Esophageal Electrocardiography

Esophageal Lead Ambulatory Monitoring with QRST Subtraction Demonstrates Left Atrial Initiation of Paroxysmal Atrial Fibrillation.

Guerra P, Sparks P, Mlynash M, Groenewegen AS, Roithinger F, Steiner P, Lesh MD. Univ of California San Francisco. Abstract presented at North American Society of Pacing and Electrophysiology, Toronto. May, 1999. Background: Recent results suggest a pulmonary vein (PV) focus triggers AF in patients with paroxysmal atrial fibrillation (PAF). Given the difficulty in inducing triggering beats in the EP laboratory, a noninvasive screening tool for left atrial (LA) triggers is desirable. Methods: We evaluated the utility of ambulatory esophageal lead monitoring (ELAM) to identify patients with LA premature beats (APBs) which initiate AF. Because of its proximity to the posterior left atrium (LA), early activation in the esophageal lead should occur at or before the onset of the surface P wave for the APBs arising from the PV region. Recognition of initiating APBs on the EKG is hampered by the superimposed T waves. A novel automatic QRST subtraction algorithm was applied to the Holter data to isolate ectopic P waves. ELAM was performed on 17 patients referred to PAF using a Mortara Instruments 12-lead recorder. A 10 French bipolar esophageal lead (CardioCommand TAPSCOPE-210) was positioned such that an adequate atrial signal was obtained. Results: ELAM was performed for a mean of 16.5 +/- 6.3 hours and the esophageal lead was well tolerated in all. Ten patients had a total of 40 PAF initiations. During sinus rhythm, the atrial signal recorded from the esophageal lead occurred 33 +/- 6 msec after the surface P wave, reflecting the expected late LA activation. All PAF episodes were initiated by an APB. Atrial activation during APB was consistently early in all the esophageal tracings, occurring a mean of 28 +/- 11 msec before the onset of the P wave revealed by QRST-subtraction of the surface tracings. These patients underwent invasive mapping of the initiating foci for PAF. Two patients had left upper PV foci, 2 hard right upper PV foci, 1 a left lower PV focus, 1 a right lower PV focus, and 2 patients had foci in both upper PVs. Two patients did not have sufficient APBs to permit mapping. Conclusions: 1) Ambulatory esophageal EKG monitoring is feasible and when compared to QRST subtraction can reveal left atrial foci as initiators of PAF. 2) Documenation of early esophageal lead activation for APBs that initiate AF is highly predictive of PV triggers, and may serve as a useful screening test for candidates for focal AF ablation.

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