Relation between ligament of Marshall and adrenergic atrial tachyarrhythmia

Background-The mechanism of the adrenergic atrial tachyarrhythmia is unclea r. We hypothesize that the ligament of Marshall (LOM) is sensitive to adren ergic stimulation and may serve as a source of the adrenergic atrial tachya rrhythmia. Methods and Results-We performed computerized mapping studies in isolated-p erfused canine left atrial tissues from normal dogs (n=9) and from dogs wit h chronic atrial fibrillation (AF) induced by 10 to 41 weeks of rapid pacin g (n=3). Before isoproterenol, spontaneous activity occurred in only one no rmal tissue (cycle length, CL >1300 ms). During isoproterenol infusion, aut omatic rhythm was induced in both normal tissues (CL=578+/-172 ms) and AE t issues (CL=255+/-29 ms, P<0.05). The origin of spontaneous activity was map ped to the LOM. In the AF tissues, hut not the normal tissues, we observed the transition from rapid automatic activity to multiple wavelet AF. Ablati on of the LOM terminated the spontaneous activity and prevented AF. Immunoc ytochemical studies of the LOM revealed muscle tracts surrounded by tyrosin e hydroxylase-positive (sympathetic) nerves. Conclusions-We conclude that the LOM is richly innervated by sympathetic ne rves and serves as a source of isoproterenol-sensitive focal automatic acti vity in normal canine atrium. The sensitivity to isoproterenol is upregulat ed after long-term rapid pacing and may contribute to the development of AF in this model.