Endocardial mapping of atrial fibrillation in the human right atrium using a non-contact catheter

Background Endocardial mapping of atrial fibrillation in humans is limited by its low resolution and by complexities in the arrhythmia and atrial anatomy. Methods and Results A catheter mounted non-contact multielectrode was deployed in the right atrium of 11 patients with atrial fibrillation and used to reconstruct 3360 electrograms, superimposed onto a computer-simulated model of the endocardium, using inverse solution mathematics. This allows construction of isopotential maps of the right atrium. Patients had either sustained atrial fibrillation (n=3) for >6 months or developed atrial fibrillation during the study (n=8). Spontaneous initiation of atrial fibrillation was recorded in one patient and was demonstrated by the non-contact system to arise from two successive atrial ectopic beats from the site of a roving contact catheter. Reconstruction of electrograms recorded during atrial fibrillation was validated by comparison with contact electrograms with cross-correlation. During established atrial fibrillation, four patients predominantly had a single right atrial wave front, two had two wave fronts and five patients had three to five wave fronts for most of the time. Periods of electrical silence were seen in the right atrium in eight patients, after which, activity emerged from consistent septal sites alone, suggesting a left atrial origin. During intravenous administration of flecainide, atrial fibrillation in two patients terminated spontaneously or following pacing manoeuvres, while in the remaining patient sinus rhythm was restored via atrial tachycardia. Conclusion Non-contact mapping of the right atrium has demonstrated modes of initiation and termination of atrial fibrillation, characterized different patterns of right atrial activation in atrial fibrillation and suggests that the left atrium may sustain atrial fibrillation in some patients. Simultaneous mapping of the right and left atrium is required to further elucidate the mechanisms of human atrial fibrillation.