Key result
Flecainide enhanced the induction of sustained ventricular arrhythmias in a postinfarction canine model, accounting for all 10 adverse proarrhythmic responses compared to D-sotalol (p<0.0001).
Why the study?
Does flecainide compared to D-sotalol affect myocardial conduction, refractoriness, and arrhythmia inducibility in a canine postinfarction model?
Population
canine occlusion-reperfusion infarction model
Comparison
flecainide vs D-sotalol
Design
Preclinical
Authors
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Suggests proarrhythmic risk with flecainide postinfarction; hypothesis-generating for differential effects of class Ic versus III agents in ischemic models.
Does flecainide compared to D-sotalol affect myocardial conduction, refractoriness, and arrhythmia inducibility in a canine postinfarction model?
p-value: p=<0.0001
In a canine postinfarction model, flecainide exhibits proarrhythmic effects related to selective slowing of myocardial conduction, whereas D-sotalol shows favorable antiarrhythmic effects by increasing refractoriness.
well et al. (1993) studied Myocardial infarction (canine occlusion-reperfusion model). Flecainide vs. D-sotalol was evaluated on Induction of sustained ventricular arrhythmias in previously noninducible dogs (p=<0.0001). Flecainide enhanced the induction of sustained ventricular arrhythmias in a postinfarction canine model, accounting for all 10 adverse proarrhythmic responses compared to D-sotalol (p<0.0001).
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