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Europace 2005 7(5):421-427; doi:10.1016/j.eupc.2005.05.015
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© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.

Complete pulmonary vein isolation guided by three-dimensional electroanatomical mapping for the treatment of paroxysmal atrial fibrillation in patients with hypertrophic obstructive cardiomyopathy

Xingpeng Liua, Feifan Ouyanga,*, Hercules Mavrakisa, Changsheng Mab, Jianzeng Dongb, Sabine Ernsta, Dietmar Bänscha, Matthias Antza and Karl-Heinz Kucka

aII. Med. Abteilung, Allgemeines Krankenhaus St. Georg Lohmühlenstrasse 5, 20099 Hamburg, Germany; bDepartment of Cardiology, Beijing Anzhen Hospital, Capital University of Medical Sciences Beijing, China

Manuscript submitted 28 October 2004. Accepted after revision 7 May 2005.

*Corresponding author. Tel.: +49 40 181885 2305; fax: +49 40 181885 4444. E-mail address: ouyangfeifan{at}aol.com (F. Ouyang).


    Abstract
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
AIMS: Evaluation of the clinical outcome of patients with hypertrophic obstructive cardiomyopathy (HOCM) and paroxysmal atrial fibrillation (AF) treated with complete pulmonary vein (PV) isolation guided by three-dimensional (3-D) electroanatomical (EA) mapping.

METHODS: Circumferential radiofrequency (RF) ablation and continuous circular lesions (CCLs) around the left and right-sided PVs were performed in 4 highly symptomatic patients (2 males; age 57.5±8.3 years) with HOCM and anti-arrhythmic drug (AAD) refractory paroxysmal AF. Ablation was guided by 3-D EA mapping combined with conventional circumferential PV mapping. The endpoints of the ablation were defined as: (1) absence of all PV spikes documented with the two Lasso catheters within the ipsilateral PVs; and (2) no recurrence of the PV spikes within all PVs following intravenous administration of adenosine.

RESULTS: The ablation endpoints were achieved in all patients. A repeat ablation was performed in one patient due to repetitive atrial tachycardia, 1 month after the initial procedure. During a follow-up of 5.8±2.7 months, all patients are free of AF recurrence. Short episodes of symptomatic AT were documented after the repeat procedure, and were well controlled with oral amiodarone in the patient. No procedure-related complications were observed.

CONCLUSION: The present study demonstrates that complete isolation of ipsilateral PVs guided by 3-D EA mapping is potentially effective for the treatment of highly symptomatic, drug refractory paroxysmal AF in patients with HOCM.

Key Words: hypertrophic cardiomyopathy, atrial fibrillation, ablation, pulmonary vein


    Introduction
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Atrial fibrillation (AF) is the most common sustained arrhythmia in patients with hypertrophic cardiomyopathy. Paroxysmal AF can result in severe haemodynamic decompensation due to the loss of atrial contraction and the uncontrolled fast ventricular rate, especially in patients with hypertrophic obstructive cardiomyopathy (HOCM) [1Go–3]Go. Recent studies have demonstrated that continuous circular lesions (CCLs) around the pulmonary veins (PVs) guided by three-dimensional (3-D) electroanatomical (EA) mapping is an effective treatment for paroxysmal AF [4Go6]Go. In the present study, we evaluate the effectiveness of complete PV isolation guided by 3-D EA mapping in patients with HOCM and paroxysmal AF.


    Methods
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Patient characteristics
We evaluated four highly symptomatic patients (two males; age 57.5±8.3 years; range 49–66 years) with HOCM and frequent episodes of paroxysmal AF. The functional status of all patients during sinus rhythm was New York Heart Association (NYHA) class II. The frequency of AF paroxysms in the 6-month period prior to ablation was 1–4 episodes per week. AF-related symptoms included palpitations, presyncope, hypotension and dyspnoea. In one patient, AF onset resulted in severe haemodynamic decompensation, requiring external electrical cardioversion. A dual-chamber pacemaker (DDD) following ablation of the atrioventricular node had been implanted for control of rapid heart rates during AF in this patient. Paroxysmal AF was first diagnosed 8±8.5 years (range 1–20 years) before referral, and had been ineffectively treated with amiodarone, verapamil and beta-blockers in all patients. All patients were on amiodarone treatment when the ablation procedure was performed and continued their treatment for 1 month after ablation. The diagnosis of HOCM was based on current established echocardiographic criteria [7]Go. The maximal thickness of interventricular septum was 27±5 mm (2.7±0.5 times thicker than the posterior wall). A left ventricular outflow tract obstruction with a resting pressure gradient of 53±14 mmHg and diastolic dysfunction were observed in our patients by Doppler echocardiography. Primary hypertension and aortic stenosis were excluded in all patients. A dual-chamber implantable cardioverter defibrillator (ICD) had been implanted due to malignant ventricular tachyarrhythmias in two patients. The mean left atrial (LA) diameter was 46.0±9.0 mm (range 37–58 mm). Transoesophageal echocardiography was performed to rule out LA thrombi in all patients. Anticoagulation treatment with warfarin was discontinued on admission and replaced by intravenous heparin to maintain the partial thromboplastin time at 2–3 times the control value in all patients.

Mapping and ablation
All patients provided informed written consent prior to the procedure. Two standard catheters were positioned: a 6-F catheter (Biosense-Webster Inc.) at the His bundle region via a femoral vein, and a 6-F catheter into the coronary sinus (CS) via the left subclavian vein. No catheter was placed inside the CS in patient #3 with a previous DDD pacemaker implantation. Three 8-F sheaths (SL1, St. Jude Medical Inc., Minnetomra, MN, USA) were advanced to the LA using a modified Brockenbrough technique: two sheaths over one puncture site and the third sheath via a second puncture site. After transeptal catheterization, intravenous heparin was administered to maintain an activated clotting time of 250 to 300 s.

The technique of complete isolation of ipsilateral PVs guided by 3-D LA mapping has been described previously in detail [6]Go. Briefly, LA geometry was reconstructed using a 3-D EA mapping system (CARTO, Biosense-Webster, USA) during CS pacing in three patients and right atrial appendage pacing in patient #3. Each PV ostium was identified by selective venography and tagged on the EA map. Two decapolar circumferential mapping catheters (Lasso, Biosense-Webster) were placed within the ipsilateral superior and inferior PVs or within the superior and inferior branches of a common PV (Fig. 1). CCLs around the ipsilateral PVs were created with continuously irrigated radiofrequency (RF) ablation using a 3.5 mm tip ablation catheter (Thermo-Cool Navi-Star, Biosence-Webster). RF energy was delivered with a temperature setting of 45 °C, a power limit of 30–40 W and infusion rate of 17 ml/min. RF energy was applied for more than 30 s at each point until the maximal local electrogram amplitude decreased by more than 70% or fragmented potentials were noted. Irrigated RF ablation was performed in the posterior wall more than 1 cm and in the anterior wall about 5 mm from the angiographically defined ipsilateral PV ostia (Fig. 2). In patient #4, ablation was performed within 5 mm of the ostium of the PVs due to the relatively narrow border between the anterior aspect of the left PVs and the posterior wall of left atrial appendage.



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Figure 1 (Left panel) Fluoroscopic right anterior oblique (RAO) view showing the angiography of left side pulmonary veins (PV), two Lasso catheters within the right superior and inferior pulmonary veins (RSPV, RIPV), a catheter inside the coronary sinus (CS), and a catheter at the His bundle region (His) in patient #1 with a dual-chamber implantable cardioverter defibrillator (ICD). Note that the selective PV angiography revealed a common ostium in the left-sided PVs in this patient. (Right panel) Fluoroscopic left anterior oblique (LAO) view showing the PV angiography and circumferential mapping with two Lasso catheters in left superior and inferior pulmonary veins (LSPV, LIPV respectively) in patient #3 with a dual-chamber pacemaker.

 



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Figure 2 Electroanatomical map of the left atrium in patient #4 (left panel: posteroanterior view; right panel: right lateral view). The PV ostia (identified by angiography) are tagged by white dots. Two continuous circular lesions marked by multiple red dots around the PVs are demonstrated.

 
The endpoints of the ablation were defined as: (1) absence of all PV spikes documented with the two Lasso catheters within the ipsilateral PVs at least 30 min after isolation; and (2) no recurrence of the PV spikes within all PVs following intravenous administration of 9–12 mg of adenosine.

Post-ablation treatment and follow-up
Intravenous heparin was administered for 3 days after the procedure, followed by warfarin for at least 3 months in all patients. All patients continued oral amiodarone treatment for 1 month after ablation. All patients were followed up with 12-lead electrocardiography (ECG), 24-h Holter recordings and echocardiography 1, 3, 6 and 9 months after ablation. Three patients had a telemetric ECG recorder (Philips Telemedizin, Germany) for 6 months to document symptomatic arrhythmias or to transfer a 30 s ECG once per week if asymptomatic. Monthly telephone interviews were conducted with all patients. Interrogation of implantable devices was also used to exclude recurrence of AF in two patients. Any episode of AF, regardless of duration, was considered as arrhythmia recurrence.

Statistical analysis
All values are expressed as mean±SD.


    Results
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Ablation
A common PV ostium was demonstrated by selective PV angiography in the left-sided PVs (LCPV) in patient #1. All ipsilateral PVs were successfully isolated by two CCLs and ipsilateral PV spikes disappeared simultaneously in all patients (Fig. 3). After intravenous adenosine administration (9–12 mg) no PV spike recurrence was observed in any PV. The mean RF duration was 1860±345 s (1540 to 2210 s) for the right-sided PVs and 1764±356 s (1459 to 2150 s) for the left-sided PVs. No vagal reflexes or cough were observed during irrigated RF delivery in all patients. After PV isolation, automatic PV activity dissociated from the atrial activity was observed in two left PVs (patient #1 and patient #4) and one right PV (patient #2) (Fig. 3). The procedure time was 234±42 min (195–290 min) with a fluoroscopic time of 31.1±4.4 min (26.2–36.5 min).



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Figure 3 Tracings are ECG leads I, II, V1 and intracardiac electrograms recorded from two Lasso catheters within the right superior and inferior pulmonary veins (RSPV, RIPV), a mapping catheter (Mp), a catheter inside the coronary sinus (CS) and a catheter at the His bundle region (HBE) during sinus rhythm in patient #2. Note both RSPV and RIPV were isolated simultaneously during the 16th radiofrequency (RF) application. After PV isolation, an automatic activity (marked by arrow) dissociated from the atrial activity was recorded in the ipsilateral PVs. Also, an atrial extrasystole (AES; marked with asterisk) was recorded after two beats of sinus rhythm, and presented with different morphology of P wave and different intracardiac atrial activation sequences. A, atrial potential; V, ventricular potential; PV, pulmonary vein potential.

 
A repeat ablation was performed in patient #1 due to repetitive atrial tachycardia 1 month after the initial procedure. During the repeat procedure, two conduction gaps in the previous CCLs were identified using two Lasso catheters within the ipsilateral PVs. One gap was located in the postero-inferior part of right-sided CCLs and the other gap was located in the inferior part the left-sided CCLs. The two conduction gaps were successfully closed by irrigated RF applications during the second procedure (Fig. 4). No procedure-related complications were observed in any patient.



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Figure 4 (Left panel) Fluoroscopic left and right anterior oblique (LAO, RAO) view showing the two Lasso catheters within the right superior and inferior pulmonary veins (RSPV, RIPV), a catheter inside the coronary sinus (CS), and a catheter at the His bundle region (His) in patient #1 with a dual-chamber implantable cardioverter defibrillator (ICD) during the repeat procedure. (Right panel) Tracings are ECG leads I, II, V1 and intracardiac electrograms recorded from two Lasso catheters within the right superior and inferior pulmonary veins (RSPV, RIPV), a mapping catheter (Mp), a catheter inside the coronary sinus (CS) and a catheter at the His bundle region (HBE) during paced rhythm in the same patient. Note that (1) PV spikes via a recovered conduction gap on the previous CCLs are widely separately from the far-field atrial activation during paced rhythm; and (2) both RSPV and RIPV were isolated simultaneously during the radiofrequency (RF) delivery at the conduction gap located on the postero-inferior part of the previous CCLs. A, atrial potential; V, ventricular potential; PV, pulmonary vein potential; CCLs, continuous circular lesions.

 
Follow-up
All patients are free of AF recurrence during a follow-up period of 5.8±2.7 (range 3–9) months (three patients without any AAD treatment). However, a symptomatic short episode of AT was documented after the repeat procedure and was well controlled with oral amiodarone in patient #1.


    Discussion
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
Atrial fibrillation in patients with hypertrophic cardiomyopathy
Paroxysmal and chronic AF ultimately occur in 20–25% of hypertrophic cardiomyopathy patients [1Go–3]Go. The ideal treatment strategy for AF in patients with hypertrophic cardiomyopathy is unclear due to the absence of large randomized trials. However, in the recent ACC/AHA/ESC guidelines for the management of patients with hypertrophic cardiomyopathy and AF, anticoagulation and anti-arrhythmic medications to prevent AF recurrence were recommended [8]Go.

In general, an aggressive strategy for maintaining sinus rhythm is especially recommended in patients with HOCM based on the following reasons: (1) paroxysmal AF may trigger life-threatening ventricular arrhythmias [9]Go; (2) paroxysmal AF can cause deterioration in the symptoms and induce syncope or heart failure [10]Go; and (3) AF is associated with substantial risk for heart failure-related mortality, stroke and severe functional disability [11,Go12]Go. However, restoring and maintaining sinus rhythm by electrical cardioversion and AADs is difficult and is often associated with adverse effects during a long-term treatment [8,Go13]Go. Additionally, although amiodarone is regarded as effective in reducing AF recurrences in hypertrophic cardiomyopathy patients, the available data are very limited [14]Go. In the present study amiodarone was ineffective in all patients. Therefore, establishment of an effective approach for maintaining sinus rhythm is critical for patients with HOCM and paroxysmal AF.

Catheter ablation for atrial fibrillation in hypertrophic cardiomyopathy
Previous studies have established circumferential ablation around PVs guided by 3-D EA mapping as a curative therapy for paroxysmal AF with a success rate of 85–88% [4,Go5]Go. In a recent study, we demonstrated that complete isolation of ipsilateral PVs guided by 3-D EA mapping and double Lasso technique is feasible and highly effective for patients with paroxysmal AF [6]Go. In this study, 95.1% of the patients were free of AF during a follow-up of median of 131±12 days after ablation [6]Go. However, the majority of patients in the previously mentioned studies were without structural heart disease and the clinical outcome of patients with HOCM and paroxysmal AF treated with this ablation strategy is unknown [4Go–6]Go. In the present study, all patients were free of AF recurrence after ablation, including one patient who underwent two procedures. Restoration of sinus rhythm was also observed in a case report of a patient with HOCM and chronic AF who underwent a transaortic septal myotomy/myectomy and a Cox maze III procedure through the right and left atrium followed by mitral valve replacement [15]Go.

Based on our findings, the mechanisms of triggers for AF are likely to be similar in patients with hypertrophic cardiomyopathy to those in patients without structural heart disease. Also, these findings indicate that PVs and PV–LA junction play an important role in the initiation and maintenance of AF not only in normal hearts but also in HOCM.

Study limitations
The study population is small and highly selective, and the follow-up period is short because the ablation strategy used has been recently established. Although further larger studies and a longer follow-up are necessary to clarify the effectiveness and safety of this approach, our findings at least indicate that complete isolation of ipsilateral PVs guided by 3-D mapping may be an alternative treatment for paroxysmal AF in HOCM patients.

Conclusion
The present study demonstrates that complete isolation of ipsilateral PVs guided by 3-D EA mapping is potentially effective for the treatment of highly symptomatic, drug refractory paroxysmal AF in patients with HOCM.


    Acknowledgements
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
We gratefully acknowledge the assistance of Detlef Henning for expert preparation of the figures.


    References
 Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Acknowledgements
 References
 
[1] Maron BJ, Casey SA, Poliac LC, et al. Clinical course of hypertrophic cardiomyopathy in a regional United States cohort. JAMA 1999; 281: 650–655.[Abstract/Free Full Text]

[2] Maron BJ, McKenna WJ, Danielson GK, et al. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy. A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol 2003; 42: 1687–1713.[Free Full Text]

[3] Nishimura RA and Holmes DR Jr. Clinical practice. Hypertrophic obstructive cardiomyopathy. N Engl J Med 2004; 350: 1320–1327.[Free Full Text]

[4] Pappone C, Oreto G, Rosanio S, et al. Atrial electroanatomical remodeling after circumferential radiofrequency pulmonary vein isolation: efficacy of an anatomic approach in a large cohort of patients with atrial fibrillation. Circulation 2001; 104: 2539–2544.[Abstract/Free Full Text]

[5] Oral H, Scharf C, Chugh A, et al. Catheter ablation for paroxysmal atrial fibrillation: Segmental pulmonary vein ostial ablation versus left atrial ablation. Circulation 2003; 108: 2355–2360.[Abstract/Free Full Text]

[6] Ouyang F, Bänsch D, Ernst S, et al. Complete isolation of the left atrium surrounding the pulmonary veins: new insights from the double Lasso technique in paroxysmal atrial fibrillation. Circulation 2004; 110: 2090–2096.[Abstract/Free Full Text]

[7] Maron BJ, Pelliccia A, Spirito P. Cardiac disease in young trained athletes: Insights into methods for distinguishing athlete's heart from structural heart disease, with particular emphasis on hypertrophic cardiomyopathy. Circulation 1995; 91: 1596.[Free Full Text]

[8] Fuster V, Rydén LE, Asinger RW, et al. ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: executive summary A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients with Atrial Fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology. Circulation 2001; 104: 2118–2150.[Free Full Text]

[9] Boriani G, Rapezzi C, Biffi M, et al. Atrial fibrillation precipitating sustained ventricular tachycardia in hypertrophic cardiomyopathy. J Cardiovasc Electrophysiol 2002; 13: 954.[CrossRef][Web of Science][Medline]

[10] Robinson K, Frenneaux MP, Stockins B, et al. Atrial fibrillation in hypertrophic cardiomyopathy: a longitudinal study. J Am Coll Cardiol 1990; 15: 1279–1285.[Abstract]

[11] Olivotto I, Cecchi F, Casey SA, et al. Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. Circulation 2001; 104: 2517–2524.[Abstract/Free Full Text]

[12] Maron BJ, Olivotto I, Bellone P, et al. Clinical profile of stroke in 900 patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2002; 39: 301–307.[Abstract/Free Full Text]

[13] The AFFIRM Investigators. Relationships between sinus rhythm, treatment, and survival in the atrial fibrillation follow-up investigation of rhythm management (AFFIRM) study. Circulation 2004; 109: 1509–1513.[Abstract/Free Full Text]

[14] McKenna WJ, Harris L, Rowland E, et al. Amiodarone for long-term management of patients with hypertrophic cardiomyopathy. Am J Cardiol 1984; 54: 802–810.[CrossRef][Web of Science][Medline]

[15] Matsui Y, Fukada Y, Imai T, et al. Combined cox maze procedure, septal myectomy, and mitral valve replacement for severe hypertrophic obstructive cardiomyopathy complicated by chronic atrial fibrillation. Ann Thorac Cardiovasc Surg 2003; 9: 323–325.[Medline]


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