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J Thorac Cardiovasc Surg 2004;127:770-778
© 2004 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Concurrent multiple left atrial focal activations with fibrillatory conduction and right atrial focal or reentrant activation as the mechanism in atrial fibrillation

^a Nippon Medical School, Tokyo, Japan

Presented at the Seventy-second and Seventy-third Scientific Sessions of The American Heart Association (Nov 7-10, 1999, in Atlanta, Ga, and Nov 12-15, 2000, in New Orleans, La).

Received for publication January 20, 2003; revisions received March 24, 2003; revisions received April 6, 2003; accepted for publication May 14, 2003.

^* Address for reprints: Takashi Nitta, MD, Associate Professor, Cardiothoracic Surgery, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
nitta{at}nms.ac.jp

OBJECTIVE: We examined the atrial activation during atrial fibrillation to validate the rationale behind simplified surgical procedures.

METHODS: Intraoperative mapping of the entire atrial epicardium was performed in 21 patients with permanent atrial fibrillation and mitral valve disease using a 256-channel, 3-dimensional dynamic mapping system.

RESULTS: Concurrent multiple repetitive activations arose from the posterior left atrium adjacent to the pulmonary veins or the left atrial appendage in all patients. The fastest activation propagated toward the right atrium conducting through Bachmann's bundle, leaving the other activations confined to a small atrial region. As the activation propagated toward the right atrium, there was a progressive conduction delay or block in the pathway. As a result, the activation in the right atrium desynchronized with the left atrial activation and became irregular and complex. The average cycle length measured at the right atrial appendage was significantly longer than that at the left atrial foci (206 ± 32 milliseconds vs 175 ± 23 milliseconds, P < .001). In addition to the passive activation, a focal activation and reentrant activation were also observed in the right atrium in 5 and 6 patients, respectively. The number of wave fronts in the right atrium was significantly greater than that in the left atrium (2.9 ± 0.8 vs 0.6 ± 0.7, P < .001).

CONCLUSIONS: Multiple left atrial focal activations with fibrillatory conduction and right atrial focal or reentrant activations are the mechanism in permanent atrial fibrillation associated with mitral valve disease. Intraoperative mapping would facilitate the indication for simplified procedures confined to the left atrium or the pulmonary veins.

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