M A Mitchell1, I D McRury, D E Haines. 1. Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
Abstract
BACKGROUND: To test the hypothesis that susceptibility to sustained atrial fibrillation may be decreased by creation of linear atrial ablations, we established a canine model of chronic atrial fibrillation and used a novel catheter design to create atrial ablations. METHODS AND RESULTS: Chronic atrial fibrillation was induced in 16 dogs by creation of mitral regurgitation and rapid pacing of the atria. Temperature-controlled radiofrequency ablations were attempted along empirically derived, preselected atrial target sites in 11 dogs (ablation group), and a sham procedure was performed in 5 dogs (control group). Follow-up electrophysiology study and pathological examination were conducted 13+/-5 days after the initial procedure. Immediately after ablation, sustained atrial fibrillation could be initiated in 1 of 9 surviving ablation dogs and 5 of 5 controls (P=.004). Four dogs died within 24 hours of the procedure. Permanent pacing was required in 4 dogs. At follow-up, 0 of 7 ablation dogs and 5 of 5 controls had atrial fibrillation (P=.001). Furthermore, 2 of 7 ablation dogs had sustained atrial tachycardias, one of which was successfully ablated. Pathological examination demonstrated frequent incomplete lesion sets and discontinuous lesions. CONCLUSIONS: In this model, a reduction in the susceptibility to sustained atrial fibrillation can be achieved by long linear atrial ablations created with specially designed coil electrode catheters. Complete lesion continuity was not required to achieve a therapeutic effect.
BACKGROUND: To test the hypothesis that susceptibility to sustained atrial fibrillation may be decreased by creation of linear atrial ablations, we established a canine model of chronic atrial fibrillation and used a novel catheter design to create atrial ablations. METHODS AND RESULTS: Chronic atrial fibrillation was induced in 16 dogs by creation of mitral regurgitation and rapid pacing of the atria. Temperature-controlled radiofrequency ablations were attempted along empirically derived, preselected atrial target sites in 11 dogs (ablation group), and a sham procedure was performed in 5 dogs (control group). Follow-up electrophysiology study and pathological examination were conducted 13+/-5 days after the initial procedure. Immediately after ablation, sustained atrial fibrillation could be initiated in 1 of 9 surviving ablation dogs and 5 of 5 controls (P=.004). Four dogs died within 24 hours of the procedure. Permanent pacing was required in 4 dogs. At follow-up, 0 of 7 ablation dogs and 5 of 5 controls had atrial fibrillation (P=.001). Furthermore, 2 of 7 ablation dogs had sustained atrial tachycardias, one of which was successfully ablated. Pathological examination demonstrated frequent incomplete lesion sets and discontinuous lesions. CONCLUSIONS: In this model, a reduction in the susceptibility to sustained atrial fibrillation can be achieved by long linear atrial ablations created with specially designed coil electrode catheters. Complete lesion continuity was not required to achieve a therapeutic effect.
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