Rh. Foster et al., IBUTILIDE - A REVIEW OF ITS PHARMACOLOGICAL PROPERTIES AND CLINICAL POTENTIAL IN THE ACUTE MANAGEMENT OF ATRIAL-FLUTTER AND FIBRILLATION, Drugs, 54(2), 1997, pp. 312-330
Ibutilide is the first 'pure' class III antiarrhythmic drug to become
available. Its predominant action is prolongation of the myocardial ac
tion potential duration. This appears to be achieved by a unique ionic
mechanism of action that involves activation of a late inward sodium
current and possibly blockade of the rapidly activating component of t
he cardiac delayed rectifier potassium current. Intravenous ibutilide
0.01 to 0.025 mg/kg or 1 to 2mg successfully converted atrial flutter
or fibrillation to sinus rhythm in 33 to 49% of patients in 2 placebo-
controlled trials involving 439 patients with sustained arrhythmia. In
a third trial in 300 patients who developed atrial flutter or fibrill
ation after cardiac surgery: ibutilide 2mg successfully converted the
arrhythmia in 57% of patients. The mean rimes to conversion were less
than or equal to 30 minutes in these trials, In 3 comparative trials,
ibutilide was significantly more effective than racemic sotalol or pro
cainamide in terminating atrial flutter or fibrillation. The pretreatm
ent duration of the arrhythmia is an important predictor of the succes
s of ibutilide treatment; the greatest conversion rates are achieved w
hen the arrhythmia is of recent onset (i.e. less than or equal to 30 d
ays' duration). Ibutilide is more effective in terminating atrial flut
ter than atrial fibrillation. Adverse events associated with ibutilide
are predominantly cardiovascular: Sustained polymorphic ventricular t
achycardia developed in 1.7%, and nonsustained polymorphic ventricular
tachycardia in 2.7%, of 586 patients treated with ibutilide in clinic
al trials. However; no proarrhythmia-related deaths have been reported
with the use of ibutilide, The drug has minimal haemodynamic effects
and is associated with few noncardiovascular adverse events. Thus, ibu
tiline is a useful agent for the pharmacological cardioversion of rece
nt-onset atrial fibrillation or flutter provided that adequate steps a
re taken to monitor for proarrhythmic events. The drug causes few nonc
ardiovascular adverse events and has minimal haemodynamic effects. Fur
thermore, it appears to be more effective than procainamide (especiall
y in patients with atrial flutter) and racemic sotalol.