September 1, 1998Journal of Cardiovascular Electrophysiology
Acceleration‐Induced Action Potential Prolongation and Early Afterdepolarizations
Population
Canine left ventricular epicardial, M region, endocardial, and Purkinje fiber preparations
Comparison
Acceleration of pacing rate in preparations… vs Baseline slow pacing rates
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Supports caution with abrupt acceleration on IKr blockers; leaves open human validation of M-cell EAD mechanisms in torsades.
Structured PICO
P
Population
Canine left ventricular epicardial (n=10), M region (n=36), endocardial (n=10), and Purkinje fiber (n=12) preparations
I
Intervention
Acceleration of pacing rate (sudden acceleration from a basic cycle length range of 900 to 4,000 msec to a range of 500 to 1,500 msec) in preparations pretreated with E-4031 (1 to 2 microM)
C
Comparator
Baseline slow pacing rates (basic cycle lengths >= 800 msec)
O
Outcome
Early afterdepolarization (EAD) activity and action potential duration (APD)surrogate
Acceleration of heart rate can induce or facilitate transient early afterdepolarizations and action potential prolongation in ventricular M cells pretreated with an IKr blocker, providing a cellular mechanism for the precipitation of torsades de pointes.
Cite This Study
Burashnikov et al. (1998) studied this question.