Background-Electrically based therapies for terminating atrial fibrillation (AF) currently fall into 2 categories:antitachycardia pacing and cardioversion. Antitachycardia pacing uses low-intensity pacing stimuli delivered via a single electrode and is effective for terminating slower tachycardias but is less effective for treating AF. In contrast, cardioversion uses a single high-voltage shock to terminate AF reliably, but the voltages required produce undesirable side effects, including tissue damage and pain. We propose a new method to terminate AF called far-field antifibrillation pacing, which delivers a short train of low-intensity electric pulses at the frequency of antitachycardia pacing but from field electrodes. Prior theoretical work has suggested that this approach can create a large number of activation sites ("virtual" electrodes) that emit propagating waves within the tissue without implanting physical electrodes and thereby may be more effective than point-source stimulation. Methods and Results-Using optical mapping in isolated perfused canine atrial preparations, we show that a series of pulses at low field strength (0.9 to 1.4 V/cm) is sufficient to entrain and subsequently extinguish AF with a success rate of 93% (69 of 74 trials in 8 preparations). We further demonstrate that the mechanism behind far-field antifibrillation pacing success is the generation of wave emission sites within the tissue by the applied electric field, which entrains the tissue as the field is pulsed. Conclusions-AF in our model can be terminated by far-field antifibrillation pacing with only 13% of the energy required for cardioversion. Further studies are needed to determine whether this marked reduction in energy can increase the effectiveness and safety of terminating atrial tachyarrhythmias clinically. Key Words: arrhythmia Ⅲ atrium Ⅲ cardioversion Ⅲ fibrillation Ⅲ mapping A trial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide, 1 affecting Ͼ2.2 million people in the United States alone. 2 Complications associated with chronic AF include increased risk for both thromboembolism and stroke. 2 Left untreated, paroxysmal AF often progresses to permanent AF, which is resistant to therapy. 3 Although underlying anatomic or pathophysiological factors may fuel this progression, 3 AF itself may lead to its own perpetuation through electric, structural, and metabolic remodeling of atrial tissue. The realization that AF begets AF 4 has led to management strategies that are designed to avoid the progression of AF by reducing the frequency and duration of AF episodes.
Clinical Perspective on p 476One such strategy, cardioversion, attempts to reset all electric activity in the atria and requires the use of large (Ͼ5 V/cm) electric field gradients. 5-7 These high energies cause pain and trauma for the patient, damage the myocardium, and reduce battery life in implanted devices. 8 Another strategy, antitachycardia pacing (ATP), seeks to avoid the development of permanent AF by suppressing paroxysmal A...