Key result
Hypokalaemia prolonged epicardial action potential durations and induced early afterdepolarizations and ventricular tachycardia in isolated mouse hearts, recapitulating the clinical phenotype.
Population
Isolated mouse hearts and whole-cell patch-clamped epicardial and endocardial myocytes
Comparison
Perfusion with hypokalaemic solutions vs Perfusion with normokalemic solutions
Design
Preclinical
Authors
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Hypokalaemia may promote VT via APD changes in murine hearts; hypothesis-generating with no clinical implications yet.
Hypokalaemia in isolated murine hearts induces early afterdepolarizations and reduces transmural dispersion of repolarization, providing a mechanistic substrate for ventricular tachycardia.
Killeen et al. (2007) studied Hypokalaemia-induced ventricular tachycardia. Hypokalaemic solutions vs. Normokalemic solution (5.2 mM K+) was evaluated on Action potential durations (APD90) and arrhythmic events. Hypokalaemia prolonged epicardial action potential durations and induced early afterdepolarizations and ventricular tachycardia in isolated mouse hearts, recapitulating the clinical phenotype.
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