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The importance of superior vena cava isolation in ablation strategy for atrial fibrillation

Higuchi, Kojia; Yamauchi, Yasuterub; Hirao, Kenzoc; Marrouche, Nassir F.a

Current Opinion in Cardiology: January 2013 - Volume 28 - Issue 1 - p 2–6
doi: 10.1097/HCO.0b013e32835b099b
ARRHYTHMIAS: Edited by Anthony Tang

Purpose of review Superior vena cava (SVC) is one of the most important nonpulmonary vein origins of atrial fibrillation, and SVC should be carefully treated in order to decrease the recurrence of atrial fibrillation after ablation. Despite the fact that pulmonary vein isolation (PVI) should be performed prophylactically for all pulmonary veins, prophylactic SVC isolation (SVCI) is still controversial. This review describes recent data on treatments for SVC focus during atrial fibrillation ablation.

Recent findings There are two different major approaches to treat SVC focus during atrial fibrillation ablation. One is the conventional approach, in which SVCI is performed only if atrial fibrillation from SVC origin is recognized using pacing maneuvers and/or isoproterenol infusions. Another approach is performing SVCI in all cases prophylactically in addition to PVI. The rate of atrial fibrillation freedom 1 year after initial atrial fibrillation ablation by prophylactic PVI along with SVCI was almost the same as with the conventional method (85–90% atrial fibrillation freedom). In addition, the conventional method also had a good result even 5 years after ablation (73.3%).

Summary Because of the good result after using the conventional approach and possible complications during SVCI, SVCI should be performed only if SVC focus is recognized, not prophylactically.

aComprehensive Arrhythmia Research & Management (CARMA) Center, University of Utah Health Sciences Center, Salt Lake City, Utah, USA

bDivision of Cardiovascular Medicine, Musashino Red Cross Hospital

cDepartment of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan

Correspondence to Koji Higuchi, MD, CARMA Center, University of Utah Health Sciences Center, 30 North 1900 East, Room 4A100, Salt Lake City, UT 84132-2400, USA. Tel: +1 801 213 4008; fax: +1 801 581 7735; e-mail: Koji.J.Higuchi@carma.utah.edu

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INTRODUCTION

Atrial fibrillation is the most commonly encountered cardiac arrhythmia in clinical practice, with a prevalence of 0.4–1% in the population [1]. Catheter ablation has emerged as a promising new treatment strategy for atrial fibrillation, which potentially cures atrial fibrillation radically and emancipates people from bothersome antiarrhythmic drug treatments. The cornerstone procedure of atrial fibrillation ablation is the electrical isolation of pulmonary veins from left atrium by ablating pulmonary vein antrum region in the left atrium, because ectopic beats initiating atrial fibrillation mostly originate from pulmonary veins [2]. Atrial fibrillation is also initiated by nonpulmonary vein ectopic beats, which may arise from the superior vena cava (SVC), left atrial posterior wall, crista terminalis, coronary sinus ostium, ligament of Marshall and interatrial septum [3]. Usually, the incidence of atrial fibrillation initiated from nonpulmonary vein foci is 26–28% in patients who undergo atrial fibrillation ablation, although it differs according to clinical studies [3,4]. Of these sites, the SVC is thought to be the most common source of ectopies, which harbours 26–30% of nonpulmonary vein foci [5,6], especially in patients with sleep apnea syndrome or obesity [7]. The SVC often becomes an important target during the atrial fibrillation ablation procedure [8,9].

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MECHANISM OF ARRHYTHMOGENICITY IN SUPERIOR VENA CAVA

The true mechanism of arrhythmogenicity in the SVC is still unclear. However, several studies are demonstrating concepts as the possible mechanism of its arrhythmogenicity. Sicouri et al. [10▪▪] demonstrated in their study using a canine model that late phase 3 early afterdepolarization (EAD) and delayed afterdepolarization (DAD)-mediated extrasystoles as well as automatic beats arising from SVC myocardial sleeves may serve as triggers of atrial fibrillation, which were also observed in pulmonary vein preparations. Chiou et al. [11] raised the concept of SVC-aorta ganglionated plexi, a third fat pad, which is located in the medial SVC and aortic root, superior to the right pulmonary artery. They concluded that the SVC-aorta ganglionated plexi serves as a relay station between extrinsic and intrinsic cardiac autonomic nervous systems [11]. Lu et al. [12] demonstrated using a canine model that high-frequency stimulation of the SVC-aorta ganglionated plexi induced a significant shortening of the effective refractory period and subsequent atrial fibrillation originating from the SVC. They also demonstrated that the hyperactivity of SVC-aorta ganglionated plexi induced by injection of acetylcholine initiated rapid firing originating from the SVC. These findings were eliminated after the ablation of SVC-aorta ganglionated plexi [12]. This suggests that the SVC-aorta ganglionated plexi plays an important role in initiating atrial fibrillation from the SVC. This is, however, not the only mechanism of SVC-related atrial fibrillation; we also have to take other mechanisms into consideration. In the study of Higuchi et al. [9] using a three-dimensional (3D) electroanatomical mapping, myocardial extensions in the SVC of patients with SVC-related atrial fibrillation were significantly longer than those of patients without SVC-related atrial fibrillation (34.7 ± 4.4 vs. 16.5 ± 11.4 mm, P < 0.0001). Some patients without SVC-related atrial fibrillation did not have any myocardial extensions in the SVC [9]. The myocardial extension also seems to play a significant role in SVC-related atrial fibrillation. The SVC-aorta ganglionated plexi may be the initiator of rapid firing from the SVC and the myocardial extension of SVC may become a substrate to maintain SVC fibrillation.

Box 1

Box 1

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HISTOLOGICAL FINDINGS OF MYOCARDIAL EXTENSION IN SUPERIOR VENA CAVA

A human histological study [13] showed that myocardial sleeves extend from right atrium (RA) into SVC for 2–5 cm. In another post-mortem study of Kholová et al. [14] using 25 human autopsied hearts, myocardial extension from RA to SVC was recognized in 19 out of 25 SVCs (76%) and SVC–RA myocardial connection was discontinuous in most cases and circumferential in a few cases, with a mean thickness of 1.2 ± 1.0 mm and a mean length of 13.7 ± 13.9 mm (maximum, up to 47 mm) [14].

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PROCEDURE OF SUPERIOR VENA CAVA ISOLATION

The arrhythmogenic focus from the SVC was found to be relatively far from the SVC–RA junction (Lin et al. [3] 25.3 ± 9.7 mm, 29 ± 19.9 mm, Tsai et al. [8] 19 ± 9.7 mm, Higuchi et al. [9] 25.4 mm, 32.2 mm). Formerly, the focal ablation at arrhythmogenic foci in the SVC was performed with the guidance of a multipolar catheter or a basket catheter placed in the SVC [8,15▪▪]. The recent standard method is the electrical isolation of SVC (SVCI) from the RA, which can be obtained by ablating 5–10 mm above the SVC–RA junction with the guidance of 3D electroanatomical mapping and a circular mapping catheter placed near the SVC–RA junction. Usually, SVCI can be achieved by ablating the earliest SVC activation during sinus rhythm in a segmental point-by-point fashion using 3D electroanatomical mapping, not by circumferential ablation [16].

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POSSIBLE COMPLICATIONS OF SUPERIOR VENA CAVA ISOLATION

Radiofrequency application in the SVC has potential risks of developing several complications: (1) SVC stenosis, (2) sinus node injury and (3) right phrenic nerve injury.

SVC stenosis is sometimes recognized after radiofrequency application in the SVC. An experimental study using mongrel dogs demonstrated variable (mild to severe) SVC narrowing after a conventional (4 mm tip, 60°C, 60 s) radiofrequency application (six to seven times) in the SVC both acutely and gradually [17]. There is also a case report that resulted in severe stenosis of the SVC after radiofrequency ablations to obtain SVCI using an irrigated-tip catheter (25 W, 10 times, 278 s, totally; Fig. 1) [18]. Sinus node injury is also a considerable complication, which usually occurs if radiofrequency ablations are applied below the SVC–RA junction. The SVC–RA junction should be determined carefully before ablation, and the circumferential line to create SVCI should be about 5–10 mm above the SVC–RA junction [19▪]. Radiofrequency applications should be ceased immediately if the acceleration of sinus rhythm is observed, which indicates damage to the sinus node. Akoum et al. [20] utilized late gadolinium enhancement MRI for detecting a preexisting sinus node dysfunction by evaluating structural remodelling in the RA. This modality can be used before performing SVCI for detecting patients with a preexisting sinus node dysfunction, who may have a greater potential risk of sinus node injury after ablations near the SVC–RA junction. Performing MRI prior to ablation may also help us understand the anatomy of RA and SVC of each patient. Right phrenic nerve injury is the most frequently recognized complication. The right phrenic nerve is close to the SVC superiorly and adjacent to the lateral border of the entrance of the inferior vena cava to the RA inferiorly. Although the right phrenic nerve is immediately adjacent to the anterolateral wall of the SVC, it veers posteriorly as it approaches the SVC–RA junction. More inferiorly, it passes close to the junction of the left atrium to the right superior pulmonary vein. The damage to the phrenic nerve usually occurs during radiofrequency applications on the posterolateral aspect of the SVC, and it turns out to be a right side diaphragm paralysis (Fig. 2). Even if the right phrenic nerve paralysis mostly recovers within 1 year [21], confirming that the right phrenic nerve is not captured by a pacing maneuver should be performed before applying radiofrequency ablations to avoid damage to the nerve. In addition, the movement of the right diaphragm should be checked periodically to detect nerve damage as soon as possible.

FIGURE 1

FIGURE 1

FIGURE 2

FIGURE 2

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STRATEGY, INDICATION AND RESULTS OF SUPERIOR VENA CAVA ISOLATION

The basic strategy to treat the SVC triggering atrial fibrillation is electrical isolation of SVC from RA. However, the attitude to the ‘indication of SVCI’ seems to be different according to facilities.

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PERFORMING SUPERIOR VENA CAVA ISOLATION ONLY IF SUPERIOR VENA CAVA TRIGGER IS RECOGNIZED

This is the standard strategy that has been performed, and the basic maneuver to induce ectopic beats is described as follows:

(1) Atrial fibrillation induction is attempted by high-frequency pacing from catheters placed in the RA, the coronary sinus or pulmonary veins with intravenous infusion of isoproterenol (0.5–2 μg/min) as necessary.

(2) Atrial fibrillation is cardioverted into sinus rhythm.

(3) Ectopic beats triggering atrial fibrillation can be recognized after cardioversion.

Interestingly, in the study of Lin et al. [3], only 7% of these foci were observed spontaneously during the procedure, while 93% of the firings were discovered following isoproterenol infusion (0.5–2 g/min) or immediately after cardioversion. This finding was also reported in the dog model [10▪▪]. Chang et al. [15▪▪] reported in their study the long-term outcome of ablation therapy in 68 patients with atrial fibrillation from SVC origin by this induction maneuver using isoproterenol infusion and cardioversion. In this study, the rate of atrial fibrillation freedom was 85.3% at 1 year, 78.7% at 2 years and 73.3% at 5 years after the initial ablation procedure. In addition, patients with pure SVC-initiating atrial fibrillation presented a better outcome than those with coexisting pulmonary vein triggers (Fig. 3). They also found that the 5-year result after segmental SVCI was same as for circumferential SVCI, which means that segmental point-by-point ablation is enough for obtaining the electrical isolation of SVC from RA (Fig. 4). They concluded that SVCI without pulmonary vein isolation (PVI) is an acceptable therapeutic strategy in patients with atrial fibrillation originating from the SVC only.

FIGURE 3

FIGURE 3

FIGURE 4

FIGURE 4

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PROPHYLACTIC SUPERIOR VENA CAVA ISOLATION IN ADDITION TO PULMONARY VEIN ISOLATION

This method has been recently proposed, in which SVCI is prophylactically performed in addition to PVI. Corrado et al. [6] demonstrated in their randomized study that the patients who underwent SVCI as an adjunctive therapy to PVI had significantly lower recurrence rate of atrial fibrillation than those who underwent only PVI [6]. Their 1-year success rate after an initial ablation procedure with PVI and PVI along with SVCI for paroxysmal atrial fibrillation patients was 77 vs. 90% (P = 0.04). On the contrary, Wang et al. [22] also conducted a randomized prospective study comparing the beneficial difference between two strategies, PVI and empiric PVI along with SVCI for patients with paroxysmal atrial fibrillation. In this study, they did not find statistical significance between these two strategies regarding the success rate 1 year after initial atrial fibrillation ablation (PVI, 81%; PVI along with SVCI, 86%; P = 0.75).

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IMPLICATION FROM TWO DIFFERENT METHODS

The success rate of atrial fibrillation ablation 1 year after initial ablation by empiric PVI along with SVCI seems to be almost the same as for the conventional method (performing SVCI only for patients who have triggers in the SVC). In addition, the conventional method also has a good result (73.3%) even 5 years after ablation. Furthermore, if patients with short myocardial extensions in the SVC do not have SVC-related atrial fibrillation, as previously reported [9], it is not necessary to isolate all SVCs to reduce atrial fibrillation recurrences. The procedure of SVCI is different from PVI in that SVCI should be performed 5–10 mm ‘inside’ the SVC from the SVC–RA junction to avoid sinus node injury, whereas PVI should be performed at the pulmonary vein antrum, which is about 10 mm ‘outside’ the pulmonary vein from the left atrium–pulmonary vein junction. Therefore, there should be enough myocardial extension in the SVC to accomplish SVCI safely, and SVC should not be ‘prophylactically’ isolated in all patients, who may have just a tiny SVC myocardial extension. We may have to spend time to induce SVC-related atrial fibrillation using pacing maneuvers and/or isoproterenol infusions. However, it will save time eventually if we can avoid unnecessary SVCI by this conventional induction method. Furthermore, we can avoid unnecessary complications of SVCI, in which the incidence of complications is remarkably higher than for PVI.

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CONCLUSION

Because of the proximity of SVC-aorta ganglionated plexi to the SVC and the good extension of myocardium in the SVC from the RA, SVC frequently becomes an important source of ectopic beats initiating atrial fibrillation. Therefore, SVC should be carefully examined, whether it has an arrhythmogenicity or not, in order to reduce the recurrence of atrial fibrillation. Performing SVCI only if SVC triggers are recognized after pacing maneuvers and/or isoproterenol infusions seems to be reasonable in order to avoid unnecessary ablations and complications.

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Acknowledgements

None.

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Conflicts of interest

There are no conflicts of interest.

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REFERENCES AND RECOMMENDED READING

Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest

Additional references related to this topic can also be found in the Current World Literature section in this issue (p. 80).

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REFERENCES

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This is the first report about long-term outcomes of catheter ablation in patients with atrial fibrillation from SVC origin. The atrial fibrillation freedom rate 5 years after initial ablation was 73.3%.

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Sinus node injury is a complication after SVC isolation, which occurred in 4.5% of this study cohort. This study reports characteristics of sinus node dysfunction after SVC isolation.

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Keywords:

atrial fibrillation; catheter ablation; electrical isolation; superior vena cava

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