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Potassium channel blockade amplifies cardiac instability numerical studies of torsades de pointes
Starmer C.F., , Namasivayam A., Singh M.
Published in National Library of Medicine
PMID: 7883289
Volume: 38
Issue: 4
Pages: 259 - 266
Suppression of responses to premature stimulation has been the guiding principle in managing many cardiac arrhythmias. Recent clinical trails revealed that sodium channel blockade increased the incidence of re-entrant cardiac arrhythmias resulting in sudden cardiac death, although the physiologic mechanism remains uncertain. Potassium channel blockade offers an alternative mechanism for suppressing responses to premature stimuli. We have developed a simple model of a 2D sheet of excitable cells. We can initiate re-entrant activation with stimuli timed to occur within a period of vulnerability (VP). Reducing the Na conductance increases the VP while reducing the K conductance increases the collective instability of the array, and arrhythmias similar to torsades de pointes seen in patients subjected to K channel blocked can be readily initiated. Thus, while K channel blockade may suppress excitability by prolonging the action potential duration, it appears to simultaneously exhibit proarrhythmic properties that result in complex re-entrant arrhythmias.
About the journal
JournalIndian Journal of Physiology and Pharmacology
PublisherNational Library of Medicine
Open AccessNo