Antiarrhythmic effect of antazoline in experimental models of acquired short- and long-QT-syndromes

Ellermann, Christian; Sterneberg, Magdalena; Kochhäuser, Simon; Dechering, Dirk G.; Fehr, Michael; Eckardt, Lars; Frommeyer, Gerrit

doi:10.1093/europace/eux383

Cited by 13 publications

(16 citation statements)

References 17 publications

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“…This resulted in an increase of atrial postrepolarization refractoriness, an antiarrhythmic mechanism shared by other AADs (amiodaron, quinidine) . An experimental model of long/short QT further reinforced this theory, demonstrating the prolongation of ventricular ERP and a remarkable increase in ventricular PPR . The clinical effect observed in both studies was the abolition of atrial fibrillation and ventricular arrhythmia.…”

Section: Discussionmentioning

confidence: 60%

“…The detailed mechanism of antiarrhythmic properties of antazoline is not entirely clear but current data point to a multichannel mode of action involving sodium and potassium channels . Animal model studies report a significant increase of atrial and ventricular effective refractory periods (ERP) leading to a remarkable increase in atrial and ventricular postrepolarization refractoriness, an antiarrhythmic mechanism observed in amiodarone or quinidine …”

Section: Introductionmentioning

confidence: 99%

“…Both experimental and clinical studies indicate that biological effects exerted by antazoline are dose‐dependent …”

Section: Introductionmentioning

confidence: 99%

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Intravenous antazoline, a first‐generation antihistaminic drug with antiarrhythmic properties, is a suitable agent for pharmacological cardioversion of atrial fibrillation induced during pulmonary vein isolation due to the lack of influence on atrio‐venous conduction and high clinical effectiveness (AntaEP Study)

Farkowski

Maciąg

Kowalik

et al. 2019

Brit J Clinical Pharma

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Aims: Antazoline is a first-generation antihistaminic drug used primarily in eye drop formulations. When administered intravenously, antazoline displays antiarrhythmic properties resulting in a rapid conversion of recent-onset atrial fibrillation (AF) to sinus rhythm (SR).The aim of the study was to assess the influence of antazoline on atrio-venous conduction and other electrophysiological parameters in patients undergoing AF ablation.Methods: An experimental prospective study. Patients scheduled for the first-time AF ablation, in SR and not on amiodarone were enrolled. Atrio-venous conduction assessment and invasive electrophysiological study (EPS) were performed before and after intravenous administration of 250 mg of antazoline. In case of AF induction during EPS, antazoline was administered until conversion to SR or a cumulative dose of 300 mg. Results:We enrolled 14 patients: 13 (93%) men, mean age 63.4 (59.9-66.8) years, mean CHA 2 DS 2 -VASc score 1.6 (1.0-2.2). Antazoline was administered in a mean dose 257.1 (246.7-267.6) mg. Pulmonary vein potentials and atrial capture during pulmonary vein stimulation were present before and after the administration of antazoline. Wenckebach point and atrial conduction times did not change significantly, but atrio-ventricular node effective refractory period improved-324.7 (275.9-373.5) ms vs 284.3 (256.2-312.4) ms, P = 0.02. Antazoline was effective in all 5 (100%) cases of AF induction during EPS. There were no serious adverse events.Conclusion: Due to the lack of influence on atrio-venous conduction and high clinical effectiveness, antazoline may be suitable for pharmacological cardioversion of AF occurring during AF ablation.The authors confirm that the Principal Investigator for this paper is Michal M. Farkowski and that he had direct clinical responsibility for patients.

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Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

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Intravenous antazoline, a first‐generation antihistaminic drug with antiarrhythmic properties, is a suitable agent for pharmacological cardioversion of atrial fibrillation induced during pulmonary vein isolation due to the lack of influence on atrio‐venous conduction and high clinical effectiveness (AntaEP Study)

Farkowski

Maciąg

Kowalik

et al. 2019

Brit J Clinical Pharma

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“…The experimental setting of the antegradely-perfused Langendorff-heart has been described earlier extensively 11 . In short, 35 hearts of female New Zealand white rabbits were explanted and mounted to a Langendorff apparatus.…”

Section: Methodsmentioning

confidence: 99%

“…With propofol, post-repolarization refractoriness was significantly lengthened. Prolongation of PRR protects the myocardium against premature beats, is therefore antiarrhythmic 11,17 and a common pharmacological property of class I antiarrhythmic drugs. Consequently, ventricular vulnerability as tested by programmed ventricular stimulation was not increased with propofol.…”

Section: Impact Of Propofol On Cardiac Electrophysiologymentioning

confidence: 99%

Propofol abolishes torsade de pointes in different models of acquired long QT syndrome

Ellermann

Könemann

Wolfes

et al. 2020

Sci Rep

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There is conflicting evidence regarding the impact of propofol on cardiac repolarization and the risk of torsade de pointes (TdP). The purpose of this study was to elucidate the risk of propofol-induced TdP and to investigate the impact of propofol in drug-induced long QT syndrome. 35 rabbit hearts were perfused employing a Langendorff-setup. 10 hearts were perfused with increasing concentrations of propofol (50, 75, 100 µM). Propofol abbreviated action potential duration (APD 90) in a concentrationdependent manner without altering spatial dispersion of repolarization (SDR). Consequently, no proarrhythmic effects of propofol were observed. In 12 further hearts, erythromycin was employed to induce prolongation of cardiac repolarization. Erythromycin led to an amplification of SDR and triggered 36 episodes of TdP. Additional infusion of propofol abbreviated repolarization and reduced SDR. No episodes of TdP were observed with propofol. Similarly, ondansetron prolonged cardiac repolarization in another 13 hearts. SDR was increased and 36 episodes of TdP occurred. With additional propofol infusion, repolarization was abbreviated, SDR reduced and triggered activity abolished. In this experimental whole-heart study, propofol abbreviated repolarization without triggering TdP. On the contrary, propofol reversed prolongation of repolarization caused by erythromycin or ondansetron, reduced SDR and thereby eliminated drug-induced TdP.

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Digitalis Promotes Ventricular Arrhythmias in Flecainide- and Ranolazine-Pretreated Hearts

et al. 2018

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Antiarrhythmic effect of antazoline in experimental models of acquired short- and long-QT-syndromes

Abstract: Antazoline significantly reduced induction of VF in an experimental model of acquired SQTS. In three experimental models of acquired LQTS, antazoline effectively suppressed TdP.

Cited by 13 publications

References 17 publications

Propofol abolishes torsade de pointes in different models of acquired long QT syndrome

Digitalis Promotes Ventricular Arrhythmias in Flecainide- and Ranolazine-Pretreated Hearts

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