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uced increase in action potential duration, while amplifying drug-induced conduction slowing, both in S1 and S2 beats. As a result, whilst the EW was increased (quinidine and procainamide), or not changed (flecainide) at the long S1 -S1 intervals, it was invariably reduced by these agents at the short S1 -S1 intervals. These findings indicate that increased heart rate prior to ectopic activation shapes the arrhythmic profiles by facilitating drug-induced EW reduction. This article is protected by copyright. All rights reserved. This articl