doi: 10.1161/CIRCULATIONAHA.106.626689
(Circulation. 2006;113:2474-2476.)
© 2006 American Heart Association, Inc.
Editorial |
Cell Therapy for Rate Control in Atrial Fibrillation
A New Approach to an Old Problem
From the Harvard-Thorndike Electrophysiology Institute and Arrhythmia Service, Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass.
Correspondence to Kevin F. Kwaku, MD, PhD, Beth Israel Deaconess Medical Center, Cardiovascular Division, 330 Brookline Ave, RW 453, Boston, MA 02215. E-mail kkwaku@bidmc.harvard.edu
Key Words: Editorials • atrioventricular node • electrophysiology • heart rate • atrial fibrillation
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Physicians and patients alike have long sought ways by which to tame the rapid and irregular heartbeats that typically accompany atrial fibrillation (AF). In addition to offering symptomatic relief from palpitations, this goal has gained further importance since the recognition that sustained rapid, and perhaps also irregular, ventricular rates can lead to adverse structural cardiac remodeling and the development of a tachycardia-induced cardiomyopathy.1 In many instances, maintenance of sinus rhythm is either impractical or unachievable, and in addition to therapeutic anticoagulation, most patients will require some strategy to control their ventricular rate during AF.
Article p 2485
The mainstays of pharmacological rate control for AF have remained unchanged for decades and consist of digoxin, ß-blockers, and the nondihydropyridine calcium channel antagonists verapamil and diltiazem alone or in combination.2,3 However, medical treatment often is limited by a lack of efficacy or intolerance of side effects. Research involving novel agents such as selective A1 adenosine agonists4,5 remains in early stages and is unlikely to overcome the drawbacks of currently available drugs.
A nearly 100% efficacious approach to ventricular rate control in AF is catheter-based radiofrequency ablation of the AV junction (AVJ).6,7 Experimentally, the same result is achievable with cryoablation,8 laser energy,9 or ethanol infusion into the AV nodal artery.10 Although appropriate in selected patients,6,11–13 radiofrequency AVJ ablation has the distinct disadvantage of rendering them permanently pacemaker dependent. An increased risk of tachyarrhythmic sudden death after AVJ ablation may be countered by pacing at higher rates early after the procedure; however, concerns exist
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