Novel pharmacological therapies for atrial fibrillation.
OBJECTIVE
Atrial fibrillation is a common yet difficult cardiac rhythm to treat. Limitations of the currently available medications, increasing complexity of atrial fibrillation patient populations and the prevalence of the condition have made new drug development crucial. Our understanding of the pathophysiology of atrial fibrillation has increased tremendously over the years. The importance of electrical remodeling and structural remodeling has been widely appreciated and has opened new avenues for pharmacological research.


RESULTS
Novel ion channel blockers have targeted atrial-specific ion channels or a combination of ion channels in order to maximize efficacy and minimize proarrhythmic risk. Understanding of atrial fibrillation as a metabolically complex condition with activation of multiple signaling cascades has fuelled drug development in a new direction. Exciting new drugs inhibiting fibrosis, cellular hypertrophy and improving cell-cell communication may help treat chronic atrial fibrillation in the future.


CONCLUSIONS
Continuing progress in our knowledge of the ionic and structural remodeling in atrial fibrillation will only accelerate the search for a safe antidote. In the future focal pharmacological modulation may help target specific targets in diverse populations. The potential of many of these pharmacotherapies, however, will need to be tested in large randomized trials before our faith in them is realized.
Bagwe
Suveer
S
Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. SDBagwe@uams.edu
Leonardi
Marino
M
Bissett
Joe
J
D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use*; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology
D000889:Anti-Arrhythmia Agents; D002317:Cardiovascular Agents; D007473:Ion Channels