A class III antiarrhythmic agent.
It is marketed under the trade name Tikosyn.
Capsules containing 125, 250, and 500 µg of dofetilide.
Due to the pro-arrhythmic potential of dofetilide, it is only available by prescription by physicians who have undergone specific training in the risks of treatment with dofetilide.
Used for the maintenance of sinus rhythm in individuals prone to the formation of atrial fibrillation and flutter, and for the chemical cardioversion to sinus rhythm from atrial fibrillation and flutter.
The half-life is approximately 10 hours, and ranges from 4.8 to 13.5 hours.
Selectively blocks the rapid component of the delayed rectifier outward potassium current, causing the refractory period of atrial tissue to increase in atrial fibrillation and atrial flutter.
Does not affect Vmax, conduction velocity, or the resting membrane potential.
THas a dose-dependent increase in the QT interval and the corrected QT interval (QTc), and as a result initiation of therapy under telemetry monitoring or if serial EKG measurements of QT and QTc can be performed.
A steady-state plasma level of dofetilide is achieved in 2–3 days.
80% of dofetilide is excreted by the kidneys via cation exchange, so the dose of should be adjusted in individuals with renal insufficiency.
Drugs that impair the renal cation exchange system including cimetidine, hydrochlorothiazide, itraconazole, ketocanazole, prochlorperazine, trimethoprim and verapamil should be avoided with the use of dofetilde.
About 20 percent metabolized in the liver via the CYP3A4 isoenzyme of the cytochrome P450 enzyme system, and drugs that interfere with CYP3A4 will increase drug levels.
Most serious side effect is torsades de pointes, with a dose related incidence of 0.3-10.5%.
During initiation of therapy patients should be hospitalized, observe serial renal function tests, have continuous cardiac monitoring and have cardiac resuscitation available.
The Danish Investigations of Arrhythmias and Mortality on Dofetilide (DIAMOND) study, indicated that the drug does not affect mortality in the treatment of patients post-myocardial infarction with left ventricular dysfunction, however it was shown to decrease all-cause readmissions as well as CHF-related readmissions.
Used in the suppression of atrial fibrillation in individuals with LV dysfunction.