Nonuniform Recovery of Excitability in Ventricular Muscle

Han, Jaok; Moe, Gordon K.

doi:10.1161/01.res.14.1.44

Cited by 903 publications

(248 citation statements)

References 14 publications

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“…Regional differences in action potential duration may cause reentry due to focal reexcitation without a preceding triggering beat. 7 Another possible mechanism is related to differences in refractory periods between hrkinje cells and ventricular myocardium, which may predispose to bundle-branch reentry.3 Although we did not note the development of right bundle-branch block or fascicular block during tachycardia induction, this mechanism cannot be excluded completely.…”

Section: Discussionmentioning

confidence: 81%

Triggered activity as arrhythmogenic mechanism after myocardial infarction: Clinical and electrophysiologic study of one case

Wiesfeld

Crijns

Veldhuisen³

et al. 1992

Clinical Cardiology

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Section: Discussionmentioning

confidence: 81%

Triggered activity as arrhythmogenic mechanism after myocardial infarction: Clinical and electrophysiologic study of one case

Wiesfeld

Crijns

Veldhuisen³

et al. 1992

Clinical Cardiology

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“…The electrophysiological background reflects the different duration of the monophasic action potentials and a delayed occurrence of some action potentials because of the slow conduction properties. 16,17 …”

Section: Discussionmentioning

confidence: 99%

Magnetic Dispersion of the Late Repolarization in Brugada Syndrome

Joung

Kim

Lee

et al. 2008

Circ J

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Background Magnetocardiography (MCG) is a new noninvasive modality for recording cardiac depolarization and repolarization and was used in the present study to evaluate abnormalities in patients with Brugada syndrome (BS). Methods and ResultsThe MCG findings of 10 BS, 21 right bundle branch block (RBBB), and 34 normal patients were compared. On the horizontal spatiotemporal activation graph (STAG), the r' waves were more frequently located on the right side in the RBBB than in the normal (p=0.001) or BS groups (p=0.001). The maximum current angles of the r' wave fell into the northwest axis in all BS patients as compared to having a right axis deviation in 19 of 21 RBBB patients (90.4%, p=0.001). In the magnetic field and current density vector maps during late repolarization, the BS group had a non-dipole pattern more frequently and a higher number of poles compared with the normal (p=0.001) and RBBB groups (p=0.001). Conclusions During depolarization, the horizontal STAG location and maximum current angle of the r' wave were beneficial in differentiating BS from RBBB and normal. The magnetic dispersion was a more frequently observed finding in BS patients than in RBBB and normal patients during late repolarization. (Circ J 2008; 72: 94 -101)

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“…This finding suggests that bepridil could be arrhythmogenic at toxic doses. Bepridil at such a high concentration might cause a slow conduction in the ventricle accompanied by a spatial inhomogeneity of refractoriness, which is an important prerequisite for the re-entrant arrhythmias precipitating ventricular fibrillation (Han & Moe, 1964;Marix, Yoon & Han, 1977). However, there is no evidence supporting this possible mechanism for the arrhythmogenic action of bepridil, and it is beyond the scope of this paper to extend the discussion in this direction.…”

Section: Discussionmentioning

confidence: 99%

Electromechanical effects of bepridil on rabbit isolated hearts

Anno

Furuta

Itoh

et al. 1984

British J Pharmacology

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Electromechanical effects of a new antianginal agent, bepridil, on Langendorff‐perfused rabbit hearts were compared with those of verapamil and lidocaine. Bepridil at concentrations above 2 × 10−7m caused a dose‐related decrease in heart rate (HR), a prolongation of the atrio‐His bundle conduction time (A‐H interval) and a prolongation of the functional refractory period (FRP) of the atrioventricular (A‐V) node. Similar changes in HR, A‐H interval and the FRP of the A‐V node were observed with verapamil at concentrations above 2 × 10−8m. Lidocaine at above 4 × 10−5m prolonged slightly the A‐H interval and the FRP of the A‐V node but did not decrease the HR. Bepridil at concentrations above 10−6m prolonged both the His bundle‐ventricular conduction time (H‐V interval) and the effective refractory period (ERP) of ventricular muscles. Similar changes in the H‐V interval and in the ERP of ventricular muscles were observed with lidocaine at above 10−5m. Verapamil ranging between 5 × 10−8m and 8 × 10−7m had no effect on the H‐V interval and appreciably shortened the ERP of ventricular muscles. Bepridil at concentrations above 2 × 10−6m reduced the developed tension as did verapamil at above 10−7m. On a molar basis, the depressant effect of bepridil on HR and the A‐V nodal conduction, which may reflect inhibitory action on the slow channels, was less than one tenth that of verapamil. Bepridil was more potent than lidocaine in prolonging the H‐V interval and the ERP of ventricular muscles indicating a possible inhibition of the fast sodium channels. Both of these electrophysiological effects of bepridil may afford significant bases for the antiarrhythmic action of the drug.

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Nonuniform Recovery of Excitability in Ventricular Muscle

Cited by 903 publications

References 14 publications

Triggered activity as arrhythmogenic mechanism after myocardial infarction: Clinical and electrophysiologic study of one case

Triggered activity as arrhythmogenic mechanism after myocardial infarction: Clinical and electrophysiologic study of one case

Magnetic Dispersion of the Late Repolarization in Brugada Syndrome

Electromechanical effects of bepridil on rabbit isolated hearts

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