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Arrhythmogenic Effects of Quinidine on Catecholamine‐Induced Delayed Afterdepolarizations in Canine Atrial Fibers
Author(s) -
WIT ANDREW L.,
TSENG GEANY,
HENNING BERTHOLD,
HANNA MICHAEL S.
Publication year - 1990
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.1990.tb01045.x
Subject(s) - quinidine , afterdepolarization , medicine , tetrodotoxin , electrophysiology , cardiology , endocrinology , repolarization
Arrhythmogenic Effects of Quinidine on Catecholamine‐induced Delayed Afterdepolarizations . We studied the effects of quinidine and tetrodotoxin (TTX), two drugs that block Na + channels, on delayed afterdepolarizations (DAD) caused by norepinepbrine in atrial fibers of the canine coronary sinus. At long stimulus cycle lengths of 10 seconds, quinidine increased the amplitude of the afterdepolarizations and caused triggered activity within 1–2 minutes. Simultaneously, action potential duration (APD) was lengthened but upstroke velocity was not decreased. Prolonged exposure to quinidine eventually decreased upstroke velocity but DAD amplitude remained larger than control and triggered activity was still induced more easily. The effects of quinidine to increase afterdepolarizations was partially related to its prolongation of the APD since shortening APD with repolarizing current decreased DAD amplitude. However, DAD amplitude remained larger than control indicating that quinidine caused triggering by other mechanisms as well. TTX, on the other hand, which blocks Na + channels but shortens APD, decreased DAD amplitude and triggered activity. Part but not all of these effects resulted from the shortening of APD by TTX since prolongation of APD with depolarizing current only partially restored DAD amplitude. Anti‐arrhythmic drugs, therefore, may have effects on DADs that partly result from changes in the APD. Quinidine may cause cardiac arrhythmias by virtue of its effects to potentiate triggered activity.