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Systematic Electrical Disconnection of Superior Vena Cava in Addition to Pulmonary Vein Ablation: Is It Worthwhile?

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Addition to Pulmonary Vein Ablation: Is It Worthwhile?

A. B

ONSO

, S. T

HEMISTOCLAKIS

, A. R

OSSILLO

, M. B

EVILACQUA

, A. C

ORRADO

, A. R

AVIELE

Introduction

Many reports have focused attention on the pulmonary veins and posterior wall of the left atrium to explain the physiopathological mechanism of atrial fibrillation [1–3].

Anatomical observations have shown that sleeves of atrial myocardial tis- sue extend inside the pulmonary veins even for several centimetres [4] and they have peculiar electrophysiological properties that can be stimulated under pathological situations, such as wall stretching, or under neurovegeta- tive stimulation [5]. In particular, the cells located inside the pulmonary veins, because of altered automatism or triggered activity [6], can provoke numerous supraventricular ectopic beats or even bursts of atrial tachycardia that are able to start paroxysmal atrial fibrillation episodes. Suppression of these ectopic foci inside the pulmonary veins by means of transcatheter ablation has provided effective treatment in about 70% of such patients [7].

The ablative techniques used to improve efficacy and safety, and to reduce the procedure time have simplified the ablative approach. Today, the electri- cal disconnection of pulmonary veins is carried out by a segmental or cir- cumferential approach at the AV-junction or with antrum extension. These techniques have increased the success rate to 80–90% [8–10]. The evolution of ablative techniques and the extension of treatment to patients with persis- tent or permanent atrial fibrillation therefore allowed us to analyse the mechanisms of onset and maintenance of atrial fibrillation. It was observed that the AV-junction is another important factor in the physiopathology of atrial fibrillation [11]. Moreover, the electrical isolation of pulmonary veins

Division of Cardiology, Cardiovascular Department, Umberto I Hospital, Mestre-

Venice, Italy

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alone loses efficacy progressively when patients with persistent or perma- nent atrial fibrillation are treated; in these patients, both the substrate and electrical remodelling probably play important roles [12, 13].

Notwithstanding the different ablative techniques and the growing num- ber of procedures, therapeutic success without antiarrhythmic treatment is rarely above 80%.

This is due to several fundamental reasons:

1. Electrical disconnection of the pulmonary veins is often incomplete, or, after a disconnection, some veins regain electrical conduction over time [14, 15].

2. It is possible that evolution of substrate and consequently of electrogenic disease is responsible for new recurrences.

3. The presence of different arrhythmogenic areas not included in the previ- ous ablation can be responsible for recurrences of atrial fibrillation [16].

It has been pointed out that the triggers of atrial fibrillation can arise also from other structures of the atria, such as superior vena cava [17], Marshall vein [18, 19], coronary sinus [20], christa terminalis, as well as the free walls of the atria [16]. The superior vena cava has anatomical and electrical charac- teristics similar to those of the pulmonary veins [21–23] and its involvement in the genesis of episodes of atrial fibrillation can explain some of the failures after disconnection of the pulmonary veins alone [24]. It has been shown that ablation of other, non-pulmonary-vein foci that initiate paroxysmal atrial fib- rillation episodes is efficient only in 60% of patients [16]. In addition, it seems that about 6% of cases of paroxysmal atrial fibrillation develop from ectopic beats starting from the superior vena cava [16, 24]. Disconnection of the superior vena cava proved successful in treating patients who had episodes of atrial fibrillation from foci arising from the superior vena cava [24, 25]. Moreover, recent findings in animals have demonstrated that the iso- lation of all thoracic veins can prevent episodes of permanent atrial fibrilla- tion, when effective [26]. In this study, the importance of systematic electrical disconnection of the superior vena cava together with the disconnection of pulmonary veins was evaluated, and initial results of this approach vs discon- nection of only the pulmonary veins are presented.

Study Conditions

From December 2004 to June 2005, 64 consecutive patients (45 males, mean

age 58 ± 12) were treated with atrial fibrillation ablation. The patients were

symptomatic for paroxysmal (28), persistent (20), permanent (16) atrial fib-

rillation and refractory to antiarrhythmic drug therapy. Structural heart dis-

ease was diagnosed in 61% (39/64) patients; 17 were hypertensive, 17 had

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mitral valvular prolapse, four had ischaemic heart disease, and 1 dilated car- diomyopathy). LVEF in this group of patients was 54 ± 10 , LAD 44 ± 6 mm. Patients were randomised in two groups: group I (30 patients) under- went circumferential electrical disconnection of the pulmonary veins and of the superior vena cava using a technique guided by intracardiac echocardio- gram phased array. Group II (34 patients) underwent only circumferential electrical disconnection of the pulmonary veins. The procedure was carried out with two transeptal punctures. Mapping was done with a Lasso decapo- lar 2-cm-diameter catheter, while ablation was done using the large-curve 8- mm catheter (Byosence Webster). Energy was delivered at the AV-junction of the pulmonary veins with antrum extension according to titration and a flow-chart guided by microbubbles production, as described by Marrouche et al. [l0]. The superior vena cava was disconnected at the junction of the vena cava and right atrium after positioning the mapping Lasso decapolar catheter, and guided by intracardiac echo. Before each radiofrequency deliv- ery the ablation area was stimulated to reveal possible involvement of the right phrenic nerve, in which case no ablation was performed. In case of sud- den sinus tachycardia during erogation in the juxta-sinus-node area, eroga- tion was immediately interrupted and the ablating catheter moved to a more proximal position. In these cases, a partial disconnection of the superior vena cava was accepted as end-point. Energy was supplied at 50 Watts and the temperature was 50°C.

The end-point of the procedure was reached with complete disappear- ance of all sharp potentials at the AV-junction of the pulmonary veins and superior vena cava, and at the antrum of the pulmonary veins. All patients were in wash-out of antiarrhythmic drugs before the procedure and had undergone anticoagulant therapy for at least 1 month, Transoesophageal echo was done immediately before the procedure.

Follow-Up

Patients were discharged without antiarrhythmic therapy but they were pro- vided with anticoagulant therapy for at least 3 months after the procedure.

Antiarrhythmic therapy was administered only to those patients with many recurrences and, when necessary, within 2 months after ablation. Therapy was withdrawn after 2 months if effective. All patients received Holter moni- toring before discharge for a week, had a routine follow-up visit and under- went further Holter monitoring at 1, 3, 6 and every 6 months. ECG and Holter monitoring were carried out at any other time if symptoms recurred.

CT scan was performed at 3 months. Success was defined as total absence of

recurrences of atrial fibrillation or atrial tachycardia/flutter.

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Preliminary Results

All pulmonary veins were disconnected in the two study groups. The superi- or vena cava was not completely disconnected in 40% (12/30) of patients because of phrenic nerve stimulation. The mean time of the procedure for disconnecting the pulmonary veins in the two groups was 4. 05 ± 0.31 h.

The mean procedure time for the vena cava disconnection was 25 ± 10 min. No lesions of the phrenic nerve were detected during the procedure and no other complications were found.

Follow-Up

The mean follow-up thus far is 3 ± 3 months. .At this writing, follow-up is incomplete and the patients are not evenly distributed between the two groups; nonetheless, early recurrence has been observed in the two groups:

30% (10/30) in group I and 38% (13/34) in group II. If we consider only the few patients with complete disconnection of the superior vena cava the rate of early recurrence is 22% (4/18) and 50% (6/12), respectively.

Conclusions

Although final results are not yet available, it is interesting to note that patients who had complete disconnection of the superior vena cava have had a good initial follow-up. However, these preliminary results must be con- firmed by studies that include a larger number of patients and a longer fol- low-up time.

References

1. Jalife J, Berenfeld O, Mansour M (2002) Mother rotors and fibrillatory conduction:

a mechanism of atrial fibrillation. Cardiovasc Res 54:204–216

2. Haïssaguerre M, Jaïs P, Shah DC et al (1998) Spontaneous initiation of atrial fibril- lation by ectopic beats originating in the pulmonary veins. N Engl J Med 339:659–666

3. Chen SA, Hsieh MH, Tai CT et al (1999) Initiation of atrial fibrillation by ectopic beats originating from the pulmonary veins: electrophysiological characteristics, pharmacological responses, and effects of radiofrequency ablation. Circulation 100:1879–1886

4. Saito T, Waki K, Becker AE (2000) Left atrial extension onto pulmonary veins in humans: anatomic observations relevant for atrial arrhythmias. J Cardiovasc Electrophysiol 11:888–894

5. Pappone C, Santinelli V, Manguso F et al (2004) Pulmonary vein denervation

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enhances long-term benefit after circumferential ablation for paroxysmal atrial fibrillation. Circulation 109:327–334

6. Wu TJ, Ong JJ, Chang CM et al (2001) Pulmonary veins and ligament of Marshall as sources of rapid activation in a canine model of sustained atrial fibrillation.

Circulation 103:1157–1163

7. Haïssaguerre M, Jaïs P, Shah DC et al (2000) Electrophysiological end point for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci. Circulation 101:1409–1417

8. Shah DC, Haïssaguerre M, Jaïs P et al (2001) Curative catheter ablation of paroxy- smal atrial fibrillation in 200 patients: strategy for presentations from sustained atrial fibrillation to no arrhythmias. PACE 24:1541–1558

9. Pappone C, Oreto G, Rosanio S et al (2001) Atrial remodeling after circumferential radiofrequency pulmonary vein ablation. Efficacy of an anatomic approach in a large cohort of patients with atrial fibrillation.Circulation 104:2539–2544

10. Marrouche NF, Martin DO, Wazni O et al (2003) Phased-array intracardiac echo- cardiography monitoring during pulmonary vein isolation in patients with atrial fibrillation. Impact on outcome and complications. Circulation 107:2710–2716 11. Hocini M, Ho SY, Kawara T et al (2002) Electrical conduction in canine pulmonary

veins: electrophysiological and anatomic correlation. Circulation 105:2442–2448 12. Ernst S, Ouyang F, Lober F et al (2003) Catheter-induced linear lesions in the left

atrium in patients with atrial fibrillation: an electroanatomic study. J Am Coll Cardiol 42:1271–1282

13. Nademanee K, McKenzie J, Kosar E et al (2004) A new approach for catheter abla- tion of atrial fibrillation: Mapping of the electrophysiologic substrate. JACC 43:2044–2053

14. Cappato R, Negroni S, Pecora D et al (2003) Prospective assessment of late conduc- tion recurrence across radiofrequency lesions producing electrical disconnection at the pulmonary vein ostium in patients with atrial fibrillation. Circulation 108:1599–1604

15. Nanthakumar K, Plumb VJ, Epstein AE et al (2004) Resumption of electrical con- duction in previously isolated veins. Rationale for a different strategy? Circulation 109:1226–1229

16. Lin WS, Tai CT, Hsieh MH et al (2003) Catheter ablation of paroxysmal atrial fibril- lation initiated by non-pulmonary vein ectopy. Circulation 107:3176–3183

17. Tsai CF, Tai CT, Hsiung MH et al (2000) Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava. Circulation 102:67–74

18. Hwang C, Wu TJ, Doshi RN et al (2000) Vein of Marshall cannulation for the analy- sis of electrical activity in patients with focal atrial fibrillation. Circulation 101:1503–1505

19. Hsu LF, Jaïs P, Keane D et al (2004) Atrial fibrillation originating from persistent left superior vena cava. Circulation 109:828–832

20. Sanders P, Jaïs P, Hocini M et al (2004) Electrical disconnection of the coronary sinus by radiofrequency catheter ablation to isolate a trigger of atrial fibrillation. J Cardiovasc Electrophysiol 15:364–368

21. Yeh HI, Lai YJ, Lee SH et al (2001) Heterogeneity of myocardial sleeve morphology and gap junctions in canine superior vena cava. Circulation 104:3152–3157 22. Ooie T, Tsuchiya T, Ashikaga K et al (2002) Electrical connection between the right

atrium and the superior vena cava, and the extent of myocardial sleeve in a patient

with atrial fibrillation originating from the superior vena cava. J Cardiovasc

Electrophysiol 13:482–485

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23. Shah DC, Haïssaguerre M, Jaïs P et al (2002) High-resolution mapping of tachycar- dia originating from the superior vena cava. J Cardiovasc Electrophysiol 13:388–392

24. Goya M, Ouyang F, Ernst S et al (2002) Electroanatomic mapping and catheter ablation of breakthroughs from the right atrium to the superior vena cava in patients with atrial fibrillation. Circulation 106:1317–1320

25. Yamane T, Miyanaga S, Inada K et al (2004) A focal source of atrial fibrillation in the superior vena cava: isolation and elimination by radiofrequency ablation with the guide of basket catheter mapping. J Interv Card Electrophysiol 11:131–134 26. Park A, Chou CC, Drury PC et al (2004) Thoracic vein ablation terminates chronic

atrial fibrillation in dogs. Am J Physiol Heart Circ Physiol 286:H2072–H2077

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