Electrophysiological mechanisms in a canine model of erythromycin-associated long QT syndrome.

Rubart, Michael; Pressler, Milton L.; Pride, Harald P.; Zipes, Douglas P.

doi:10.1161/01.cir.88.4.1832

Cited by 104 publications

(67 citation statements)

References 65 publications

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“…They also showed that drug-induced LQTS was detected in wedge preparations, Purkinje fibers, HERG (the human ether-a-gogo-related gene), and isolated heart (rank order), although APD prolongation associated with only 3 of 4 drugs was detected in isolated heart. 20) In our in vivo canine model, the extent of EMinduced RV and LV MAPD prolongation was similar to that reported by Rubart,et al,17) and EAD and PVC occurred only rarely under administration of DP or EM alone. However, EADs were observed in 8 of the 12 dogs given both DP and EM (in either order), and PVC/TdP/VF developed in 3 dogs.…”

Section: Discussionsupporting

confidence: 89%

“…15,16) However, Rubart, et al reported that erythromycin at doses exceeding 20 mg/L prolonged APD both in vitro and in vivo, but the relative rare occurrence of EAD and ventricular arrhythmias suggested that other predisposing factors contribute to the acquired LQTS associated with erythromycin. 17) Eckardt, et al reported that ventricular tachyarrhythmias occurred in erythromycin-treated atrioventricular-blocked isolated rabbit hearts only in the presence of hypokalemia. 18) In contrast, Farkas, et al reported that despite being given in high doses, erythromycin neither prolonged repolarization nor induced proarrhythmia in an in vivo rabbit model of intact atrioventricular conduction.…”

Section: Discussionmentioning

confidence: 99%

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Combined Effect of Disopyramide and Erythromycin on Ventricular Repolarization in Dogs With Complete Atrioventricular Block

et al. 2011

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SummaryThe combined effects of disopyramide (DP) and erythromycin (EM) on ventricular repolarization and the incidences of ventricular premature contractions (VPCs) and torsades de pointes (TdP) were investigated in 12 anesthetized dogs with complete atrioventricular block. Monophasic action potentials (MAPs) were measured from the left and right ventricular (LV and RV) endocardium. The right or left ventricle was paced at a cycle length of 750-1000 msec. Dogs were divided into 2 groups and given either intravenous DP at 3 mg/kg and then intravenous EM at 50 mg/kg (group 1, n = 8), or intravenous EM at 50 mg/kg and then intravenous DP at 3 mg/kg (group 2, n = 4). MAP duration at 90% repolarization (MAPD 90 ) was measured before drug administration (baseline) and again after administration of each drug. RV MAPD 90 and LV MAPD 90 increased significantly (P < 0.02) after administration of each drug in group 1 (RV MAPD 90 : from 247.0 ± 36.3 [baseline] to 283.5 ± 38.3 to 321.8 ± 56.7; LV MAPD 90 : from 262.6 ± 49.1 (baseline) to 296.1 ± 58.8 to 351.0 ± 80.6). Early afterdepolarizations developed in 2 group 1 dogs after administration of DP and in 4 additional dogs after administration of EM. Frequent VPCs occurred in 1 dog after administration of DP and in 2 additional dogs after administration of EM, and TdP and ventricular tachycardias developed in 2 of the 3 dogs after administration of EM. Similar trends occurred in group 2. These results indicate a potentially fatal interaction between DP and EM administered in clinically relevant doses. (Int Heart J 2011; 52: 393-397)

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Combined Effect of Disopyramide and Erythromycin on Ventricular Repolarization in Dogs With Complete Atrioventricular Block

et al. 2011

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“…36 It has been suggested that, potentially, these oscillations may be arrhythmogenic by forming impulses repetitively in the myocardium. 36,37 A hallmark feature of the afterdepolarizations is their frequency dependence. The incidence of an EAD is increased as the BCL is increased, with the opposite effect seen with delayed afterdepolarizations (DADs 37 ).…”

Section: Eads In the Mouse Conduction Systemmentioning

confidence: 99%

Action Potential Characteristics and Arrhythmogenic Properties of the Cardiac Conduction System of the Murine Heart

Anumonwo

Tallini

Vetter

et al. 2001

Circulation Research

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Abstract-Studies have characterized conduction velocity in the right and left bundle branches (RBB, LBB) of normal and genetically engineered mice. However, no information is available on the action potential characteristics of the specialized conduction system (SCS). We have used microelectrode techniques to characterize action potential properties of the murine SCS, as well as epicardial and endocardial muscle preparations for comparison. In the RBB, action potential duration at 50%, 70%, and 90% repolarization (APD 50,70,90

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“…Erythromycin causes QT prolongation by inhibiting the delayed rectifier K + current (Rubart et al, 1993;Daleau et al, 1995). When combined with terfenadine or cisapride (discussed above), erythromycin enhances QT prolongation by blocking drug-metabolizing enzymes.…”

Section: Macrolide Anti-bioticsmentioning

confidence: 99%

Medicines and QT Prolongation

Kato¹,

Ijiri²,

Tanaka³

2012

Advances in Electrocardiograms - Methods and Analysis

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Electrophysiological mechanisms in a canine model of erythromycin-associated long QT syndrome.

Cited by 104 publications

References 65 publications

Combined Effect of Disopyramide and Erythromycin on Ventricular Repolarization in Dogs With Complete Atrioventricular Block

Combined Effect of Disopyramide and Erythromycin on Ventricular Repolarization in Dogs With Complete Atrioventricular Block

Action Potential Characteristics and Arrhythmogenic Properties of the Cardiac Conduction System of the Murine Heart

Medicines and QT Prolongation

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