Mechanisms of Vein of Marshall-Related Tachyarrhythmias and the Impact of Ethanol Infusion

Abstract

The Ligament of Marshall (LOM) is a remnant of the embryonic sinus venosus and the left cardinal vein, containing a combination of fat, fibrous tissue, blood vessels, muscle bundles, nerve fibers, and ganglia. Various muscular connections exist between the LOM and the left atrium (LA) and the coronary sinus (CS). The LOM is richly innervated by autonomic nerves, with ganglion cells distributed around it. The unique characteristics of the LOM are responsible for generating focal electrical activities and enable it to serve as a substrate for micro- and macro-reentrant circuits. This, in turn, leads to the initiation and perpetuation of atrial fibrillation (AF) and atrial tachycardia (AT). Endocardial ablation in this region does not consistently succeed due to anatomical constraints within the left lateral LA, including the presence of a thicker and longer mitral isthmus (MI), anatomical variations between the MI and epicardial structures such as the CS and vein of Marshall (VOM) and circumflex artery, and the presence of fibrofatty tissue insulating the LOM. Furthermore, epicardial ablation is challenging for inexperienced institutions because of its invasive nature. Ethanol infusion into the VOM (EI-VOM) represents an effective and safe approach that can be employed in conjunction with radiofrequency ablation to eliminate this arrhythmogenic structure.

Keywords: chemical ablation; ethanol infusion; ligament of Marshall; vein of Marshall.

Fig. 1.

Histology of Ligament of Marshall. (a) Gross photo showing location on posterior surface of heart. (b) Immunohistochemical staining for tyrosine hydroxylase showing positively in nerve (brown staining—arrow). M, myocardium; F, fat. (avidin-biotin-peroxidase, $\times$120). (c–e) Subserial sections showing the LOM, isolated from the left atrial wall (in c), with 3 tracts (arrows) emerging from it (in d) and eventually inserting into the atrial wall (in e) (hematoxylin and eosin [H&E] stain $\times$10). (f) Section from lower end of LOM showing tract inserting into the left atrial wall (arrow) and coronary sinus (CS) (H&E stain $\times$10). This figure is reproduced from the original manuscript [3] with permission from Elsevier. CS, coronary sinus; LAA, left atrial appendage; LOM, ligament of Marshall; PV, pulmonary vein; LA ENDO, left atrial endocardium.

Fig. 2.

Variations of LOM anatomy. (A1–A3) Pictures from autopsy specimens. (B1–B3) Pictures taken during surgery. A black circle in (A1) indicates the proximal connection of the LOM to the CS. (A2) A different view of the same heart. The distal end of the LOM inserts into the LSPV. (A3) A second heart in which LOM was completely attached to the epicardium. A discrete ligament was not identified. (B1) Proximal connection (arrow) between the LOM and the CS. (B2) Both the proximal and distal connections of the LOM (2 arrows) in a second heart. (B3) A third heart, which seems to have multiple muscle fibers (arrows) connecting the LOM and the LA. CS, coronary sinus; LA, left atrium; LAA, left atrial appendage; LIPV, left inferior pulmonary veins; LOM, ligament of Marshall; LSPV, left superior pulmonary vein; LV, left ventricle; PV, pulmonary vein; LPV, left pulmonary vein. This figure is reproduced from the original manuscript [15] with permission from Elsevier.

Fig. 3.

Mechanism of LOM-related tachyarrhythmias. (A) The source of triggers. (B) Drivers or micro-reentries forming the substrates of reentry. (C) Macroreentrant or localized circuits totally or partially using the LOM. (D) Rich autonomic innervation (e.g., parasympathetic ganglions around the ostium of the VOM and adrenergic nerves around the distal sympathetic nerves). CS, coronary sinus; LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MV, mitral valve; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; LOM, ligament of Marshall; VOM, vein of Marshall.

Fig. 4.

Location of epicardial-to-endocardial insertion from the ligament of Marshall. Diverse connections between the ligament of Marshall and endocardial left atrium are observed along the ridge between the LAA and LPV. Centrifugal activation is identified at the endocardial insertion point of the epicardial structures, which is one of the clues to predict LOM-related ATs. AT, atrial tachycardia; CS, coronary sinus; LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; MV, mitral valve; PMF, perimetral flutter; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; VOM, vein of Marshall; LPV, left pulmonary vein; LOM, ligament of Marshall.

Fig. 5.

Two main approaches for EI-VOM. Jugular vein approach with a guide sheath (A-i) or without (A-ii) and femoral vein approach (B). CS, coronary sinus; Eso, esophageal temperature monitoring; EI-VOM, ethanol infusion to the vein of Marshall; LAO, left anterior oblique view; RA, right atrium; RAO, right anterior oblique view; SVC, superior vena cava; VOM, vein of Marshall.

Fig. 6.

Various distribution of VOM branches. Various distribution of VOM branches are observed. A posterior branch from the main VOM-tract (A). A plexus-like short-VOM without a main tract (B). A roof branch from the distal part of the main VOM-tract (C). Stump-like VOM with two branches from the VOM-ostium; one is a posterior-inferior branch and the other is inferior branch (D). AP, antero-posterior view; LAO, left anterior oblique view; RAO, right anterior oblique view; VOM, vein of Marshall.