Key result
AVE0118 terminates persistent AF in ~43% of canine models, outperforming disopyramide, cibenzoline, and aprindine.
Why the study?
Information is limited regarding whether atrial IK,ACh may serve as a potential therapeutic target to terminate persistent AF.
Do IK,ACh inhibitors and class I drugs terminate persistent atrial fibrillation in a canine model?
Do IK,ACh inhibitors and class I drugs terminate persistent atrial fibrillation in a canine model?
IK,ACh inhibition combined with open-state INa suppression with slow dissociation kinetics may synergistically exert potent antiarrhythmic action against persistent AF.
May support IK,ACh inhibition for persistent AF; leaves open translation to human therapy.
Since information is still limited whether atrial IK,ACh may become a potential therapeutic target to terminate persistent atrial fibrillation (AF), we assessed it by using the persistent AF canine model with representative IK,ACh inhibitor AVE0118 and class I drugs. AVE0118 (6 mg/kg, n = 7), disopyramide (3 mg/kg, n = 7) and cibenzoline (3 mg/kg, n = 6) terminated the AF in 3/7, 1/7 and 2/6 animals, respectively, whereas aprindine (3 mg/kg, n = 6) did not suppress it. These findings suggest that IK,ACh inhibition in addition to open-state INa suppression with slow dissociation kinetics can synergistically exert potent antiarrhythmic action against persistent AF.
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Kambayashi et al. (2022) studied Persistent atrial fibrillation (n=26). AVE0118, disopyramide, cibenzoline, and aprindine was evaluated on Termination of atrial fibrillation. The IK,ACh inhibitor AVE0118 terminated persistent atrial fibrillation in 42.9% (3/7) of canine models, compared to 14.3% with disopyramide, 33.3% with cibenzoline, and 0% with aprindine.
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