The use of beta-adrenergic receptor blocking drugs in dysrhythmias

Gibson, D G; Sowton, Edgar

doi:10.1016/0033-0620(69)90033-4

Cited by 163 publications

(47 citation statements)

References 87 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The characteristics of the 32 patients in this study are shown in table 1 Evidence that arrhythmia reduction is due to drug efficacy is seen in the dose-response curves for each patient ( fig. 1).…”

Section: Resultsmentioning

confidence: 99%

“…That this designation is a reflection of drug effect in this selected group of patients is supported in several ways: 1) Comparison of control hourly VED frequency with that at the dosages that produced 70% VED suppression was highly significant using a nonparametric statistical test felt to be an appropriate test for analysis of this type of data (Wilcoxon rank-sum test). 18 2) Patients in this study were selected to exclude low arrhythmia frequency, thereby reducing the The ordinate is percent of controlfrequency of ventricular tachycardia vs dosage expressed as the percent of the dosage that produced >70% VED suppression for that patient.…”

Section: Discussionmentioning

confidence: 96%

See 1 more Smart Citation

Suppression of chronic ventricular arrhythmias with propranolol.

Woosley¹,

Kornhauser²,

Smith³

et al. 1979

Circulation

130

View full text Add to dashboard Cite

SUMMARY The antiarrhythmic efficacy of propranolol was evaluated in 32 patients with chronic high frequency ventricular arrhythmias in a placebo-controlled protocol. After a placebo control period, propranolol was begun and the dosage increased sequentially until arrhythmia suppression was achieved, side effects appeared, or a maximum dosage of 960 mg/day was reached. Computerized analysis of ambulatory recordings was used to quantify the arrhythmias. Twenty-four patients had 70-100% arrhythmia suppression at plasma levels ranging from 12-1100 ng/ml (end of dosing interval). Eight patients in this group had frequent episodes of ventricular tachycardia that were totally suppressed at or below the dosage that produced >70% suppression of ventricular ectopic depolarizations (VEDs). A biphasic dose-response curve was seen in five patients who responded with a decrease in arrhythmia frequency in the lower ranges of dosages but had increased frequency of ectopic rhythms as the dosage was increased above the optimal level. Only one-third of patients

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 96%

Suppression of chronic ventricular arrhythmias with propranolol.

Woosley¹,

Kornhauser²,

Smith³

et al. 1979

Circulation

130

View full text Add to dashboard Cite

show abstract

“…In this way, beta blockers may have a beneficial effect in the conversion to sinus rhythm, mainly for the control of patients with tachyarrhythmias (Gibson and Sowton, 1969). Propranolol, the most studied and most widely employed drug, increases the basic sinus cycle length, and the atrioventricular intranodal conduction time, lowers the artificial atrial rate of the Wenckebach point, and has no effect on the His-Purkinje system.…”

Section: Discussionmentioning

confidence: 99%

Effects of atenolol in patients with reciprocating supraventricular tachycardia

Pimenta

Pereira

1986

Clinical Cardiology

View full text Add to dashboard Cite

Summary:We studied 12 patients with crisis of paroxysmal reciprocating supraventricular tachycardia before and after intravenous injection of 5 mg of atenolol. The patients were then followed for periods ranging from 6 to 50 months (median 34 months). During this time, they received oral atenolol therapy, at 200 mg for the first two weeks, and 100 mg daily thereafter. Tachycardia was due to reciprocation within the atrioventricular node in 9 patients, and to pre-excitation in 3 patients. Atenolol slowed the sinus rate, prolonged the atrioventricular conduction time, and increased the atrial cycle length at which atrioventricular nodal Wenckebach phenomenon occurred. During the tachycardia, atenolol increased the tachycardia cycle length, due to prolongation of the intranodal atrioventricular conduction time. Of the 11 patients who were observed for the full period, 7 had no further episodes of arrhythmia. One patient (with left-sided pre-excitation) failed to respond to any antiarrhythmic medication, one patient remained free of symptoms for two years, but received an atrial pacemaker for control of the tachycardia at the end of this period. Two patients (one with dual atrioventricular nodal pathways, and one with concealed leftsided pre-excitation) await other treatment for their tachycardia, after remaining free of symptoms for one and two years, respectively. These findings suggest that atenolol is an effective beta blocker for use in controlling arrhythmias in patients with reciprocating supraventricular tachycardia, for use in once daily dosage, and is a medication largely free of side effects.

show abstract

“…j3-Adrenergic blockade exerts a multitude of metabolic, hemodynamic, and electrophysiologic effects and has been shown to be clinically efficacious in the treatment of certain forms of ventricular tachyarrhythmias (1)(2)(3)(4). However, the mechanisms by which f3-adrenergic blockade suppresses ventricular tachyarrhythmias remain incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias.

Sung

Keung²,

Nguyen³

et al. 1988

J. Clin. Invest.

View full text Add to dashboard Cite

IntroductionTo assess effects of el-adrenergic blockade on ventricular tachycardia (VT) of various mechanisms, electrophysiology studies were performed before and after intravenous infusion of propranolol (0.2 mg/kg) in 33 patients with chronic recurrent VT, who had previously been tested with intravenous verapamil (0.15 mg/kg followed by 0.005 mg/kg/min infusion). In the verapamil-irresponsive group, 10 patients (group IA) had VT that could be initiated by programmed ventricular extrastimulation and terminated by overdrive ventricular pacing, and 11 patients (group IB) had VT that could be provoked by isopro- (5) found that intravenous propranolol slowed the sinus rate but did not affect the VT rate and its inducibility. We and others (6-9), in contrast, observed that intravenous propranolol was effective in suppressing VT inducibility in patients in whom VT was provocable with intravenous infusion of isoproterenol. The disparity in responses to ,B-adrenergic blockade connotes that the occurrence of VT may be accounted for by different electrophysiologic mechanisms.Using the technique of programmed electrical stimulation along with pharmacologic testing with intravenous verapamil, we have previously separated three "presumptive" mechanisms of VT in human beings: reentry, catecholamine-sensitive automaticity, and triggered activity related to delayed afterdepolarizations (10). In the present study, we assessed effects of ,B-adrenergic blockade on these three forms ofVT. Our findings indicate that f3-adrenergic blockade is only specifically effective in suppressing VT suggestive of catecholamine-sensitive automaticity. MethodsPatients. Between July 1983 and July 1986, we studied 33 patients with clinically documented sustained VT that could be reproduced during the course of electrophysiologic evaluation. Sustained VT was defined as VT that lasted longer than 30 s. We excluded patients who were hemodynamically unstable and who had a prior history of congestive heart failure or who had an ejection fraction of < 40% as measured by radionuclide angiography (1 1). All 33 patients had had echocardiography and treadmill exercise testing using the standard Bruce protocol (12) before electrophysiology studies. Additionally, 24 patients had undergone cardiac catheterization with coronary angiography as clinically indicated. There were 22 men and 11 women ranging in ages from 18 to 66 (mean 42.5) yr (Tables I-III). 10 patients had arteriosclerotic heart disease with prior myocardial infarction of > 6 mo, 5 patients had idiopathic cardiomyopathy, and 18 patients had no clinical evidence of structural heart disease. All patients were clinically symptomatic with palpitations, dizziness, and/or syncope. Plasma concentrations ofcatecholamines. In patients with VT provocable with treadmill exercise testing, blood samples were drawn for measurements of plasma epinephrine and norepinephrine levels 1. Abbreviations used in this paper: VT, ventricular

show abstract

The use of beta-adrenergic receptor blocking drugs in dysrhythmias

Cited by 163 publications

References 87 publications

Suppression of chronic ventricular arrhythmias with propranolol.

Suppression of chronic ventricular arrhythmias with propranolol.

Effects of atenolol in patients with reciprocating supraventricular tachycardia

Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias.

Contact Info

Product

Resources

About