Key result
Intracoronary endothelin-1 prolongs action potential and increases dispersion, supporting a direct arrhythmogenic effect.
Why the study?
Does intracoronary endothelin-1 infusion cause direct arrhythmogenic electrophysiological changes compared to myocardial ischemia in a canine model?
Population
Canine model (n=26)
Comparison
Intracoronary endothelin-1 infusion at 30… vs 30 min left anterior descending artery occlusion…
Design
Preclinical
Follow-up
90 minutes (30 min intervention + 60 min reperfusion)
Authors
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Endothelin-1 may promote arrhythmias via direct effects independent of ischemia in canines; leaves open human translation and therapeutic relevance.
Does intracoronary endothelin-1 infusion cause direct arrhythmogenic electrophysiological changes compared to myocardial ischemia in a canine model?
p-value: p=<0.05
Endothelin-1 exerts direct arrhythmogenic effects independent of ischemia, characterized by action potential prolongation, increased dispersion, and early afterdepolarizations.
Gellér et al. (2000) studied Myocardial ischemia and arrhythmogenesis (n=26). Intracoronary endothelin-1 (ET-1) infusion vs. LAD occlusion was evaluated on Changes in monophasic action potential duration (MAPD90), dispersion (MAPDISP), and upstroke velocity (UV) (p=<0.05). Intracoronary endothelin-1 infusion prolonged monophasic action potential, increased dispersion, and caused early afterdepolarizations, supporting a direct arrhythmogenic effect.
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