Retrograde ethanol infusion in the vein of Marshall: regional left atrial ablation, vagal denervation and feasibility in humans

Abstract

Background: The vein of Marshall (VOM) is an attractive target during ablation of atrial fibrillation due to its autonomic innervation, its location anterior to the left pulmonary veins and drainage in the coronary sinus.

Methods and results: We studied 17 dogs. A coronary sinus venogram showed a VOM in 13, which was successfully cannulated with an angioplasty wire and balloon. In 5 dogs, electroanatomical maps of the left atrium were performed at baseline and after ethanol infusion in the VOM, which demonstrated a new crescent-shaped scar, extending from the annular left atrium towards the posterior wall and left pulmonary veins. In 4 other dogs, effective refractory periods (ERP) were measured at 3 sites in the left atrium, before and after high-frequency bilateral vagal stimulation. The ERP decreased from 113.6+/-35.0 ms to 82.2+/-25.4 ms (p<0.05) after vagal stimulation. After VOM ethanol infusion, vagally-mediated ERP decrease was eliminated (from 108.6+/-24.1 ms to 96.4 +/-16.9ms, p=NS). The abolition of vagal effects was limited to sites near the VOM (ERP: 104+/-14 ms, vs 98.6+/-12.2 ms post vagal stimulation, p=ns), as opposed to sites remote to VOM (ERP: 107.2+/-14.9 ms, vs 78.6+/-14.7ms post vagal stimulation, p<0.05). To test feasibility in humans, 5 patients undergoing pulmonary vein antral isolation had successful VOM cannulation and ethanol infusion: left atrial voltage maps demonstrated new scar involving the infero-posterior left atrial wall extending towards the left pulmonary veins.

Conclusions: Ethanol infusion in then VOM achieves significant left atrial tissue ablation, abolishes local vagal responses and is feasible in humans.

Keywords: ablation; atrial fibrillation; ethanol; vagal; vein of Marshall.

Figures

Figure 1

Angiographic appearance of the VOM in dogs in balloon occlusion venograms. The VOM (black arrows) can be readily identified in the right anterior oblique radiographic projection (A through E) as a posteriorly-directed branch of the coronary sinus. In the left anterior oblique projection (F), it is superiorly directed. Significant variations in caliber and length are obvious.

Figure 2

VOM cannulation technique and VOM ethanol infusion results. A, Cannulation technique. After balloon occlusion venogram, the VOM was indentified. For reference, an angioplasty wire was inserted in the main lumen of the coronary sinus. An angiographic left internal mammary artery (LIMA) catheter was then inserted to probe the roof of the coronary sinus with an angioplasty wire until the VOM was cannulated. In the case shown, significant expansion of the VOM lumen was present upon selective VOM venogram (rightmost panel). B, Bipolar voltage three-dimensional maps of the left atrial geometry before (left) and after VOM ethanol infusion (right), in the posterior-anterior view (top) and in a left lateral view (bottom). The color tubes indicate the pulmonary veins (left inferior vein not shown). At baseline, the left atrial wall had bipolar voltage signals with amplitudes exceeding 1.5 mV throughout the atrium. After VOM ethanol infusion a new area of low voltage amplitude is apparent in the anatomical distribution of the VOM, which in this case runs superiorly towards the anterior aspect of the left pulmonary veins.

Figure 3

Posterior left atrial ablation after VOM ethanol infusion. A, Course of the VOM on the coronary sinus venogram (left panel), wire cannulation (mid panel: top wire is in the VOM advanced via a left internal mammary artery angiographic catheter, bottom wire in the main coronary sinus lumen), and selective VOM venogram via an inflated angioplasty balloon. B, Bipolar voltage three-dimensional maps of the left atrial geometry before (left) and after VOM ethanol infusion (right), in the posterior-anterior view (top) and in an inferior view (bottom). The low-voltage area created by VOM ethanol infusion is posteriorly directed, in between left and right pulmonary veins.

Figure 4

Anatomical factors leading to reduced ablation area. A, Small VOM. On CS venogram (left panel, left anterior oblique projection), the VOM is a small twig arising from the roof of the coronary sinus. Cannulation was successful, but the angioplasty balloon could only be advanced in the very proximal VOM (mid panel). A small annular area of ablation was created (right panel). B, Communication between VOM and left innominate vein superiorly. Despite a large VOM on the coronary sinus venogram (panel Ba, right anterior oblique projection), and successful VOM cannulation with an angioplasty balloon (panel Bb, left anterior oblique projection), multiple ethanol infusions only created small ablation lesions on voltage maps (panel Bd). A communication between the VOM and the superior vena cava was obvious when the VOM was cannulated from above (panel Bc).

Figure 5

Ethanol ablation lesions. A, Epicardial aspect, showing the VOM and ligament of Marshall (LOM) areas, with pale discoloration of the ablated areas (arrowheads). B, Endocardial aspect after incision in the left atrial appendage. A pale area of discoloration is shown anterior to the left pulmonary veins (PV), surrounded by small areas of tissue hemorrhage (arrowheads).

Figure 6

VOM ethanol infusion abolishes vagally-mediated decreases in effective refractory periods (ERP). A, ERPs measured in three left atrial sites before and after VOM ethanol infusion, showed blunting for vagal decreases in ERP after VOM ethanol infusion. This was particularly obvious at sites fluoroscopically adjacent to the VOM (B).

Figure 7

Representative example of VOM ethanol infusion in humans. A, Large VOM shown by contrast injection through a LIMA catheter pointing towards the VOM ostium. B, Selective VOM venogram via angioplasty balloon. C, Echocardiographic contrast injection shows earliest contrast appearance in the left atrial lumen close to the left pulmonary veins. D, Bipolar voltage map after ethanol infusion showing a large are of lower voltage (