blocker , is more effective in reducing portal pressure than propranolol ; however , there have been no clinical studies assessing the efficacy of carvedilol in primary prophylaxis . The goal of this study was to compare carvedilol and VBL for the prevention of the first variceal bleed in a r and omized controlled multicenter trial . One hundred fifty-two cirrhotic patients from five different centers with grade II or larger esophageal varices were r and omized to either carvedilol 12.5 mg once daily or VBL performed every 2 weeks until eradication using a multib and er device . Seventy-seven patients were r and omized to  carvedilol and 75 to VBL . Baseline characteristics did not differ between the groups ( alcoholic liver disease , 73 % ; median Child-Pugh score , 8 ; median age , 54 years ; median follow-up , 20 months ) . On intention-to-treat analysis , carvedilol had lower rates of the first variceal bleed ( 10 % versus 23 % ; relative hazard 0.41 ; 95 % confidence interval 0.19 - 0.96 [ P = 0.04 ] ) , with no significant differences in overall mortality ( 35 % versus 37 % , P = 0.71 ) , and bleeding-related mortality ( 3 % versus 1 % , P = 0.26 ) . Six patients in the VBL group bled as a result of b and ing ulcers . Per- protocol analysis revealed no significant differences in the outcomes . CONCLUSION Carvedilol is effective in preventing the first variceal bleed .  Carvedilol is an option for primary prophylaxis in patients with high-risk esophageal varices BACKGROUND AND AIMS Newer studies suggest that carvedilol , a beta-blocker with a moderate anti-alpha-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 r and omised 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 QTc 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 OBJECTIVE : Propranolol is known to decrease portal pressure in cirrhotic patients with portal hypertension ; however , a substantial number of patients do not respond to propranolol administration . The addition of isosorbide-5-mononitrate may enhance portal pressure reduction in patients receiving propranolol . Carvedilol is a nonselective β-blocker with α1-adrenergic blocking activity . It has been shown to decrease portal pressure in cirrhotic patients . Additionally , carvedilol has a greater portal hypotensive effect than propranolol alone in patients with cirrhosis . The current study is aim ed at comparing the acute hemodynamic effects of carvedilol with the effects of propranolol plus isosorbide-5-mononitrate in patients with viral cirrhosis . METHODS : Patients with viral cirrhosis were r and omly assigned to receive an oral administration of carvedilol of 25 mg ( n = 11 ) or an oral administration of propranolol 40 mg plus isosorbide-5-mononitrate 20 mg ( n =  11 ) . Hemodynamic values were measured at basal and 90 min after drugs administration . RESULTS : Both carvedilol and propranolol plus isosorbide-5-mononitrate significantly decreased cardiac index , heart rate , and HVPG . The magnitude of changes in HVPG observed between the basal and after drugs administration was greater in patients receiving carvedilol than in those receiving propranolol plus isosorbide-5-mononitrate ( −18.6 ± 3.6 % vs−10.1 ± 3.6 % , p < 0.05 ) . Hepatic blood flow increased following carvedilol administration but remained unchanged in patients receiving propranolol plus isosorbide-5-mononitrate . The magnitude of decrease in mean arterial pressure ( MAP ) did not differ between the two groups of patients . CONCLUSION : In our patients with viral cirrhosis  , carvedilol is more effective than propranolol plus isosorbide-5-mononitrate in the reduction of HVPG  . Carvedilol administration causes an increase in hepatic blood flow , but its systemic effects were similar to those of propranolol plus isosorbide-5-mononitrate BACKGROUND Carvedilol , a non-selective beta- and alpha-1 blocking agent , has portal hypotensive action . This study evaluates the acute and 7-day response to carvedilol , and compares it to that of propranolol . METHODS Thirty-six cirrhotics were r and omized into two groups of 18 each , and treated with carvedilol or propranolol .  Hepatic venous pressure gradient ( HVPG ) was measured before and 90 min after either 25 mg carvedilol or 80 mg propranolol was administered orally , and again 7 days after 12.5 mg carvedilol daily or 80 mg propranolol daily , respectively . ' Responders ' were defined as those with HVPG reduction of > or = 20 % . RESULTS With carvedilol , 11/18(61.1 % ) and 11/17(64.7 % ) patients responded acutely and after 7 days , respectively , while 9/18(50 % ) and 10/16(62.5 % ) did so to propranolol . However , HVPG reduction ( percent ) by carvedilol was not superior to that by propranolol either acutely ( 27.67 + /- 31.49 compared to 22.98 + /- 27.40 , P = 0.6 ) or after 7 days ( 28.2 + /- 29.05 compared to 23.25 + /- 20.15 , P = 0.6 ) . With carvedilol , the acute HVPG response ( P < 0.001 ) and responder status ( P = 0.018 ) were good predictors of the response after 7 days , but were weak predictors in the case of propranolol ( 0.1 > P > 0.05 and P = 0.059 , respectively ) . On carvedilol , only one patient ( with ascites ) developed symptomatic systemic hypotension with oliguria . CONCLUSION Carvedilol is a relatively safe , effective portal hypotensive agent , both acutely and over 7 days , but not superior to propranolol , at least in Indians . The acute hemodynamic response seems promising in predicting long-term response BACKGROUND AND AIMS Our aim was to identify predictors of clinical decompensation ( defined as the development of ascites , variceal hemorrhage [ VH ] , or hepatic encephalopathy [ HE ] ) in patients with compensated cirrhosis and with portal hypertension as determined by the hepatic venous pressure gradient ( HVPG ) . METHODS We analyzed 213 patients with compensated cirrhosis and portal hypertension but without varices included in a trial evaluating the use of beta-blockers in preventing varices . All had baseline laboratory tests and HVPG . Patients were followed prospect ively every 3 months until development of varices or VH or end of study . To have complete information , until study termination , about clinical decompensation , medical record review was done . Patients who underwent liver transplantation without decompensation were censored at transplantation . Cox regression models were developed to identify predictors of clinical decompensation . Receiver operating characteristic ( ROC ) curves were constructed to evaluate diagnostic capacity of HVPG . RESULTS Median follow-up time of 51.1 months . Sixty-two ( 29 % ) of 213 patients developed decompensation : 46 ( 21.6 % ) ascites , 6 ( 3 % ) VH , 17 ( 8 % 
    Output:
    
Adverse events were nonsignificantly more frequent and serious with carvedilol .
CONCLUSIONS Carvedilol  reduces portal hypertension significantly more than propranolol .
However , available data do not allow a satisfactory comparison of adverse events .