Europace Advance Access originally published online on March 16, 2007
Europace 2007 9(5):302-304; doi:10.1093/europace/eum024
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ATRIAL TACHYARRHYTHMIA
Bidirectional superior vena cava: right atrial conduction delay during tachycardia
Department of Clinical Electrophysiology, Room Bd416, Thoraxcentre, Erasmus MC, Dr. Molewaterplein 40, Rotterdam 3015 GD, The Netherlands
Manuscript submitted 26 December 2006. Accepted after revision 26 January 2007.
* Corresponding author. Tel: +31 10 4633991; fax: +31 10 4634420. E-mail address: a.thornton{at}erasmusmc.nl
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Abstract |
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The superior vena cava, like all the thoracic veins, has myocardial sleeves and plays a role in initiation and perpetuation of atrial fibrillation. Conduction delay between it and the right atrium has been shown previously. This case study shows delay in both directions during different arrhythmias in the same patient.
Key Words: Arrhythmia, Magnetic navigation, Superior vena cava, Atrial tachycardia
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Introduction |
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The thoracic veins, the pulmonary veins (PVs), coronary sinus (CS), and superior vena cava (SVC), have been shown to play a major role in the initiation and perpetuation of atrial fibrillation (AF). Some groups even include SVC isolation as part of their routine for AF ablation.1
Both focal sources and reentry have been suggested as the underlying causal mechanism within these veins.2–4 In the SVC, myocardial sleeves may extend for up to 47 mm into the vein, and mostly have a circular orientation.5 Slow conduction and block have been shown at the SVC-right atrial (RA) junction.6 In the following case study, we show evidence of bidirectional conduction block in this region during two different tachycardias. |
Case report |
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A 40-year-old man with a long history of paroxysmal palpitations had undergone slow pathway cryoablation 1 year previously for atrioventricular nodal reentry tachycardia (AVNRT). He was well for 6 months off all medication, following which he again complained of much shorter and less frequent paroxysmal palpitations. These were difficult to document, and because of a suspicion of recurrence of tachycardia a new electrophysiological study was planned.
He was studied under light conscious sedation. Sustained AVNRT could be induced under an isoprenaline infusion and after aggressive burst pacing. The slow pathway region was mapped with a 4-mm tip cryocatheter (Freezor, Cryocath Technologies Inc., Kirkland, Canada) and a single cryoablation was performed. Under Isoprenaline AVNRT was no longer inducible, but a number of atrial tachycardias were induced of which one was sustained for up to 10 minutes and was mapped.
Remote magnetic navigation (Niobe, Stereotaxis Inc., St Louis, MO, USA) using an electroanatomic mapping and ablation catheter (7-F Navistar RMT, Biosense Webster, Diamond Bar, CA, USA.) was undertaken via the right femoral vein. Under high dose Isoprenaline a 52-point map was constructed and the earliest activation was noted high in the RA. As we advanced the ablation catheter into the SVC (Figure 1) it was apparent that there was 2 to 1 conduction from the SVC to the atria (Figure 2). The episode we were mapping terminated during catheter manipulation in the SVC via a short transition to AF in the SVC with variable conduction to the atria. The point of breakthrough from the SVC to the RA was in the anterolateral border where phrenic nerve stimulation over a broad area was present with pacing at low output (Figure 3). During further stimulation, we were able to induce AF in the atria with high grade block from the RA into the SVC (Figure 4). We were never able to map fully the initial tachycardia and could not show whether this was an SVC flutter or a focal tachycardia. On a high-dose Isoprenaline infusion, we were no longer able to induce the initial tachycardia and off Isoprenaline no tachycardia was inducible. No further ablation was performed. Without medication he has had no recurrence of symptoms after 12 months.
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Discussion |
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The thoracic veins, including the SCV, have been shown to play a major role in the initiation and perpetuation of AF. Tsai et al., suggested that this may be the case in up to 6% of patients with AF.4
Enhanced automaticity and triggered activity giving rise to focal atrial tachycardias, and reentry (in both structurally normal and previously operated hearts) have been suggested as the underlying mechanism.2–4,7
There is a complex arrangement of muscle sleeves around all the thoracic veins, including the venae cavae. Myocardial sleeves are found in both the superior and inferior vena cava (IVC), although those in the SVC appear to be the most arrhythmogenic. This may relate to the presence of better connections between these sleeves and the right atrium than those in the IVC. The sleeves may in some cases extend as far up the SVC as the insertion of the azygos vein. Mostly these sleeves appear to have a circular orientation.5 The connections may be discontinuous and have degenerative changes.
Not surprisingly, given their anatomical features, mapping shows electrical heterogeneity and slow, discontinuous conduction within the SVC extensions.3 There seems to be a higher degree of conduction block within the SVC (70%) than within PVs (30%).4 Decremental conduction from the SVC to the RA has been seen during tachycardia and pacing,6,8,9 while the same has been shown for conduction from the RA to the SVC during sinus rhythm or pacing.3
As with the connections from the PVs to the left atrium, there frequently appear to be more than one connection from the SVC to the RA, with some connections conducting bidirectionally, while others may conduct from SVC to RA only (exit sites) or vice versa (entrance sites). While the entrance and exit sites are frequently the same,3,10 in some cases where connections have been mapped, it appears as though they may be found in different areas.11 This may suggest either unidirectional conduction block or possibly an oblique orientation of the connection. The position of the connections may vary around the entire SVC-RA junction. Goya et al., performed electroanatomic mapping in 16 patients and showed one or 2 connections per patient, with connections located anteriorly in 3, laterally in 4, posteriorly in 10, and septally in 6. Others have also shown a predominance of more posterior connections.3,6,11–13
While direct ablation of the focus or interruption of a reentry circuit may be associated with a permanent cure, others have suggested an alternative approach of segmental, or wide area SVC isolation in a similar fashion to the approach of pulmonary vein isolation for AF. This may require a mean of four applications in a more focal approach,10 to ablation of two-thirds or more of the circumference of the SVC using a wider approach.14 Whichever approach is used, it should be remembered that both the sinus node and the phrenic nerve are in close proximity to this area on the lateral border of the RA-SVC junction. Occurrence of phrenic nerve palsy, fortunately not permanent, has been recorded after ablation of these arrhythmias in humans.15
This case demonstrates two different, although related, arrhythmias with SVC to RA block during an SVC tachycardia, as well as RA–SVC conduction block during AF.
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A.S. Thornton has received payment for presentations given for Stereotaxis Inc. L. Jordaens and Erasmus MC received a research grant from Stereotaxis Inc.
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References |
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[1] Kanj MH, Wazni OM, Natale A. How to do circular mapping catheter-guided pulmonary vein antrum isolation: the Cleveland Clinic approach. Heart Rhythm 2006; 3: 866–9.[CrossRef][ISI][Medline]
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