Propranolol in the Treatment and Prevention of Cardiac Arrhythmias

Gianelly, Ralph E.; Griffin, John R.; Harrison, Donald C.

doi:10.7326/0003-4819-66-4-667

Cited by 63 publications

(9 citation statements)

References 15 publications

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“…For example, Coltart and Shand22 found that 50% inhibition of exercise tachycardia occurred with about 30 ng/ml plasma propranolol and that almost maximal inhibition was produced by 100-150 ng/ml. Chidsey et al 21 found ,7(8) 0 (3) I-" (2) ,.-' (2) 7<5) (4) that concentrations of 14 and 8 ng/ml were associated with 50% reduction in renin levels and exerciseinduced tachycardia, respectively. They also showed that the plasma concentration-response curve for reduction in anginal attacks and exercise heart rate were superimposable.…”

Section: Discussionmentioning

confidence: 99%

“…Ventricular arrhythmias were suppressed in 98 cases (44%) and decreased in 27 additional cases (total response 57%). Gianelly et al 2 did not observe benefit in any of the five patients given propranolol for ventricular arrhythmias, but dosages were less than 120 mg/day and plasma levels were not reported. Another series of 10 patients with the prolapsing mitral valve syndrome had only a 50% response rate with the maximum dosage of 160 mg/day.3 Winkle et al 4 observed a decrease in VEDs in only five of nine patients with mitral valve prolapse.…”

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confidence: 99%

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Suppression of chronic ventricular arrhythmias with propranolol.

Woosley¹,

Kornhauser²,

Smith³

et al. 1979

Circulation

132

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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

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Suppression of chronic ventricular arrhythmias with propranolol.

Woosley¹,

Kornhauser²,

Smith³

et al. 1979

Circulation

132

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“…In an early report, this effect could be demonstrated in vitro at only very high concentrations of propranolol that are not routinely achieved during clinical use (7). 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).…”

mentioning

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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“…One of its two principal effects is to depress or block the ac tions of various catecholamines upon the beta receptors (59), the main � adrenergic cardiac actions being acceleration of heart rate and A-V conduc tion, and strengthening of cardiac contraction. Thus, the antiarrhythmic application of �-adrenergic blockage may be the slowing of supraventricular tachycardias, increasing the degree of A-V blockade in atrial fibrillation or flutter, and the neutralization of the excessive irritability of the various car diac pacemakers in response to excessive catecholamine stimulation (60). Propranolol also has been found to possess antiarrhythmic properties other than those related to this �-blockade.…”

Section: Antiarrhythmic Drugsmentioning

confidence: 98%

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

Selzer¹,

Cohn²

1970

Annu. Rev. Med.

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Two developments at the beginning of this decade exerted a profound influence upon clinical management of acute myocardial infarction: the in troduction of closed-chest resuscitation with electric shock therapy for ven tricular fibrillation, and the availability of continuous monitoring of the electrocardiogram by means of the cathode-ray oscilloscope. As a result of this, the coronary care unit has become a standard facility for the treatment of myocardial infarction. I t should be recognized that the concept of thera peutic centers for patients with myocardial infarction encompasses a broad range of facilities available in such units (1). On the one end of the spectrum, one can place the comprehensive cardiology center, equipped to treat all as pects and complications of myocardial infarction, including the use of emer gency surgery and artificial pump-support. On the other end, is the small area in a hospital in which nurses can observe the patient's rhythm displayed upon the monitoring oscilloscope. The great majority of coronary care units ap proach the latter end of the spectrum-based primarily on the availability of electrocardiographic monitoring units. Thus, the role of such units is the identification, early recognition, treatment, and prevention of dangerous arrhythmias. The most common arrhythmias that are potentially life-threat ening are related to increased "irritability" of the ventricular myocardium. The purpose of this review is to examine the rationale for the therapy of ventricular arrhythmias in acute myocardial infarction-both the fundamen tal and practical considerations. INCIDENCE OF ARRHYTHMIASDuring the earlier era, when the diagnosis of arrhythmias was based on their occurrence during routine examination of the patient or during record ing of an electrocardiographic tracing, the incidence of arrhythmias was es timated to range between 9 and 27 percent, with an average of 18 percent

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Propranolol in the Treatment and Prevention of Cardiac Arrhythmias

Cited by 63 publications

References 15 publications

Suppression of chronic ventricular arrhythmias with propranolol.

Suppression of chronic ventricular arrhythmias with propranolol.

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

Treatment of Ventricular Extrasystoles and Tachyarrhythmias in Acute Myocardial Infarction

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