In a randomized controlled trial, addition of simvastatin to standard therapy did not reduce rebleeding, but was associated with a survival benefit for patients with Child-Pugh class A or B cirrhosis. Survival was not the primary end point of the study, so these results require validation. The incidence of rhabdomyolysis in patients receiving 40 mg/d simvastatin was higher than expected. European Clinical Trial Database ID: EUDRACT 2009-016500-24; ClinicalTrials.gov ID: NCT01095185.

Nonselective b-blockers are useful to prevent bleeding in patients with cirrhosis and large varices but not to prevent the development of varices in those with compensated cirrhosis and portal hypertension (PHT). This suggests that the evolutionary stage of PHT may influence the response to b-blockers. To characterize the hemodynamic profile of each stage of PHT in compensated cirrhosis and the response to b-blockers according to stage, we performed a prospective, multicenter (tertiary care setting), cross-sectional study. Hepatic venous pressure gradient (HVPG) and systemic hemodynamic were measured in 273 patients with compensated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG !10 mm Hg (clinically significant PHT [CSPH]), with either no varices (n 5 80) or small varices (n 5 114), and 79 had an HVPG >5 and <10 mm Hg (subclinical PHT). Patients with CSPH had higher liver stiffness (P < 0.001), worse Model for End-Stage Liver Disease score (P < 0.001), more portosystemic collaterals (P 5 0.01) and splenomegaly (P 5 0.01) on ultrasound, and lower platelet count (P < 0.001) than those with subclinical PHT. Patients with CSPH had lower systemic vascular resistance (1336 6 423 versus 1469 6 335 dyne Á s Á cm -5 , P < 0.05) and higher cardiac index (3.3 6 0.9 versus 2.8 6 0.4 L/min/m 2 , P < 0.01). After propranolol, the HVPG decreased significantly in both groups, although the reduction was greater in those with CSPH (-16 6 12% versus -8 6 9%, P < 0.01). The HVPG decreased !10% from baseline in 69% of patients with CSPH versus 35% with subclinical PHT (P < 0.001) and decreased !20% in 40% versus 13%, respectively (P 5 0.001). Conclusion: Patients with subclinical PHT have less hyperdynamic circulation and significantly lower portal pressure reduction after acute b-blockade than those with CSPH, suggesting that b-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than in earlier stages. (HEPATOLOGY 2016;63:197-206) P ortal hypertension (PHT) is the most common complication of cirrhosis and the main determinant for developing varices or clinical decompensation (appearance of ascites, variceal bleeding, or hepatic encephalopathy). Decompensation, in turn, is the leading cause of mortality in cirrhosis. 1,2 The primary factor in the development of PHT in cirrhosis is an increased vascular resistance to portal flow through Abbreviations: CI, confidence interval; CO, cardiac output; CSPH, clinically significant portal hypertension; HR, heart rate; HVPG, hepatic venous pressure gradient; MELD, Model for End-Stage Liver Disease; PHT, portal hypertension; RCT, randomized controlled trial; SVR, systemic vascular resistance.From the

; for the Variceal Bleeding Study GroupBalloon tamponade is recommended only as a "bridge" to definitive therapy in patients with cirrhosis and massive or refractory esophageal variceal bleeding (EVB), but is frequently associated with rebleeding and severe complications. Preliminary, noncontrolled data suggest that a self-expandable, esophageal covered metal stent (SX-ELLA Danis; Ella-CS, Hradec Kralove, Czech Republic) may be an effective and safer alternative to balloon tamponade. We conducted a randomized, controlled trial aimed at comparing esophageal stent versus balloon tamponade in patients with cirrhosis and EVB refractory to medical and endoscopic treatment. Primary endpoint was success of therapy, defined as survival at day 15 with control of bleeding and without serious adverse events (SAEs). Twenty-eight patients were randomized to Sengstaken-Blakemore tube (n 5 15) or SX-ELLA Danis stent (n 5 13). Patients were comparable in severity of liver failure, active bleeding at endoscopy, and initial therapy. Success of therapy was more frequent in the esophageal stent than in balloon tamponade group (66% vs. 20%; P 5 0.025). Moreover, control of bleeding was higher (85% vs. 47%; P 5 0.037) and transfusional requirements (2 vs 6 PRBC; P 5 0.08) and SAEs lower (15% vs. 47%; P 5 0.077) in the esophageal stent group. TIPS was used more frequently in the tamponade group (4 vs. 10; P 5 0.12). There were no significant differences in 6-week survival (54% vs. 40%; P 5 0.46). Conclusion: Esophageal stents have greater efficacy with less SAEs than balloon tamponade in the control of EVB in treatment failures. Our findings favor the use of esophageal stents in patients with EVB uncontrolled with medical and endoscopic treatment. (HEPATOLOGY 2016;63:1957-1967 SEE EDITORIAL ON PAGE 1768A cute bleeding from esophageal varices (AVB) carries a death rate ranging from 12% to 20% during the acute episode, which, by consensus, is defined as the first 5 days after the patient reaches the hospital.(1-3) Failure to control bleeding or early rebleeding leads to a very high mortality, ranging from 30% to 50%, suggesting that failure of initial treatment should be considered a strong predictor of mortality in patients with AVB. (2)(3)(4)(5) Treatment for AVB according to current guidelines is based on early and cautious blood volume resuscitation, early administration of IV vasoactive drugs (terlipressin, somatostatin, or analogs) and of prophylactic