November 1, 1991Pacing and Clinical Electrophysiology
Afterdepolarizations and Triggered Activity Develop in a Select Population of Cells (M Cells) in Canine Ventricular Myocardium: The Effects of Acetylstrophanthidin and Bay K 8644
Population
Canine ventricular myocardium
Design
Preclinical
Authors
Discussion
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Implication
Identifies M-cell specificity for afterdepolarizations in canine models; leaves open relevance to clinical digitalis toxicity and human arrhythmogenesis.
Key Points
- To determine whether early and delayed afterdepolarizations and triggered activity are preferentially induced in a specialized subpopulation of ventricular myocytes (M cells).
- Exposed canine ventricular myocardial tissue preparations to the cardiotonic agent acetylstrophanthidin and the calcium channel agonist Bay K 8644.
- Evaluated electrical repolarization, afterdepolarizations, and triggered activity across epicardial, deep subepicardial (M cell), and endocardial layers.
- Prominent early afterdepolarizations, delayed afterdepolarizations, and triggered action potentials were restricted to or far more readily induced in deep subepicardial M cells.
- Triggered activity induced by afterdepolarizations was never observed in the epicardial or endocardial cell layers.
Structured PICO
P
Population
Canine ventricular myocardium
I
Intervention
Acetylstrophanthidin (AcS) and Bay K 8644
O
Outcome
Induction of early afterdepolarizations (EADs), delayed afterdepolarizations (DADs), and triggered activitysurrogate
Demonstrates that afterdepolarizations and triggered activity induced by acetylstrophanthidin and Bay K 8644 occur specifically in the M cells of the canine ventricular myocardium.
Cite This Study
Sicouri et al. (1991) studied this question.