Molecular biology of atrial fibrillation.
Atrial fibrillation (AF) is the most common arrhythmia seen in medical practice. Despite the overall advance in the treatment of the cardiac dysrhythmias with the introduction of radiofrequency ablation, therapeutic options in AF have remained largely unchanged and aimed at controlling the heart rate and anticoagulation. New surgical and ablation techniques are being developed. While promising, they are still extremely laborious and available only to a handful of patients. The limited success in the therapy of AF is in part due to our poor understanding of its molecular pathophysiology. Molecular research of AF has focused on 2 main fields, identification of the genes that play a role in the initiation of the disease and altered gene expression during the disease state. These studies are aimed at identifying not only the triggering factors in the acute form but also those that perpetuate the arrhythmia and convert it into a chronic form. Advances in genetics and molecular biology will likely give new insights into the development of the disease and improve our understanding and therapeutic options.
Brugada
R
R
Masonic Medical Research Laboratory, Utica, NY 13501, USA. brugada@mmri.edu
D000200:Action Potentials; D000367:Age Factors; D000818:Animals; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D002412:Cations / Q000378:metabolism; D004285:Dogs; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007473:Ion Channels / Q000235:genetics / Q000502:physiology; D009206:Myocardium / Q000473:pathology; D010375:Pedigree
D002412:Cations; D007473:Ion Channels