Ablating the Obscure: The Curious Case of the Vein of Marshall

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The ligament of Marshall (LOM) is an intriguing but incompletely understood vestigial epicardial fold. It is an embryologic remnant of the connection between the left anterior cardinal vein and coronary sinus (CS).1 The LOM is composed of fibrous tissue, a myocardial sleeve (Marshall bundle) innervated by sympathetic and parasympathetic fibers,2 and a vein of Marshall (VOM). The vein courses along the epicardial surface of the lateral mitral isthmus, originating at its junction with CS epicardial muscle sleeves, and extends to the epicardial surface of left atrial (LA) ridge that separates the left atrial appendage (LAA) from the left‐sided pulmonary veins (PVs). Several arrhythmogenic phenomena are attributed to the LOM, including focal and macroreentrant atrial tachycardia as well as initiation and perpetuation of atrial fibrillation (AF).3 Since the LOM is a remote threadlike structure that is not usually accessed during a standard electrophysiologic study, electrograms from the Marshall bundle are not routinely recorded or evaluated for their participation in atrial arrhythmias. Because this arrhythmogenic source often operates “under the radar,” its precise significance remains to be elucidated.
Like the VOM, the Marshall bundles emerge from their interface with CS muscle sleeves and follow the superior route of the VOM, inserting into the epicardial region of the LA ridge.6 These muscle bundles can provide a direct electrical connection (epicardial bridge) between the LA ridge/left PVs and the muscle sleeves of the CS, and likely account for the failure to isolate electrically some left PV––LA connections and to create bidirectional mitral isthmus block in refractory cases.5 An LOM trigger of AF should be suspected when ectopic beats from the mid or distal CS appear to trigger AF, particularly if the CS electrograms are associated with double potentials (one corresponding to LA activation and the other corresponding to the Marshall bundle).6
There are several approaches to mapping and ablating the muscle fibers of the VOM. A transvenous approach includes an occlusive CS venogram to identify the origin of the VOM. The ostium of the VOM is then engaged with a 7‐F luminal CS catheter and a small‐diameter mapping catheter is advanced through its inner lumen to cannulate the VOM. The VOM catheter is used to guide the corresponding endocardial site(s) for ablation and to confirm elimination of LOM potentials. Ablation is performed with an open irrigation catheter, typically positioned along the left lateral ridge, just below the left inferior PV. LOM potentials are eliminated in 90% of patients whose potentials can be mapped.2 Mapping can also be performed epicardially by focusing on the region between the LAA and left PVs and identifying Marshall bundle potentials.2 An alternative approach uses ethanol infusion to ablate the Marshall bundle. After the VOM is cannulated with a coronary vein subselection catheter, an angioplasty balloon is advanced over a guidewire into the proximal VOM. A selective venogram is performed during balloon inflation. Two to 4 serial injections of ethanol are then administered over 2 minutes through the catheter (1 mL, 98% ethanol).8 With each injection, the balloon is retracted slightly until the final injection is delivered at the most proximal junction of the VOM with the CS.
The study by Lee and colleagues published in this issue of the Journal adds several modifications to the techniques described above, essentially simplifying the method for ablating the Marshall bundle of the LOM.11 The study population was culled from a retrospective analysis of 367 consecutive patients who underwent ablation for AF and/or atypical atrial flutter. Five percent or 16 patients had persistence of PV potentials deep within a left‐sided PV, despite extensive antral and carinal ablation.
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