Protection Against Programmed Electrical Stimulation-Induced Ventricular Tachycardia and Sudden Cardiac Death by NE-10064, a Class III Antiarrhythmic Drug

Black, Shawn C.; Butterfield, James L.; Lucchesi, Benedict R.

doi:10.1097/00005344-199312000-00006

Cited by 59 publications

(15 citation statements)

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“…In VF-resistant dogs in the exercise plus ischemia sudden-death protocol, azimilide did not induce VF (57). In neither inducible nor noninducible dogs in PES studies did azimilide cause or worsen arrhythmias (3,16,47).…”

Section: Safety Pharmacologymentioning

confidence: 99%

Pharmacology of Azimilide Dihydrochloride (NE‐10064), A Class III Antiarrhythmic Agent

Salata

Brooks

1997

Cardiovascular Drug Reviews

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Section: Safety Pharmacologymentioning

confidence: 99%

Pharmacology of Azimilide Dihydrochloride (NE‐10064), A Class III Antiarrhythmic Agent

Salata

Brooks

1997

Cardiovascular Drug Reviews

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“…In isolated human atrial and ventricular myocytes, azimilide produces a concentration-dependent inhibition of both the I Ks and I Kr [9•,10,28,33]. In intact animal models, azimilide has been shown to suppress both atrial [35,36] and ventricular arrhythmias, and has the potential to prevent sudden death following coronary artery occlusion [37,38]. Of particular interest, the drug has been found to be unusually and consistently effective in terminating AF and AFL in various canine experimental models [35,36].…”

Section: Pure Class III Antiarrhythmic Drugs Under Development: Focusmentioning

confidence: 99%

What niche will newer class III antiarrhythmic drugs occupy?

Singh

Sarma

2001

Curr Cardiol Rep

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The decline in the use of sodium channel blockers has led to an expanding use of b-blockers and complex class III agents such as sotalol and amiodarone for controlling cardiac arrhythmias. Success with these agents in the context of their side effects has spurred the development of compounds with simpler ion channel-blocking properties with less complex adverse reactions. The resulting so-called pure class III agents were found to have antifibrillatory effects in atrial fibrillation (AF) and flutter, as well as in ventricular tachyarrhythmias. Pure class III compounds are effective in inducing acute chemical conversion of AF, in preventing paroxysmal AF, and in maintaining sinus rhythm in patients with persistent AF restored to sinus rhythm. Examples of such compounds are dofetilide, which selectively blocks IKr, and ibutilide, available only as an intravenous agent, which blocks the IKr and augments the inactivated Na+ current in atrial myocytes. Dofetilide and ibutilide have been introduced into clinical practice. Azimilide is the first of the class III agents that blocks both components (IKr and IKs) of the delayed rectifier current, which may confer certain electrophysiologic advantages. The potential therapeutic niche of ibutilide, dofetilide, and azimilide in the control of cardiac arrhythmias forms the basis of this review.

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“…Early data does indeed show that drugs, designed to block IKs, increase the action potential duration (APD) with reverse use dependence [7,8]. In intact animal models, azimilide, which predominantly inhibits this current, has suppressed both atrial and ventricular arrhythmias and has the potential to prevent sudden death following coronary artery occlusion [9,10]. The results of clinical trials with azimilide are awaited.…”

Section: Advent Of the Patch Clamp Techniquementioning

confidence: 99%

The impact of recent ion channel science on the development and use of antiarrhythmic drugs

Langan

1999

Curr Cardiol Rep

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In the past 20 years in the basic laboratory, tools have been developed to further our understanding of the mechanism of arrhythmias and of the effect of compounds on these or their substrates. Patch clamp studies have better defined the cardiac channels. A new classification of antiarrhythmic drugs was devised, coined the Sicilian Gambit. Drugs, aimed at blocking specific channels, are now being developed. With the cloning of channels, information about their molecular structure became available. One can begin to understand the molecular determinants of antiarrhythmic drug action on specific ion channels, and how this is modulated by effectors. Molecular and electrophysiologic techniques also have been used to collect information about the way disease states affect the cardiac channels, and how this can alter the response to ion channel blockers. This has proceeded utilizing a few technologies. Diseased heart cells from patients, from animal models of disease, or from transgenic mice are studied to examine the change in current expression and channel protein quantity in different stages of disease. Hopefully this new information will make drug therapy more target-oriented.

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Protection Against Programmed Electrical Stimulation-Induced Ventricular Tachycardia and Sudden Cardiac Death by NE-10064, a Class III Antiarrhythmic Drug

Cited by 59 publications

References 0 publications

Pharmacology of Azimilide Dihydrochloride (NE‐10064), A Class III Antiarrhythmic Agent

Pharmacology of Azimilide Dihydrochloride (NE‐10064), A Class III Antiarrhythmic Agent

What niche will newer class III antiarrhythmic drugs occupy?

The impact of recent ion channel science on the development and use of antiarrhythmic drugs

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