Bretylium tosylate in treatment of refractory ventricular arrhythmias complicating myocardial infarction.

Terry, G; Vellani, C W; Higgins, Michael R.; Doig, A.

doi:10.1136/hrt.32.1.21

Cited by 60 publications

(5 citation statements)

References 5 publications

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“…Bretylium acts via two electrophysiologic mechanisms. First, it impairs the neuronal release at lower doses and in partially depolarized myocardium, and decreases ERP and the excitability threshold [231]. At higher doses and in normal fibers, bretylium lengthens APD and ERP [244].…”

Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Zehender

Hohnloser

Just

1991

Cardiovasc Drug Ther

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The antiarrhythmic principle of drug-induced QT-interval prolongation is well known. However, with the widespread use of the presently known and new Class III antiarrhythmic agents under investigation, and the growing number of agents not primarily designed as antiarrhythmic drugs that potentially cause QT prolongation, we have also become aware of the proarrhythmic hazards associated with many of these agents. The proarrhythmic risk differs markedly from one agent to another and interferes with many individual clinical variables (e.g., hypokalemia, sinus bradycardia). This paper summarizes the present data on the proarrhythmic risk of drug-induced QT prolongation, including the value and problems of the rate-corrected QT interval, the mechanisms involved in the genesis of proarrhythmia, and the clinical cofactors that facilitate the occurrence of proarrhythmic events. In addition, an extensive database provides information on the known proarrhythmic risk of all currently used QT-prolonging agents.

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Section: Characteristics Of Proarrhythmia After Drug-lnduced Qt Prolomentioning

confidence: 99%

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Zehender

Hohnloser

Just

1991

Cardiovasc Drug Ther

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“…It is recognized that late-occurring arrhythmias during recovery from AMI have a poor outcome unless treated with bretylium. 194 …”

Section: In-hospital Mortalitymentioning

confidence: 97%

“…This is consistent with other reports of bretylium's salvage of virtually moribund patients with drug and countershock refractory VF. [142][143][144]170,177,184,185,188,190,192,194,195,[197][198][199][200][201][202] It should be noted that the crossover patients who received bretylium later than 24 hours after admission all developed confirmed infarctions.…”

Section: Crossover Patientsmentioning

confidence: 99%

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Bacaner

Brietenbucher²,

LaBree³

2004

American Journal of Therapeutics

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It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholestero...

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“…However, almost every controlled study has failed to show a reduction in the incidence of ventricular fibrillation by prophylactic administration of lidocaine even when arrhythmias per se were suppressed (2)(3)(4)(5)(6)(7)(8)(9)(10)(11). In contrast, ventricular fibrillation can be suppressed by bretylium tosylate and its pharmacologic analog, bethanidine sulphate (2,(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31). Both drugs (termed class 3) increase ventricular fibrillation threshold manyfold, facilitate electrical defibrillation, and induce episodes of pharmacologic (spontaneous) defibrillation under conditions where it does not normally occur (refs.…”

Section: Introductionmentioning

confidence: 99%

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

Bacaner¹,

Clay²,

Shrier³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The suppression of ventricular fibrillation by antidysrhythmic drugs is well correlated with their ability to block potassium channels in nerve and cardiac membranes. Blockade of potassium channels reduces electrical inhomogeneities in action potential and conduction parameters that lead to ventricular fibrillation. These actions tend to effectively decrease the electrical size of the heart, which suggests a mechanism for antifibrillatory drug action. The receptor sites for antifibrillatory drug action (IK blockade) appear to be on the outside of the cardiac membrane whereas receptors for antiarrhythmic drug action (INa blockade) appear to be on the inside of the cardiac membrane.

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Bretylium tosylate in treatment of refractory ventricular arrhythmias complicating myocardial infarction.

Cited by 60 publications

References 5 publications

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

QT-Interval prolonging drugs: Mechanisms and clinical relevance of their arrhythmogenic hazards

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

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