Future directions of electrotherapy for atrial fibrillation.
Suboptimal treatment of atrial fibrillation (AF) by pharmacotherapy alone has given rise to multiple novel electrotherapeutic modalities including pacing, ablation, and atrial defibrillation. These treatment approaches offer physicians the opportunity to evaluate their patients more extensively to better optimize therapy. AV junctional node ablation followed by full-time pacing improves quality of life and reduces the incidence of tachycardia-induced cardiomyopathy. Physicians who are reluctant to ablate the AV node may opt for either an AV nodal modification procedure or therapeutic modalities that attempt to maintain sinus rhythm. Both biatrial and dual site pacing have met with some success in preventing AF in a limited patient population. Studies also have evaluated the extent to which pacing may be used to terminate AF. These initial studies showed that, in general, pacing was ineffective. Radiofrequency catheter ablation is another therapeutic modality receiving considerable interest. The creation of multiple lesions mimicking the maze procedure, isthmus ablation to prevent the onset of atrial flutter that may degrade into AF, and ablation of tachycardia foci are all potential treatment alternatives to consider either as the primary therapy or as a synergistic procedure designed to augment another electrical therapy. Internal atrial defibrillation is being shown to be both safe and efficacious. This therapy appears uniquely able to repeatedly restore sinus rhythm in a segment of the AF population. Any of these therapies, either alone or more likely in some form of combined therapy, is likely to significantly influence and improve the care of patients with AF in the future.
Reuter
D
D
InControl, Inc., Redmond, Washington 98052, USA.
Ayers
G M
GM
D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy*; D002304:Cardiac Pacing, Artificial; D017115:Catheter Ablation; D004554:Electric Countershock / Q000295:instrumentation / Q000639:trends*; D006801:Humans