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1.
The impact of propranolol on nitric oxide and total antioxidant capacity in patients with resistant hypertension-evidence from the APPROPRIATE trial.
Ranasinghe, HN, Fernando, N, Handunnetti, S, Weeratunga, PN, Katulanda, P, Rajapakse, S, Galappatthy, P, Constantine, GR
BMC research notes. 2020;(1):228
Abstract
OBJECTIVES The objective was to assess the effect of propranolol on oxidative stress and anti-oxidant potential in patients with resistant hypertension as a secondary analysis of the APPROPRIATE trial. This randomized double blinded clinical trial recruited patients with resistant hypertension and allocated forty patients to propranolol and placebo in 1:1 ratio. The pro-oxidant state (nitrate and nitrite) was assessed using modified Griess assay. The total anti-oxidant capacity was measured using ABTS assay. RESULTS Analysis was performed for 18 patients from the propranolol group and 15 from the placebo group. A decline in end point ambulatory blood pressure (p = 0.031) and greater mean reduction in office SBP (29.7 ± 13.0 mmHg, p = 0.021) was noted in the propranolol arm. Nitrate and nitrite levels were lower at the end of a 90 day follow up period in both arms, with a greater mean reduction with propranolol. A significant increase in the AOC was noted in both arms with higher incremental value with Propranolol. The findings of this study do not demonstrate a statistically significant effect of propranolol on the oxidative stress/antioxidant balance in patients with resistant hypertension. The observed trends merit further evaluation.
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2.
Carvedilol versus propranolol effect on hepatic venous pressure gradient at 1 month in patients with index variceal bleed: RCT.
Gupta, V, Rawat, R, Shalimar, , Saraya, A
Hepatology international. 2017;(2):181-187
Abstract
BACKGROUND AND AIMS Endoscopic variceal ligation (EVL) plus beta blocker is the mainstay treatment after index bleed to prevent rebleed. Primary objective of this study was to compare EVL plus propranolol versus EVL plus carvedilol on reduction of HVPG after 1 month of therapy. METHODS Patients of cirrhosis presenting with index esophageal variceal bleed received standard treatment (Somatostatin therapy f/b EVL) following which HVPG was measured and patients were randomized to propranolol or carvedilol group if HVPG was >12 mmHg. Standard endotherapy protocol was continued in both groups. HVPG was again measured at 1 month of treatment. RESULTS Out of 129 patients of index esophageal variceal bleed, 59 patients were eligible and randomized into carvedilol (n = 30) and propranolol (n = 29). At 1 month of treatment, decrease in heart rate, mean arterial blood pressure (MAP) and HVPG was significant within each group (p = 0.001). Percentage decrease in MAP was significantly more in carvedilol group as compared to propranolol group (p = 0.04). Number of HVPG responders (HVPG decrease >20 % or below 12 mmHg) was significantly more in carvedilol group (22/29) as compared to propranolol group (14/28), p = 0.04. CONCLUSION Carvedilol is more effective in reducing portal pressure in patients with cirrhosis with esophageal bleed. Though a larger study is required to substantiate this, the results in this study are promising for carvedilol. Clinical trials online government registry (CTRI/2013/10/004119). Trial registration number CTRI/2013/10/004119.
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3.
Efficacy and safety of cinnarizine in the prophylaxis of migraine headaches in children: an open, randomized comparative trial with propranolol.
Togha, M, Malamiri, RA, Rashidi-Ranjbar, N, Asa, S, Mahvelati, F, Ashrafi, MR
Acta neurologica Belgica. 2012;(1):51-5
Abstract
Migraine headaches are common in children. Early diagnosis and appropriate interventions are mandatory to prevent decades of suffering and diminished quality of life. There is need for data regarding the efficacy and safety of prophylactic agents in children with migraine; therefore, we designed a randomized clinical trial to compare the efficacy and safety of cinnarizine with that of a well-known prophylactic agent (propranolol) in the prophylaxis of pediatric migraine headache. A total of 120 patients aged between 6 and 17 years were recruited and 113 patients succeeded in completing all phases of the trial. Of them, 57 patients were given cinnarizine, and propranolol was administered in 56 patients. Reduction in headache frequency was the main response to treatment. Cinnarizine reduced the baseline headache frequency by more than 50% in 74.6% of patients and the mean headache frequency per month was reduced from 11.851 ± 0.739 (mean ± SEM) to 3.358 ± 0.739 (mean ± SEM) attacks per month (P < 0.001). In the propranolol group, more than 50% reduction of the baseline headache frequency was seen in 72.5% of patients and the mean headache frequency per month was reduced from 10.264 ± 0.830 (mean ± SEM) to 2.774 ± 0.830 (mean ± SEM) attacks per month (P < 0.001). No significant difference was seen in 50% reduction of the baseline headache frequency between treatment groups (P = 0.358). No significant adverse effects were reported. In this open study, cinnarizine appeared thus as effective as propranolol and safe for the prophylaxis of migraine in children, but this remains to be confirmed in a double-blind placebo-controlled trial.
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4.
Efficacy and safety of oral propranolol premedication to reduce reflex tachycardia during hypotensive anesthesia with sodium nitroprusside in orthognathic surgery: a double-blind randomized clinical trial.
Apipan, B, Rummasak, D
Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons. 2010;(1):120-4
Abstract
PURPOSE The present study sought to determine whether premedication with oral propranolol 10 mg before hypotensive anesthesia with sodium nitroprusside could reduce reflex tachycardia, the amount of sodium nitroprusside used, and blood loss during hypotensive anesthesia for orthognathic surgery. PATIENTS AND METHODS A total of 60 patients undergoing bimaxillary surgery were studied in a prospective, randomized, and double-blind study of oral propranolol 10 mg or placebo as premedication before hypotensive anesthesia with sodium nitroprusside. Hemodynamic variables, the amount of sodium nitroprusside used, and blood loss were statistically analyzed. RESULTS The heart rate and amount of sodium nitroprusside used were highly significantly less (P < .01) in the propranolol group, but no significant difference was found in blood loss between the 2 groups. No clinically significant complications were observed in either group. CONCLUSION Premedication with oral propranolol 10 mg before hypotensive anesthesia with sodium nitroprusside is safe and effective to reduce reflex tachycardia and the amount of sodium nitroprusside used.
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5.
The beta-adrenergic antagonist propranolol partly abolishes thermogenic response to bioactive food ingredients.
Belza, A, Gille, MB, Schultz John, S, Kondrup, J
Metabolism: clinical and experimental. 2009;(8):1137-44
Abstract
A combination of tyrosine, capsaicin, catechins, and caffeine has been shown to possess a thermogenic effect in humans. The present objective was to investigate whether the thermogenic response to the bioactive combination (BC) could be diminished or abolished by propranolol. Twenty-two men (age, 29.0 +/- 7.1 years; body mass index, 26.0 +/- 3.6 kg/m(2); mean +/- SD) participated in a 4-way, randomized, double-blind, placebo-controlled crossover study. The effect of the following was tested: (1) placebo, (2) BC, (3) BC + 5 mg propranolol, and (4) BC + 10 mg propranolol. Resting metabolic rate, respiratory quotient, and the thermogenic response were measured for 5 hours postintake. Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate, and appetite ratings were assessed every half hour. The BC increased resting metabolic rate by 5% (73 [36; 110] kJ/5 h, mean [95% confidence interval], P < .0001) compared with placebo. Both propranolol doses blunted the thermogenic response by 50% compared with placebo (P < .01). The BC increased SBP by 3% (4 +/- 1 mm Hg, P = .003) compared with placebo. The effect of BC on SBP was reduced by 25% by propranolol (P = .07). The BC (with or without propranolol) increased DBP by 6% (4 +/- 1 mm Hg, P ≤ .0002). Propranolol decreased heart rate by 5% (3 +/- 1 beats per minute, P < .0001) compared with placebo and BC. No effects were observed on appetite ratings. In conclusion, the study confirms the thermogenic properties of BC. The 50% reduction of the thermogenic response by propranolol indicates that beta-adrenergic pathways are partly responsible for the thermogenic response.
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6.
Distal myocardial protection with intracoronary beta blocker when added to a Gp IIb/IIIa platelet receptor blocker during percutaneous coronary intervention improves clinical outcome.
Uretsky, BF, Birnbaum, Y, Osman, A, Gupta, R, Paniagua, O, Chamoun, A, Pohwani, A, Lui, C, Lev, E, McGehee, T, et al
Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions. 2008;(4):488-97
Abstract
OBJECTIVE The present study tested the hypothesis that intracoronary (IC) propranolol improves clinical outcomes with percutaneous coronary intervention (PCI) when used with background Gp IIb/IIIa receptor blockade. BACKGROUND We have previously shown that administration of a relatively large weight-based IC dose of the beta blocker propranolol before PCI decreases the incidence of post-PCI myocardial infarction (MI) and improves short- and long-term outcome. It has previously been shown that administration of a Gp IIb/IIIa receptor blocker decreases post-PCI MI and improves short- and long-term clinical outcome. METHODS Patients undergoing PCI (n = 400) were randomized in a prospective double-blind fashion to IC propranolol (n = 200) or placebo (n = 200) with eptifibatide administered to all the patients. Myocardial isoform of creatine kinase was measured during the first 24 hr and clinical outcomes at 30 days and 1 year. RESULTS MI after PCI was seen in 21.5% of placebo and 12.5% of propranolol patients (relative risk reduction 0.42; 95%CI 0.09, 0.63; P = 0.016). At 30 days, the composite end point of death, post-procedural MI, urgent target lesion revascularization, or MI after index hospitalization occurred in 22.5% of placebo vs. 13.5% of propranolol patients (risk reduction 0.43; 95%CI 0.08, 0.65; P = 0.018). Similar results were observed at 1 year with adverse outcomes in 21.5% of propranolol and 32.5% of placebo patients (P = 0.01). CONCLUSION IC propranolol administration with the background Gp IIb/IIIa receptor blockade significantly reduces the incidence of post-PCI MI and improves the short- and long-term clinical outcome when compared with a Gp IIb/IIIa blocker alone.
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7.
Irbesartan plus low-dose propranolol versus low-dose propranolol alone in cirrhosis: a placebo-controlled, double-blind study.
Schepke, M, Wiest, R, Flacke, S, Heller, J, Stoffel-Wagner, B, Herold, T, Ghauri, M, Sauerbruch, T
The American journal of gastroenterology. 2008;(5):1152-8
Abstract
OBJECTIVES Angiotensin II receptor antagonists have been shown to moderately lower portal pressure in some patients with cirrhosis but may have adverse effects on kidney function. This study aimed at comparing the effects of a combined treatment using irbesartan plus propranolol with propranolol monotherapy on portal pressure and kidney function in patients with cirrhosis. METHODS Thirty-two patients were included (Child A/B/C: 13/18/1, etiology: 16 alcohol, 13 viral, 3 other; bilirubin 1.4 +/- 1.1 mg/dL, creatinine 0.86 +/- 0.20 mg/dL, baseline hepatic venous pressure gradient 18.7 +/- 5.3 mmHg). All patients received 20 mg propranolol b.i.d. Additionally, they randomly received either placebo (N = 15) or irbesartan (step-up dosage titration up to 300 mg/d, N = 17). Patients were followed at weekly intervals, re-evaluation of hepatic venous pressure gradient (HVPG) was performed after 8 wk. RESULTS One patient in the propranolol/irbesartan group was excluded due to variceal bleeding. No other adverse events occurred. Portal pressure declined in both groups (propranolol/irbesartan group 19.6 +/- 1.5 mmHg to 16.6 +/- 1.2 mmHg, P= 0.037, propranolol/placebo group 17.8 +/- 1.1 mmHg to 15.1 +/- 1.2 mmHg, P= 0.019). Sodium excretion significantly increased in the propranolol/irbesartan group (from 122 +/- 20 mmol/d to 230 +/- 23 mmol/d, P= 0.045), but not in the propranolol/placebo group. CONCLUSIONS Combination treatment of propranolol plus irbesartan is well tolerated in cirrhotic patients when titrating the angiotensin II antagonist in a step-up manner, and it increases sodium excretion in patients with compensated or moderately decompensated cirrhosis. Addition of irbesartan has no effect on portal pressure.
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8.
Sodium Valproate versus Propranolol in paediatric migraine prophylaxis.
Ashrafi, MR, Shabanian, R, Zamani, GR, Mahfelati, F
European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society. 2005;(5):333-8
Abstract
In a randomized clinical trial the effect of Sodium Valproate in pediatric migraine prophylaxis was compared with that of Propranolol. One hundred and twenty patients with common migraine (migraine without aura) aged from 3 to 15 years who met the defined criteria enrolled into the study. Randomly the patients were divided in two groups of A and B, treating with sodium Valproate and Propranolol, respectively. Three phases of baseline period (phase I), titration and adjustment period (phases II) and fixed -dose treatment period (phase III) have been designed. A total of 57 patients in group A, and 58 patients in group B completed all phases of the trial. Seventy two percent of patients in group A and 69% of patients in group B have responded to Sodium Valproate and Propranolol, respectively, as a reduction of more than 50% in headache frequency per month. Further more both drugs have shown efficacy in reducing the severity and duration of headache and also better response to rescue medications (p value <0.01). There was no significant difference in all previously mentioned therapeutic effects between two groups (p value <0.05).
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9.
The effect of propranolol on glyceryltrinitrate-induced headache and arterial response.
Tvedskov, JF, Thomsen, LL, Thomsen, LL, Iversen, HK, Williams, P, Gibson, A, Jenkins, K, Peck, R, Olesen, J
Cephalalgia : an international journal of headache. 2004;(12):1076-87
Abstract
Prophylactic drug trials in migraine are long-lasting and expensive and require long-term toxicology information. A human migraine model would therefore be helpful in testing new drugs. Immediate headache and delayed migraine after glyceryltrinitrate (GTN) has been well characterized. We have recently shown that sodium valproate has prophylactic effect in the GTN model. Here we report our experience with propranolol in this model. Nineteen subjects with migraine without aura and 16 sex- and aged-matched healthy subjects were included in a two-centre randomized double-blind cross-over study. Fourteen migraine subjects and 14 healthy subjects completed the study and results from comparison of the 28 subjects are reported. Randomly propranolol 160 mg or placebo were each given daily for 14 days to both migraine and healthy subjects. A 20-min intravenous infusion of GTN 0.25 microg/kg per min was administered on a study day at the end of both pretreatment periods. Headache was registered for 12 h after GTN infusions. Its intensity was scored on a numerical verbal rating scale from 0 to 10. Fulfilment of International Headache Society (HIS) criteria was recorded for 24 h. Radial and superficial temporal artery diameters and blood velocity of both middle cerebral arteries were measured. All migraine subjects developed headache after GTN. No reduction of overall peak headache was found after propranolol (median 5, range 0-7) compared with placebo (median 5, range 0-10) (P = 0.441). Eight of the 14 completing migraine subject developed IHS 1.1 migraine after GTN, two subjects on both days, three subjects only after placebo, and three subjects only after propranolol. No reduction of GTN-induced migraine was found after propranolol compared with placebo (5 vs. 5, P = 1.000). All healthy subjects developed headache after GTN. No reduction of overall peak headache was found after propranolol (median 2, range 1-5) compared with placebo (median 1, range 1-7) (P = 0.315). Two subjects fulfilled IHS criteria 1.1 for migraine without aura after propranolol but not after placebo. The fulfilment was short lasting and did not require rescue medication. Headache after GTN was more pronounced in migraine subjects than in healthy subjects both with (P = 0.003) and without pretreatment with propranolol (P = 0.017). We found that 2 weeks of propranolol constricted the radial artery in healthy subjects but not in migraine subjects. GTN-induced vasodilatation abolished this difference. Mean maximum blood flow velocity in the middle cerebral artery was higher in healthy subjects than in migraine patients (P = 0.003-0.033) and unaffected by propranolol. We observed no effect of propranolol on GTN-induced headache and migraine. This could indicate that GTN induces migraine at a deeper level of the pathophysiological cascade of migraine than the prophylactic effect of propranolol. Propranolol does not constrict cerebral arteries, which therefore cannot be part of its mechanism of action in migraine.
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10.
Distal myocardial protection during percutaneous coronary intervention with an intracoronary beta-blocker.
Wang, FW, Osman, A, Otero, J, Stouffer, GA, Waxman, S, Afzal, A, Anzuini, A, Uretsky, BF
Circulation. 2003;(23):2914-9
Abstract
BACKGROUND Experimental studies have demonstrated that intravenous beta-blocker administration before coronary artery occlusion significantly reduces myocardial injury. Clinical studies have shown that intracoronary (IC) propranolol administration before percutaneous coronary intervention (PCI) delays myocardial ischemia. The present study tested the hypothesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardial infarction (MI) and short-term adverse outcomes after PCI. METHODS AND RESULTS Patients undergoing PCI (n=150) were randomly assigned in a double-blind fashion to receive IC propranolol (n=75) or placebo (n=75). Study drug was delivered before first balloon inflation via an intracoronary catheter with the tip distal to the coronary lesion. Biochemical markers were evaluated through the first 24 hours and clinical outcomes to 30 days. Evidence of MI with creatine kinase-MB elevation after PCI was seen in 36% of placebo and 17% of propranolol patients (P=0.01). Troponin T elevation was seen in 33% of placebo and 13% of propranolol patients (P=0.005). At 30 days, the composite end point of death, postprocedural MI, non-Q-wave MI after PCI hospitalization, or urgent target-lesion revascularization occurred in 40% of placebo versus 18% of propranolol patients (hazard ratio 2.14, 95% CI 1.24 to 3.71, P=0.004). CONCLUSIONS IC administration of propranolol protects the myocardium during PCI, significantly reducing the incidence of MI and improving short-term clinical outcomes.