Anti-arrhythmic drugs

Abstract

Anti-arrhythmic drugs (AAD's) alter the electrical properties of the heart principally by either prolonging the cardiac action potential, decreasing conduction velocity, reducing focal automaticity or a combination of these effects. Despite the fact that a large number of AAD's were initially developed for ventricular arrhythmias the most common current indication is actually AF. Although the majority of these drugs act relatively specifi cally on certain receptors the overall general distribution of these receptors throughout the ventricular and atrial myocardium may result in unwanted effects such as Torsades de Pointes (TdP) predominantly with class IA and class III drugs, prolongation of AV conduction, QRS widening and monomorphic VT with class IC drugs. A meta-analysis of 44 trials involving 11,322 patients showed that all AAD's were associated with an increased risk of proarrhythmia with the exception of amiodarone and propafenone (Lafuente-Lafuente et al. Arch Intern Med 166:719-28, 2006). Although amiodarone is a very useful agent in the treatment of both atrial and ventricular arrhythmias its use is often limited as a result of its potential long term non-cardiac side effects which limit its use (Rothenberg et al. Heart Dis Stroke 3:19-23, 1994). More recently, "atrial selective" AAD's have been developed which may have improved effi cacy with better side effect profi le. Additionally some drugs (such as renin-angiotensin aldosterone inhibitors and anti-infl ammatory agents) may affect the underlying substrate and be indirectly antiarrhythmic.