88 ± 2.956 while in Group B was 16.78 ± 5.559 and respectively. A significantly higher proportion of variceal bleeds were seen in Group A (6 of 17, 35.3%) compared to Group B (1 of 17, 5.8%) at 12 months (p=0.03). The onset of first variceal bleed was at 9.2 ± 0.96 weeks in Group A and 11.8 ± 0.21 weeks in Group B which was statistically significant (p- 0.02) (Fig.1). No mortality and
adverse events were reported in either group. Conclusions: This is the first RCT (NCT01196481) showing that carvedilol is effective in about 50% patients with large varices. However, in BB non-responders, combining VSL#3 with carvedilol is not effective and EVL remains the first choice for primary prophylaxis for large esophageal varices. Disclosures: The following people have nothing to disclose: Ankit Bhardwaj, Avinash Kumar, NVP-BGJ398 order Devraj Rangegowda, Chandan K. Kedarisetty, Manoj Kumar, Chitranshu Vash-ishtha, Ajeet S. Bhadoria,
Shiv K. Sarin Background and aims: Non-Selective β-Blockers (NSBBs) have been associated with increased incidence of Paracentesis Induced Circulatory Dysfunction (PICD) and reduced survival in patients with cirrhosis and refractory ascites; however, causes of death were not related to worsening haemodynamics. We have prospectively evaluated intra-individual central and peripheral hemodynamic effects produced by NSBBs introduction and the incidence of PICD in patients undergoing large volume paracentesis (LVP). Methods: Patients with cirrhosis and refractory ascites, having indication to initiate or discontinue NSBBs were enrolled. During two consecutive LVP (while EPZ-6438 cell line been respectively on and off NSBBs therapy), for each patient cardiac output (CO), systemic vascular resistances (SVR), peripheral vascular resistances (PVR), and Plasma Renin Activity (PRA) before and 60′ after LVP were recorded, using impedance cardiography and plethysmography. Results: Eleven patients were enrolled, 6 completed the study; all the patients did have diuretic intractable refractory ascites and new indication to introduce propranolol (mean dose±SD 60±21.9 mg/day). Before NSBBs initiation, SVR (1808±358.3 vs 1398±332.4 dyn.s.cm-5; p= .02) and PVR (45.9±7.0 vs 27.7±5.9
mmHg. min.dl.ml-1; p= .04) significantly decreased 60′ after LVP than pre-paracentesis; CO consequently showed an increasing trend (3.8±0.67 Non-specific serine/threonine protein kinase vs 4.4±1.14 l/min; p= .06). PICD was diagnosed in 2/6 patients. While on NSBBs therapy, CO did not increase after LVP (3.3±0.9 vs 3.6±1.0 l/min; p= .1), but this was counterbalanced by a smaller decrease of SVR (1981.12±314.2 vs 1763.29±555.05 dyn.s.cm-5; p= .1) and PVR (44.17±12.2 vs 32.1 ±7.86 mmHg.min.dl.ml-1; p= .2). Three of six patients showed an increase in PRA values post-LVP, consistent with PICD. Conclusions: In patients with cirrhosis undergoing LVP, the inotropic negative effect of NSBBs seems to be counterbalanced by smaller decrease of vascular resistances, probably due to splanchnic β2-blockade.