Pharmacological prevention of atrial tachycardia induced atrial remodeling as a potential therapeutic strategy.
Atrial fibrillation (AF) is the most common cardiac arrhythmia requiring medical therapy, and present treatment modalities are inadequate. Over the past few years, we have learned a great deal about the phenomenon of electrical remodeling, by which rapid atrial activation leads to changes in atrial electrical properties that promote AF initiation and maintenance. This knowledge opens up the possibility that electrical remodeling may itself be a novel therapeutic target in AF. The present paper reviews what is known about the basic mechanisms of atrial electrical remodeling and then discusses the experimental and clinical evidence that remodeling can be prevented by drug therapy. Despite great potential value, the development of pharmacological interventions to prevent atrial electrical remodeling is still in its infancy.
Shinagawa
Kaori
K
Montreal Heart Institute, Research Center, 5000 Belanger Street East, Montreal, Quebec, Canada H1T 1C8.
Derakhchan
Katayoun
K
Nattel
Stanley
S
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D000975:Antioxidants / Q000494:pharmacology; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000503:physiopathology*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004594:Electrophysiology; D006325:Heart Atria / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D026902:Potassium Channel Blockers / Q000627:therapeutic use; D026941:Sodium Channel Blockers / Q000627:therapeutic use; D013610:Tachycardia / Q000503:physiopathology / Q000517:prevention & control*; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D000889:Anti-Arrhythmia Agents; D000975:Antioxidants; D002121:Calcium Channel Blockers; D026902:Potassium Channel Blockers; D026941:Sodium Channel Blockers