Key result
Class I antiarrhythmic drugs produced use-dependent QRS prolongation with characteristic kinetics for each agent that differed significantly among the drugs tested (p=0.0002).
Why the study?
Do class I antiarrhythmic agents produce use-dependent ventricular conduction slowing in humans with kinetics similar to in vitro sodium channel blockade?
Population
27 patients undergoing electrophysiological evaluation for antiarrhythmic therapy, and 8 age- and…
Comparison
Antiarrhythmic drugs vs Age- and disease-matched control patients not…
Design
Cohort
Follow-up
Acute (during electrophysiological evaluation)
Authors
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Supports sodium channel mechanism for class I conduction slowing in humans; leaves open clinical translation to arrhythmia risk.
Observational (n=35)
Do class I antiarrhythmic agents produce use-dependent ventricular conduction slowing in humans with kinetics similar to in vitro sodium channel blockade?
p-value: p=0.0002
Class I antiarrhythmic agents produce use-dependent QRS prolongation in humans with characteristic kinetics similar to in vitro Vmax depression, suggesting the mechanism is use-dependent sodium channel blockade.
Ranger et al. (1991) conducted an observational in Arrhythmia requiring electrophysiological evaluation (n=35). Class I antiarrhythmic drugs vs. Age- and disease-matched control patients not taking class I antiarrhythmic drugs was evaluated on Onset time course of ventricular conduction slowing (mean time constants for QRS duration changes) (p=0.0002). Class I antiarrhythmic drugs produced use-dependent QRS prolongation with characteristic kinetics for each agent that differed significantly among the drugs tested (p=0.0002).
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