The American journal of gastroenterology · 2000
Propranolol in primary and secondary prophylaxis of variceal bleeding among cirrhotics in India: a hemodynamic evaluation.
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De B K, Sen S, Biswas P K, Sengupta D, Biswas J, Santra A, Hazra B, Maity A K
Аннотация
OBJECTIVE: In the present study, we attempted to complete the hemodynamic assessment of propranolol response in cirrhotics with esophageal varices at high risk of bleeding, in one sitting, so as to identify nonresponders at the earliest. Some noninvasive indicators of this response were also evaluated.
METHODS: Hepatic venous pressure gradient (HVPG) was measured in 33 such cases (18 nonbleeders, 15 bleeders) before and 90 min after an oral dose of 80 mg propranolol, and reduction by > or =20% taken as responder.
RESULTS: Twenty-two patients (66.67%) responded (HVPG reduction > or =26%), whereas 11 (33.33%) did not (HVPG reduction < or =6%). Postdrug HVPG between responders and nonresponders showed a significant difference (p < 0.001). Neither baseline HVPG (p > 0.1), baseline CI (p = 0.665), nor baseline stroke volume index (p > 0.1) could predict responder status. Difference of HVPG reduction (percent) between bleeders (21.49 +/- 35.53) and nonbleeders (40.58 +/- 23.95) approached, but did not reach, statistical significance (p = 0.076). However, logistic regression showed this difference to be significant (p = 0.026). Age of responders was found to be significantly lower than that of nonresponders (p approximately equals 0.05). During a follow-up of 9-38 months, only one of 22 responders (on propranolol) had an episode of variceal bleed. None in whom HVPG fell to < or = 12 mm Hg bled.
CONCLUSION: The study suggests that single-sitting hemodynamic assessment of acute response to high-dose oral propranolol clearly differentiates between responders and nonresponders. Moreover, it appears that prior history of variceal bleeding and old age negatively influences the effect of propranolol.
METHODS: Hepatic venous pressure gradient (HVPG) was measured in 33 such cases (18 nonbleeders, 15 bleeders) before and 90 min after an oral dose of 80 mg propranolol, and reduction by > or =20% taken as responder.
RESULTS: Twenty-two patients (66.67%) responded (HVPG reduction > or =26%), whereas 11 (33.33%) did not (HVPG reduction < or =6%). Postdrug HVPG between responders and nonresponders showed a significant difference (p < 0.001). Neither baseline HVPG (p > 0.1), baseline CI (p = 0.665), nor baseline stroke volume index (p > 0.1) could predict responder status. Difference of HVPG reduction (percent) between bleeders (21.49 +/- 35.53) and nonbleeders (40.58 +/- 23.95) approached, but did not reach, statistical significance (p = 0.076). However, logistic regression showed this difference to be significant (p = 0.026). Age of responders was found to be significantly lower than that of nonresponders (p approximately equals 0.05). During a follow-up of 9-38 months, only one of 22 responders (on propranolol) had an episode of variceal bleed. None in whom HVPG fell to < or = 12 mm Hg bled.
CONCLUSION: The study suggests that single-sitting hemodynamic assessment of acute response to high-dose oral propranolol clearly differentiates between responders and nonresponders. Moreover, it appears that prior history of variceal bleeding and old age negatively influences the effect of propranolol.