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Unusual Presentation of Superior Vena Cava Trigger in a Patient with Atrial Fibrillation

David Singh, MD
Chief, Department of Cardiovascular Diseases
The Queen’s Medical Center
Associate Professor of Medicine
John A. Burns School of Medicine
Honolulu, Hawaii

David Singh, MD
Chief, Department of Cardiovascular Diseases
The Queen’s Medical Center
Associate Professor of Medicine
John A. Burns School of Medicine
Honolulu, Hawaii

Introduction

Ablation of atrial fibrillation (AFib) typically involves electrical isolation of pulmonary veins (PVs). It is often important to identify non-PV triggers among patients with AFib in order to maximize the effectiveness of ablation. Non-PV triggers can arise from various cardiac locations, including the coronary sinus, crista terminalis, posterior wall of the left atrium, and superior vena cava (SVC). Supraventricular tachycardias (SVTs) such as atrioventricular reciprocating tachycardia (AVRT), atrioventricular nodal reentrant tachycardia (AVNRT), and atrial tachycardia (AT) can also serve as triggers for AFib.

In this article, we present an unusual case of a patient referred for ablation of supravwentricular tachycardia and atrial fibrillation. The patient was found to have a rapid atrial tachycardia arising from the SVC with 2:1 exit block to the surrounding atria. The AT was observed to degenerate into atrial fibrillation on several occasions during the procedure. This case highlights the importance of recognizing non-PV triggers in AFib, and the phenomenon of rapid focal firing with exit block to the surrounding structures.

Case Description

A 53-year-old male was referred for symptomatic SVT and AFib. He had no prior history of cardiac surgery or other cardiac interventions. He was brought to the electrophysiology lab for evaluation and treatment of his arrhythmias. A multielectrode catheter was placed in the coronary sinus, and programmed electrical stimulation resulted in a SVT with P-wave morphology and atrial cycle length consistent with prior documented electrocardiograms (Figure 1). An SVT with an atrial cycle length of 356 ms was observed. Activation mapping of the right atrium was undertaken utilizing a multielectrode mapping catheter (PENTARAY, Biosense Webster, Inc., a Johnson & Johnson company). When the mapping catheter was advanced into the SVC, a simultaneous tachycardia with a cycle length of 178 ms was noted. There was a 2:1 relationship between the tachycardia in the SVC and the surrounding atria (Figure 2). An activation map of the right atrium revealed a focal activation pattern with earliest activation in the SVC (Figure 3, Video 1).

Discussion

Figure 1 demonstrates a long RP tachycardia with 2:1 conduction to the ventricles. Examination of the P-wave morphology reveals a biphasic P wave in lead V1 (positive-negative) with an inferior axis. The inferior axis P wave effectively rules out atypical AVNRT and AVRT. Moreover, the 2:1 atrioventricular relationship rules out AVRT, as the ventricle is an obligate part of the AVRT circuit. Therefore, the most likely SVT mechanism is atrial tachycardia. The P-wave morphology in V1 would suggest an origin near the crista terminalis or SVC.1,2 Figure 2 demonstrates that the true cycle length of the tachycardia was twice as fast as the cycle length suggested by the surface ECG. A macroreentrant atrial tachycardia (or atypical atrial flutter) should also be considered. Distinguishing between macroreentrant and focal arrhythmias can be accomplished with detailed activation mapping. Focal arrhythmias (including mechanisms such as microreentry, triggered activity, and enhanced automaticity) should demonstrate a discrete region of early activation with centrifugal spread. In contrast, macroreentrant atrial tachycardias should display an activation pattern that reveals a large circuit encompassing the entire tachycardia cycle length. An activation map of the right atrium revealed a region of focal activation that was earliest in the posterior SVC region (Figure 3). A voltage map (not shown) did not reveal any regions of scar in this right atrium. Taken together, these findings would suggest a focal arrhythmia with functional block to the surrounding atria.

Given the proximity of the posterior SVC to the right upper pulmonary vein (Figure 4), mapping of this region was undertaken to determine whether this could be the source of the arrhythmia. Shortly after transseptal puncture, the AT degenerated into atrial fibrillation. Despite cardioversion, attempts to re-initiate the AT were unsuccessful. Therefore, isolation of the pulmonary veins was undertaken. Following this, isoproterenol was initiated and programmed electrical stimulation produced the same rhythm seen in Figures 1 and 2. The right-sided veins remained isolated, and the SVT was characterized by the same 2:1 relationship to the atria and 4:1 relationship to the ventricles. Ablation was directed toward the region of earliest activation in the SVC. This resulted in termination of the tachycardia and restoration of sinus rhythm (Figure 5). Both AT and AFib remained non-inducible thereafter. We concluded that the patient had a focal SVC AFib trigger with 2:1 block to the surrounding atria.

It is well recognized that AFib may be triggered from arrhythmogenic foci arising from myocardial sleeves that extend from the right atrium into the SVC.3 SVC triggers are observed in up to 12% of patients undergoing ablation for AFib, and are important sites of origin for non-PV triggers.4 Isolation of the SVC has been shown to be a safe and effective strategy for patients with AFib triggers arising from this region.4 When performing SVC isolation, great care must be taken to avoid collateral damage to nearby structures, including the right phrenic nerve and sinus node. An increase in the sinus rate during ablation in the SVC region may portend injury to the sinus node.2 Delineation of the right phrenic nerve with high-output pacing can also help to avoid damage to this structure. Frequently, an SVC trigger can be identified by rapid firing associated with early activation in this region. Because SVC triggers often degenerate rapidly into AFib, it can be challenging to localize their precise origin within the SVC. In these instances, SVC isolation is an appropriate strategy. Because the SVC trigger was sustained in this case, detailed activation mapping could be undertaken. As a result, targeted ablation of the trigger could be pursued without the need for electrical isolation. Following his ablation, the patient has remained free from AFib and SVT for approximately 1.5 years.

Summary

This case represents an unusual presentation of a focal SVC trigger in a patient with AFib, with 2:1 exit block to the atria and frequent degeneration into atrial fibrillation. Recognition and ablation of non-PV triggers continues to be an important strategy for effective ablation of AFib. In addition, when detailed activation of an SVC trigger is possible, SVC isolation may not be necessary. 

Disclosure: Dr. Singh has no conflicts of interest to report regarding the content herein.

References
  1. Kistler PM, Roberts-Thomson KC, Haqqani HM, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol. 2006;48:1010-1017.
  2. Santangeli S, Marchlinski FE. Techniques for the provocation, localization, and ablation of non–pulmonary vein triggers for atrial fibrillation. Heart Rhythm. 2017;14:1087-1096.
  3. Kholova I, Kautzner J. Morphology of Atrial Myocardial Extensions Into Human Caval Veins: A Postmortem Study in Patients With and Without Atrial Fibrillation. Circulation. 2004;110:483-488.
  4. Arruda M, Mlcochova H, Prasad SK, et al. Electrical isolation of the superior vena cava: an adjunctive strategy to pulmonary vein antrum isolation improving the outcome of AF ablation. J Cardiovasc Electrophysiol. 2007;18:1261-1266.
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