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International Journal of Arrhythmia 2014;15(2): 39-43.
A Case of Atrial Tachycardia
Originating from the Ligament
of Marshall with Migration of
the Earliest Atrial Activation



   The ligament of Marshall (LOM) is a vestigial fold of the epicardium that contains fibrous bands, small blood vessels, and nervous filaments enveloped in fat.1 The LOM extends from the coronary sinus (CS) to the orifice of the left superior PV (LSPV). It is well known that the LOM is a non-PV focus of atrial fibrillation (AF) or atrial tachycardia (AT).2-4
   In this report, we describe a case of AT with migration of the earliest atrial activation along the pathway of LOM that was terminated by radiofrequency (RF) ablation inferior to LIPV.


   A 50-year-old man with a history of AT was admitted for electrophysiological study (EPS) and RF ablation. He was diagnosed with bladder cancer 2 years prior to the admission. Three months earlier, he began to experience palpitation. Supraventricular tachycardia was diagnosed and mild left ventricular (LV) dysfunction (ejection fraction [EF]=45%) was noted. Rate control for supraventricular tachycardia was not effective.
   During the EPS, the index arrhythmia was an AT with variable tachycardia cycle length (440-520 ms; Figure 1A). The earliest activation of AT was localized at the distal CS during tachycardia (Figure 1B).

A three-dimensional (3D) electroanatomic mapping system (NavX; St. Jude Medical, Inc, St. Paul, MN) was used for activation mapping of the left atrium during tachycardia. Activation mapping revealed focal AT arising from the anterior wall of the LIPV (Figure 2A). However, the earliest site of AT migrated to the ostium of the LIPV and the anterior ridge of the LSPV during mapping. RF ablation was performed targeting the earliest atrial activation at the anterior wall of the LIPV. During ablation, sudden PR interval prolongation and atrioventricular block developed. AT was terminated during ablation, but recurred soon afterwards. A second activation mapping revealed the earliest atrial activation at the anterior ridge of the left atrial appendage (LAA) base (Figure 2B). AT slowed during ablation, but was not terminated. A third activation mapping showed the earliest atrial activation at the anterior ridge of the LSPV (Figure 2C). Endocardial ablation was performed that targeted the earliest atrial activation site of the anterior ridge of the LSPV. Epicardial ablation was performed at the earliest atrial activation site of the vein of Marshall (VOM) inside the CS. Because of continued tachycardia after several attempts at RF and migration of the earliest atrial activation site, empirical isolation of the antral circumference of the LSPV and LIPV was attempted. However, AT was sustained. A last activation mapping revealed that the earliest atrial activation site of the AT moved again to a region inferoanterior to the LIPV (Figure 2D). RF ablation was performed at the earliest activation site (Figure 3A, blue dot), but was not effective. However, discrete electrical activity was observed inferior to the earliest atrial activation site of AT, which was considered a Marshall potential (Figure 3B, red arrow). We decided to ablate at this site, which is a suspected location of the LOM (Figure 3A yellow dot & 3C). AT was terminated by RF application at a site where activation occurred later than at the site of earliest activation of AT (Figure 3D). No AT was induced after RF ablation. Follow-up echocardiography showed improved LV function (EF=52%). The patient has been well with no recurrence of any tachyarrhythmias during the 1-year followup period.


   In this case, we reported an AT with a migrating earliest activation site considered to be the LOM.
   The 3D activation map showed that the earliest activation site of AT migrated from the anterior wall of the LIPV to the base of the LAA and then to the anterior ridge of the LSPV. The earliest activation site was later observed inferior to the LIPV. The morphology of the P wave was changed subtly according to the migration of the earliest atrial activation site of AT. Surprisingly, AT was not terminated during ablation at the earliest atrial activation site, but during ablation inferior to the earliest activation site. A preceding discrete potential was observed at the successful ablation site, which was considered a Marshall potential. Thus, we decided to perform RF ablation at that site and terminated AT. These earliest activation sites were located along the LOM, which courses from the CS obliquely above the LAA and lateral to the LSPV.5 The migration of the earliest activation site of AT could be explained by the complexity of the LOM, which has multiple myocardial insertions at the LA free wall and CS, forming a substrate for reentry.1 In this case, several insertion tracts into the left arterial (LA) free wall might be present, and thus the earliest activation site of AT could migrate to another site after RF ablation.
   The cycle length of AT was prolonged during ablation at each earliest activation site of AT, and sometimes AT was terminated but recurred after ablation. This phenomenon also supports the contention that AT originated from the LOM.
   The successful ablation site was located inferoposterior to the earliest activation site of AT. Endocardial recording at the successful ablation site showed double component potentials. Recently, Kuroki et al. also reported an AT arising from the LOM with a successful ablation site posteroinferior to the initial earliest activation site.2 In that case, a fractionated local electrogram preceding P wave onset was found at the successful ablation site. Another report of focal AT originating from the LOM also showed discrete a electrical potential (Marshall potential) preceding the atrial electrogram.4 The difference between the earliest activation site and the successful ablation site during AT could be because the earliest activation site in the activation map might be the exit site from the LA during AT arising from LOM, however, the successful ablation site with double potential might be the area of insertion of the Marshall bundle into the LA endocardial wall. In our case, local fractionated potentials were observed at the successful ablation site, albeit later than the earliest atrial activation of AT. The initial potential was regarded as a Marshall potential, whereas the second potential might be atrial activation (Figure 3B).
   In this case, we failed to terminate AT during epicardial ablation inside the CS, but succeeded in terminating AT during endocardial ablation. Previously, Hwang et al. reported successful ablation of AF arising from the LOM by RF application from the LA endocardium with the guidance of a catheter within VOM.6 Subsequently, the endocardial approach was supported by an anatomical study showing that the Marshall bundle could directly insert distally into the posterior atrial free wall superior to the CS.1
   In conclusion, we reported AT originating from the LOM, which showed migration of the earliest atrial activation during AT. The successful ablation site could be different from the earliest activation site, and local fractionated potentials could be promising markers for ablation of AT.


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