Antiarrhythmic Therapy for Atrial Tachyarrhythmias

Antiarrhythmic therapy can have a key role in prolonging the lives of patients with most common atrial tachyarrhythmias such as atrial flutter (AFL) or atrial fibrillation (AF). The optimal use of antiarrhytmic drug therapy depends in part on understanding the underlying mechanisms of AFL and AF and pharmacodynamis of each antiarrhythmic drug. Currently, there is a large body of experimental and clinical evidence that documents that AFL is associated with a macro-reentry mechanism associated with a largeaaa excitable gap in the right atrium and an area of slow conduction in the triangle of Koch. The common and uncommon types share the same mechanism on location. AF is a complex arrhythmia. Theories underlying the mechanism of AF are: the cirrcus movement, the multiple foci, the fractionate contactions, the unifocal theory, and the combination of theories. The mechanism of focal atrial tachycardia has been the subject of dabete, with abnormal automaticity, triggered activity, microreentry and all considered possibilities. Currently available antiarrhythmic drugs have limited efficacy for acute termination of AF and AFL, especially if the arrhythmia is not of recent onset. Intravenous Ibutilide given in repeated doses and i.v. procainamide hydrochloride have been recommended for acute termination of AF and AFL. Efficacy is highest in AFL and in AF with either a short arrhythmia duration or a normal left atrial size. For the prevention of AFL and AF, the following drugs have been recommended: disopyramide, quinidine, propafenone, flecainide, sotalol and amiodarone. Currently, catheter ablation using radiofrequency electrical energy is the preferred first therapy, when feasible for treatment of atrial tachyarrhytmisa, including ablation of ectopic atrial tachycardia, AFL. and AF (the Maze procedure). The surgical ablation (the corridor operation or the Maze operation for AF) has a limited role in the management of patients in whom catheter ablation has failed.