Suppression of chronic ventricular arrhythmias with propranolol.

Woosley, Raymond L.; Kornhauser, David M.; Smith, Raymond A.; Reele, Stots B.; Higgins, Stanley B.; Nies, Alan S.; Shand, David G.; Oates, John A.

doi:10.1161/01.cir.60.4.819

Cited by 133 publications

(22 citation statements)

References 22 publications

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“…24 The bioavailability of propranolol varies considerably both within and between patients after long-term treatment,25 and adequate beta-blockade cannot be achieved in all patients if a fixed dose is used. Nevertheless, for practical purposes, we chose a regimen of 40 mg four times a day.…”

Section: Discussionmentioning

confidence: 99%

One year's treatment with propranolol after myocardial infarction: preliminary report of Norwegian multicentre trial.

Hansteen¹,

Møinichen²,

Lorentsen³

et al. 1982

BMJ

195

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A prospective, randomised, double-blind study was performed to compare the effects of propranolol and placebo on sudden cardiac death in a high-risk group of patients who survived acute myocardial infarction. Altogether 4929 patients with definite acute myocardial infarction were screened for inclusion: 574 (116%) died before randomisation, and 3795 (77%) were excluded.Five hundred and sixty patients aged 35 to 70 years were stratified into two risk groups and randomly assigned treatment with propranolol 40 mg four times a day or placebo. Treatment started four to six days after the infarction. By one year there had been 11 sudden deaths in the propranolol group and 23 in the placebo group (p <0 038, two-tailed test analysed according to the "intention-to-treat" principle). Altogether there were 25 deaths in the propranolol group and 37 in the placebo group (p <0 12), with 16 and 21 non-fatal reinfarctions respectively. A quarter of the patients were withdrawn from each group. Withdrawal because of heart failure during the first two weeks of treatment was significantly more common among propranolol-treated patients than among the controls, but thereafter the withdrawal rate was the same.The significant reduction in sudden death was comparable with that after alprenolol, practolol, and timolol, which suggests that the mechanism of prevention is beta-blockade rather than any other pharmacological property of the individual drugs.

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Section: Discussionmentioning

confidence: 99%

One year's treatment with propranolol after myocardial infarction: preliminary report of Norwegian multicentre trial.

Hansteen¹,

Møinichen²,

Lorentsen³

et al. 1982

BMJ

195

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“…Intravenous administration of the same dose of L-propranolol, on the other hand, produced cerebrospinal fluid levels of only 1.2-1.4 ng/ml, while 6.7-62.5 and 2-15.4 ng/ml were detected in the plasma at 5 and 10 minutes, respectively ( 28 Thus, the measured plasma concentration of 9+3.2 ng/ml observed after intracerebroventricular injection should be below therapeutic antiarrhythmic blood levels. Cerebrospinal fluid levels, on the other hand, were on the order of 200-300 -fold higher.…”

Section: Propranolol Pharmacokineticsmentioning

confidence: 94%

Central beta-adrenergic mechanisms may modulate ischemic ventricular fibrillation in pigs.

Parker

Michael

Hartley

et al. 1990

Circulation Research

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A central noradrenergic process may permit expression of the stress-related increase in cardiac vulnerability to ventricular fibrillation (VF). Thus, the effect of central j8-adrenergic receptor blockade with L-propranolol (0.01 The high dose of L-propranolol also reduced the incidence of VF (7/15 fibrillated) compared with Ringer's solution (12/12 fibrillated) and D-propranolol (6/7 fibrillated). The lower dose of L-propranolol was without effect on VF vulnerability (7/9 fibrillated). The plasma concentration resulting from central administration of 0.05 mg/kg L-propranolol was found to be 9.05+±3.25 ng/ml, which is significantly below therapeutic antiarrhythmic blood levels. We conclude that the reduced vulnerability to ischemia-induced VF after intracerebroventricular administration of propranolol is due to alteration of a central P-adrenergic receptor-mediated phenomenon as opposed to an effect on the heart directly or to nonspecific membrane stabilization. (Circulation Research 1990;66:259-270) V arious psychological risk factors have been related epidemiologically to cardiac rhythm disturbances in the presence and absence of coronary artery disease.1-6 These rhythm disturbances include ventricular tachycardia and ventricular fibrillation (VF), the underlying mechanisms of sudden cardiac death. Although some of the psychological stressors are clearly related to acute phasic stress and imminent emotional distress accompanied by hemodynamic alterations consistent with autonomic imbalance, many are related to more tonic From the section of Cardiovascular Sciences (G.W.P., L.H.M.,

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“…Because of these data as well as the fact that propranolol is generally less effective than standard antiarrhythmic agents such as quinidine in suppressing ventricular arrhythmias (8)(9)(10), many investigators have attributed its antiarrhythmic effects to beta-adrenergic receptor blockade (11,12). In a more recent study (13) using a wide range of propranolol dosages to treat frequent VEDs, 40% of the patients with arrhythmia suppression required plasma propranolol concentrations > 150 ng/ml, a level associated with a high degree of beta blockade (14,15). These results raised the possibility that some property other than beta-adrenergic receptor blockade was responsible for ventricular arrhythmia suppression in some patients.…”

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confidence: 99%

Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade.

Murray¹,

Reilly²,

Koshakji³

et al. 1990

J. Clin. Invest.

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To investigate the mechanisms of ventricular arrhythmia suppression by propranolol, we determined the antiarrhythmic efficacy of d-propranolol in 10 patients with frequent ventricular ectopic depolarizations (VEDs) and nonsustained ventricular tachycardia. After an initial placebo phase, 40 mg d-propranolol was administered orally every 6 h with dosage increased every 2 d until arrhythmia suppression (> 80% VED reduction), intolerable side effects, or a maximal dosage (1,280 mg/d) was reached. Response was verified by documenting return of arrhythmia during a final placebo phase. Arrhythmia suppression occurred in six patients while two more had partial responses. Effective dosages were 320-1,280 mg/d (mean 920±360, SD) of d-propranolol with corresponding plasma concentrations of 60-2,280 ng/ml (mean 858±681). For the entire group, the QTc interval shortened by 4±4% (P = 0.03). Arrhythmia suppression was accompanied by a reduction in peak heart rate during exercise of 0-29%. To determine whether arrhythmia suppression could be attributed to betablockade, racemic propranolol was then administered in dosages producing the same or greater depression of exercise heart rate. In 3/8 patients, arrhythmias were not suppressed by racemic propranolol indicating that d-propranolol was effective via a non-beta-mediated action. By contrast, in 5/8 patients racemic propranolol also suppressed VEDs. We conclude that propranolol suppresses ventricular arrhythmias by both beta-and non-beta-adrenergic receptor-mediated effects. (J. Clin. Invest. 1990.85:836-842.) propranolol * antiarrhythmic * ventricular arrhythmias * dextropropranolol-betaadrenergic receptor blockade

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Suppression of chronic ventricular arrhythmias with propranolol.

Cited by 133 publications

References 22 publications

One year's treatment with propranolol after myocardial infarction: preliminary report of Norwegian multicentre trial.

One year's treatment with propranolol after myocardial infarction: preliminary report of Norwegian multicentre trial.

Central beta-adrenergic mechanisms may modulate ischemic ventricular fibrillation in pigs.

Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade.

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