Abstract

Background: Portal hypertension leads to most of the complication of cirrhosis: both bleeding and non-bleeding. Most complications due to portal hypertension can be ameliorated by β-blockers in those who are hemodynamic responders. To identify hemodynamic responder, a repeat hepatic venous pressure gradient (HVPG) is required 4–6 weeks after initiation of beta-blocker therapy. Acute hemodynamic response is a recent modality of determining HVPG response immediately during the baseline HVPG by giving high dose of injectable or oral beta-blocker. Aims: To assess the acute effect of Carvedilol on HVPG and its impact on outcome in cirrhotics over a 6-month period of follow up. Patients and Methods: Patients requiring β-blocker therapy, for primary (25/69) or secondary (44/69) prevention of variceal bleeding, were subjected to HVPG measurement. Acute Responder were defined as HVPG <12 mmHg or >10% fall in HVPG from baseline. Immediately after HVPG they were given Tab. Carvedilol 25 mg and a repeat HVPG was performed after one hour. On the basis of hemodynamic response 2 groups were made, Acute responders and non-responders. Both these groups were followed for 6 months. A repeat HVPG was done in acute responder group after 6 month. Both these group of patients were offered standard medical therapy with beta-blocker (Carvedilol) and regular EVL. All complications, hospitalization and outcome of patient noted at the end of 6 month. Results: Out of 69 patients, 49 (71%) patients showed acute reduction in HVPG of >10% after oral Carvedilol. There were no baseline differences between the two groups. On follow-up, complications like ascites was significantly less common in acute responder group as compared to non-responder group (P < 0.001). However, there was no statistically significant difference in mortality between acute responder and non-responder groups (P > 0.05). Repeat HVPG after a median period of 6 months could be performed in 41 of 49 patients in the acute responder group, while 2 patients was not willing for a repeat HVPG and 6 patients had died during this period. Out of 41 patients 35 (85%) patients were still responders (long term responders) and 6 (15%) patient were non long term responders. Conclusions: Determination of acute response to carvedilol is not only a convenient and rapid way to identify beta-blocker hemodynamic responders; it also is an excellent prognostic marker as acute responders develop less portal hypertensive complication like ascites than non-responders on beta-blocker therapy. Also the most of acute responders are found to be longstanding responder. Keywords: HVPG; portal hypertension; cirrhosis; esophageal varices

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