Key result
Endothelin-1 infusion prolongs endocardial action potential duration by ~14% and induces afterdepolarizations in dogs.
Population
32 anesthetized, open-chest mongrel dogs
Comparison
Endothelin-1 administered into the left anterior… vs Control group with atrioventricular node ablation
Design
Preclinical
Authors
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No change to clinical practice; extends experimental evidence on endothelin-1 arrhythmogenesis but leaves open human relevance.
Absolute Event Rate: 290% vs 255%
p-value: p=<0.05
In a canine model, endothelin-1 induces malignant ventricular arrhythmias primarily through the prolongation of monophasic action potential duration and the development of early afterdepolarizations.
Merkely et al. (1998) studied Ventricular arrhythmias (n=32). Endothelin-1 (ET-1) vs. Baseline/Control was evaluated on Endocardial monophasic action potential (MAP) 90% duration at 70 beats/min ventricular pacing (p=<0.05). Endothelin-1 infusion significantly increased endocardial monophasic action potential duration (290 vs 255 ms; p<0.05) and induced afterdepolarizations in dogs.