Atrial fibrillation (AF) is the most common cardiac arrhythmia in developed countries. AF is associated with increased mortality and morbidity due to thromboembolism, stroke and worsening of pre-existing heart failure. Currently available pharmacological therapies for AF suffer from unsatisfying efficacy and/or are associated with major side effects such as bleeding complications or proarrhythmia. These limitations largely result from the fact that most of the currently available drugs were developed on an empirical basis, without precise knowledge of the molecular mechanisms underlying the arrhythmia. During the last decade substantial progress has been made in understanding the molecular mechanisms contributing to the initiation and maintenance of AF. This knowledge is expected to stimulate the development of safer and more effective drugs. Here, we review new antiarrhythmic drug targets, which have emerged based on this increasing knowledge about the molecular mechanisms of AF.
Keywords: atrial remodeling; delayed after depolarizations (DADs); re-entry; triggered/ectopic activity.