To reduce portal pressure, the only recommended medication is nonselective beta blocker(NSBB). However, NSBB has some limitation to apply clinically because of poor response rate and compliance.

Recent literature has supported the role of bacterial translocation as a mediator of splanchnic vasodilatation and portal hypertension. This stimulates the release of pro-inflammatory cytokines and the activation of the vasodilator NO resulting in a more pronounced deterioration of the baseline hyperdynamic circulatory state. Selective gut decontamination with Rifaximin can induce inhibition of bacterial translocation and associated worsening of portal hypertension. The investigators hypothesized that Rifaximin plus NSBB could result in decrease of portal pressure in cirrhotic patients with esophageal varices.

Inclusion Criteria:

• Liver cirrhosis:diagnosed based on histology or unequivocal clinical, sonographic, and laboratory findings
• 19≤age≤75
• Hepatic venous pressure gradient > 12 mmHg
• Informed consent

Exclusion Criteria:

• Shock status requiring vasopressor
• Active infection, for example Spontaneous bacterial peritonitis
• Acute renal failure patients of any cause
• Clinically relevant coronary artery disease(NYHA functional angina classification III/IV),congestive heart failure NYHA III/IV), clinically relevant cardiomyopathy, history of myocardial infarction in the past 12 months
• Poorly controlled hypertension (BP 150/100mmHg)
• Hepatocellular carcinoma
• History of another primary malignancy ≤ 3years
• Medical or psychological conditions that would not permit the subject to complete thte study or sign informed consent
• Pregnancy or lactation period
• Serum creatinine ≧ 6mg/dL
• Involvement in the conduct of other study within 30 days
• Known hypersensitivity to Rifaximin or propranolol
• Dysarrhythmia, inappropriate for study on investigator's judgment