Differential Analysis of the Frequency-Dependent Effects of Class 1 Antiarrhythmic Drugs According to Periodical Ligand Binding

Weirich, J.; Antoni, H.

doi:10.1097/00005344-199006000-00019

Cited by 79 publications

(21 citation statements)

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“…In the presence of a fast recovery drug (kD, 4 second-1; e, 4 second-1), we found that the window width increased from 6 to 9 msec. Decreasing the unbinding rate from 4 the unbinding rate resulted in progressive increases in the duration of the VW and reductions in conduction velocity.…”

Section: Resultsmentioning

confidence: 82%

“…Decreasing the unbinding rate from 4 the unbinding rate resulted in progressive increases in the duration of the VW and reductions in conduction velocity.…”

Section: Resultsmentioning

confidence: 99%

“…However, with an 8-cm circumference, premature stimulation in the absence of drug yielded a premature response and one additional response. In the presence of drug (kD, 4 second-1; e, 4 second-') there was a continuously reentrant action potential. Although such a demonstration is to a certain extent arbitrary (we can select any circumference), it demonstrates that given a sufficiently long path, the unidirectional block we studied in detail can initiate reentrant activation.…”

Section: Resultsmentioning

confidence: 99%

“…Computer modified sodium channel conductance.3 All of these drugs interact with the cardiac sodium channel and modify the time course of availability of sodium channels for recruitment in the excitatory process. 4 Reentrant rhythms occur in a variety of settings, and it has been proposed that unidirectional block, perhaps resulting from a dispersion of the refractory states of individual cells, is a requirement for initiation. 5 Investigators have discussed dispersion of refractoriness as a reflection of cellular variations of the repolarization process derived from structural differences between cells.…”

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confidence: 99%

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Proarrhythmic response to sodium channel blockade. Theoretical model and numerical experiments.

et al. 1991

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Background. The use of flecainide and encainide was terminated in the Cardiac Arrhythmia Suppression Trial because of an excess of sudden cardiac deaths in the active treatment group. Such events might arise from reentrant rhythms initiated by premature stimulation in the presence of anisotropic sodium channel availability. Drugs that bind to sodium channels increase the functional dispersion of refractoriness by slowing (a result of the drug-unbinding process) the transition from an inexcitable state to an excitable state. It is interesting that encainide and flecainide unbind slowly (15-20 seconds), whereas lidocaine and moricizine unbind rapidly (0.2-1.3 seconds).Methods and Results. With a computer representation of a cable with Beeler-Reuter membrane

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Section: Resultsmentioning

confidence: 82%

“…Decreasing the unbinding rate from 4 the unbinding rate resulted in progressive increases in the duration of the VW and reductions in conduction velocity.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Proarrhythmic response to sodium channel blockade. Theoretical model and numerical experiments.

et al. 1991

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“…Flecainide is classified as a slow kinetic drug and is known to have a strong sodium channel-blocking action. 39 It is also reported that flecainide has a direct effect on I to.…”

Section: Mechanism Of St a Due To Flecainidementioning

confidence: 96%