(Circulation. 1999;100:876-883.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Relation Between Ligament of Marshall and Adrenergic Atrial Tachyarrhythmia
From the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, Calif; the Department of Pathology (M.C.F.), UCLA School of Medicine, Los Angeles, Calif; and the Utah Valley Regional Medical Center (C.H.), Provo.
Correspondence to Peng-Sheng Chen, MD, Rm 5342, CSMC, 8700 Beverly Blvd, Los Angeles, CA 90048-1865. E-mail chenp{at}csmc.edu
Background—The mechanism of the adrenergic atrial tachyarrhythmia is unclear. We hypothesize that the ligament of Marshall (LOM) is sensitive to adrenergic stimulation and may serve as a source of the adrenergic atrial tachyarrhythmia.
Methods and Results—We performed computerized mapping studies in isolated-perfused canine left atrial tissues from normal dogs (n=9) and from dogs with chronic atrial fibrillation (AF) induced by 10 to 41 weeks of rapid pacing (n=3). Before isoproterenol, spontaneous activity occurred in only one normal tissue (cycle length, CL >1300 ms). During isoproterenol infusion, automatic rhythm was induced in both normal tissues (CL=578±172 ms) and AF tissues (CL=255±29 ms, P<0.05). The origin of spontaneous activity was mapped to the LOM. In the AF tissues, but not the normal tissues, we observed the transition from rapid automatic activity to multiple wavelet AF. Ablation of the LOM terminated the spontaneous activity and prevented AF. Immunocytochemical studies of the LOM revealed muscle tracts surrounded by tyrosine hydroxylase-positive (sympathetic) nerves.
Conclusions—We conclude that the LOM is richly innervated by sympathetic nerves and serves as a source of isoproterenol-sensitive focal automatic activity in normal canine atrium. The sensitivity to isoproterenol is upregulated after long-term rapid pacing and may contribute to the development of AF in this model.
Key Words: tachyarrhythmias • mapping • catecholamines • atrial fibrillation
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