Azimilide is a potassium channel antagonist that, in contrast to existing c
lass III antiarrhythmic agents, blocks both the rapidly (I-Kr) and slowly (
I-Ks) activating components of the delayed rectifier potassium current.
In animal and clinical studies, azimilide prolonged repolarisation by incre
asing the action potential duration and effective refractory period. In ani
mal models, azimilide was effective In terminating both atrial and ventricu
lar arrhythmias. Azimilide also demonstrated antifibrillatory efficacy in a
canine model of sudden cardiac death.
In patients with a history of atrial fibrillation/flutter, oral azimilide c
ontrolled arrhythmias mon effectively than placebo in a 6-month randomised
double-blind study. At a dosage of 125mg once daily, azimilide significantl
y Increased the time to first symptomatic recurrence of atrial fibrillation
/flutter. However, no significant difference between placebo and azimilide
was found in another study.
Oral azimilide 100mg once daily demonstrated clinically significant treatme
nt effects in patients with paroxysmal supraventricular tachycardia.
In clinical trials, azimilide was generally well tolerated and headache was
the most commonly occurring adverse event. Azimilide is associated with a
low incidence of proarrhythmic events, such as torsades de pointes, and few
serious adverse events have been reported.