Impact of an acute hemodynamic response-guided protocol for primary prophylaxis of variceal bleeding

Table 3 Clinical outcomes during follow-up in patients with acute response treated with traditional nonselective beta-blockers and in patients without acute response treated with carvedilol

Variable1	Traditional NSBB, n = 52	Carvedilol, n = 24	P value
Decompensation (global)2	12 (23.1)	8 (33.3)	0.405
First decompensation	3 (14.3)	2 (22.2)	0.622
Further decompensation	9 (29.0)	6 (40.0)	0.514
Portal hypertension-related bleeding	2 (3.8)	3 (12.5)	0.318
Ascites
Overall	7 (13.5)	4 (16.7)	0.734
De novo ascites	3 (5.8)	1 (4.2)	1
Spontaneous bacterial peritonitis	1 (1.9)	2 (8.3)	0.233
Hepatorenal syndrome	1 (1.9)	1 (4.2)	0.535
Hepatic encephalopathy
Overall	7 (13.5)	5 (20.8)	0.502
De novo hepatic encephalopathy	3 (5.8)	4 (16.7)	0.191
Hepatocellular carcinoma (de novo)	3 (6.1)	0 (0)	0.546
Portal thrombosis	5 (9.6)	3 (12.5)	0.702
Nonselective beta-blocker
Propranolol dose, n/mg per day	35 / 107.6
Nadolol dose, n/mg per day	17 / 83.5
Carvedilol dose, n/mg per day		24 / 9.2
Chronic hemodynamic response
Change from baseline HVPG, %	-11.9 ± 21.8	-12.2 ± 18.5	0.965
≥ 10% reduction in HVPG	15 (55.6)	9 (69.2)	0.503
≥ 20% reduction in HVPG	8 (29.6)	4 (30.8)	1
Decrease to < 12 mmHg	3 (11.1)	4 (30.8)	0.187
Lost to follow-up, n/%	14 (26.9)	3 (12.5)	0.238
Betablocker intolerance	6 (11.5)	1 (4.2)	0.421
Change to carvedilol after second hemodynamic study	5 (7.7)
Ceased follow-up	3 (5.8)	2 (8.3)	0.648

¹Quantitative variables were expressed as mean ± standard deviation and qualitative variables as absolute value (proportion);

²Decompensation: Development of de novo or worsening ascites, hepatic encephalopathy, portal hypertension-related bleeding, hepatorenal syndrome or spontaneous bacterial peritonitis. The number of decompensation events in each group is lower than the total sum of each complication because some patients suffered more than one complication during follow-up. NSBB: Nonselective beta-blockers.