ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Alain F. Carpentier
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chauvaud, S. M.
Right arrow Articles by Carpentier, A. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chauvaud, S. M.
Right arrow Articles by Carpentier, A. F.
Related Collections
Right arrow Congenital - cyanotic

Ann Thorac Surg 2001;71:1547-1552
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Cardiac arrhythmia in patients undergoing surgical repair of Ebstein’s anomaly

Sylvain M. Chauvaud, MDa, Gianluca Brancaccio, MDa, Alain F. Carpentier, MD, PhDa

a Department of Cardiovascular Surgery, Hôpital Européen Georges Pompidou, Paris, France

Accepted for publication January 19, 2001.

Address reprint requests to Dr Chauvaud, Département de Chirurgie Cardio-Vasculaire, Hôpital Européen Georges Pompidou, 20, rue Leblanc, 75015 Paris, France
e-mail: sylvain.chauvaud{at}egp.ap-hop-paris.fr


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Arrhythmias remain an unsolved problem in Ebstein’s anomaly. The aim of this study was to investigate the evolution of arrhythmias after surgical repair.

Methods. Forty-five patients with Ebstein’s anomaly and arrhythmias were studied. Mean age was 33 ± 15 years. Twenty-four patients (53%) had paroxysmal supraventricular tachycardia, 12 (27%) had atrial fibrillation or flutter, 8 (18%) had ventricular preexcitation (Wolff-Parkinson-White syndrome), and 1 (2%) had a nonsustained ventricular tachycardia. Surgical technique included detachment of the tricuspid anterior leaflet and suture on the atrioventricular annulus associated with right ventricular longitudinal plication.

Results. There were four hospital deaths (9%). A pacemaker was implanted early after operation in 5 patients (11%). During a mean follow-up of 57 ± 50 months (range, 4 to 226 months), there were six additional deaths, three of which were sudden. Two patients were lost to follow-up. Of the 33 surviving patients, 8 (24%) continued to have symptomatic arrhythmias, and 15 (45%) were in permanent sinus rhythm. Of the 24 patients with preoperative paroxysmal supraventricular tachycardia and the 12 with atrial fibrillation or flutter preoperatively, 9 and 2 of the survivors, respectively, have had no further episodes of arrhythmia. The incidence of arrhythmia with or without symptoms was reduced to 39% (13/33) of the surviving patients.

Conclusions. Arrhythmia is not totally abolished after operation. However, patients with Ebstein’s anomaly and arrhythmia show substantial improvement after conservative surgical intervention.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Ebstein’s anomaly is a congenital cardiac malformation in which the tricuspid septal and posterior leaflets attach below the valve annulus. The effective tricuspid valve orifice is displaced downward into the right ventricle at the junction of the inlet and trabecular components of the ventricle. [1] It was first described in 1866 by Wilhelm Ebstein in a 19-year-old laborer who died of tricuspid regurgitation caused by severe malformation of the tricuspid valve [2]. The incidence of Ebstein’s anomaly is reported to be approximately 1 in 20,000 live births and is 0.5% or less among patients with congenital heart disease. Ebstein’s anomaly is often associated with paroxysmal supraventricular tachycardia. The incidence of arrhythmias ranges between 22% and 42% of patients, 5% to 10% of whom have Wolff-Parkinson-White (WPW) syndrome [3]. These arrhythmias have an important impact on the quality of life of the patient and on midterm and long-term survival [4].

Different surgical techniques have been used to repair the anomaly, but the results in regard to arrhythmias are uncertain [5–9]. The present study reports our experience in a consecutive series of patients referred for surgical repair of Ebstein’s anomaly, with particular emphasis on patients with documented preoperative arrhythmias. The purpose of the study was to evaluate whether the technique of Carpentier and associates [10] not only improves the underlying structural and hemodynamics problems but also reduces the incidence of cardiac arrhythmias.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Between January 1980 and July 1999, 98 patients underwent operation to correct Ebstein’s anomaly at Hôpital Broussais. Early in this experience, the diagnosis and the assessment of tricuspid valve insufficiency in each patient were performed with invasive methods, catheterization and angiography. Since 1985, echocardiography and Doppler echocardiography only have been used. Before operation, 45 (46%) of the 98 patients had documented arrhythmias. Arrhythmias and atrioventricular (AV) conduction before operation were assessed by routine 12-lead electrocardiograms in all patients and by electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, and treadmill exercise testing when clinically indicated. All patients were monitored by electrocardiograms intraoperatively and for 3 to 7 days postoperatively.

Preoperative electrophysiologic assessment was carried out in only 12 patients. Indications were palpitations or electrocardiographic evidence of ventricular preexcitation. At the time of electrophysiologic study, inducible orthodromic reciprocating tachycardia was found in 6 patients, 2 of whom had inducible sustained atrial flutter or fibrillation. The accessory AV connections were located in the right posteroseptal or lateral free wall in all 12 patients. One patient (patient 2) had radiofrequency ablation preoperatively.

The arrhythmias documented preoperatively in the 45 patients were as follows: paroxysmal supraventricular tachycardia in 24, permanent atrial fibrillation or flutter in 12, ventricular preexcitation (WPW syndrome) in 8, and nonsustained monomorphic ventricular tachycardia in 1. The 45 patients with a cardiac arrhythmia were significantly older than the 53 patients who did not have symptoms or a documented arrhythmia (mean age, 33 years versus 21 years; p < 0.01). There were no other significant differences in preoperative functional or hemodynamic data between patients with and patients without symptoms of preoperative arrhythmia (Table 1).


View this table:
[in this window]
[in a new window]
  		Table 1. Characteristics of Patients With and Without Arrhythmiasa

 
The tricuspid valve lesions were classified using a functional approach, which includes assessment of the motion of the anterosuperior leaflet and the size and contractility of the atrialized chamber [10]. Eleven patients had severe dysplasia of the leaflets with muscularization of the tensile apparatus and attachment of the anterosuperior leaflet to the right ventricular wall by abnormal chordae. In these patients, there was a muscular continuity between the right atrial wall, the tricuspid anterior leaflet, and the ventricular wall.

The indications for operation were cyanosis, severe symptoms, severe tricuspid regurgitation, or arrhythmias. Four patients who had mild tricuspid regurgitation and were in New York Heart Association functional class I or II underwent surgical repair for symptoms of arrhythmia associated with cyanosis (3 patients) or after an unsuccessful noninvasive attempt to oblate the accessory pathways (1 patient).

Operative technique
The operative technique has been described in detail [10, 11]. Operation was undertaken using cardiopulmonary bypass at 28°C. The tricuspid valve was approached through a right atriotomy. The corrective procedure as used at Hôpital Broussais has four basic steps, and the goals are to restore normal function to the tricuspid valve and to incorporate the inlet of the right ventricle in the repair. The anterosuperior leaflet is temporarily detached, and the restrictive trabeculations and cords are divided to restore normal motion (Fig 1). The anterolateral papillary muscle is fully mobilized by detaching the muscular bands, which were inserted into the lateral wall of the right ventricle. The atrialized right ventricle is plicated longitudinally, a measure achieving a reduction in the diameter of the tricuspid annulus. The anterosuperior leaflet is rotated in a clockwise direction and reattached to the newly reduced annulus. In adult patients, the annulus is reinforced with a Carpentier prosthetic ring.



View larger version (80K):
[in this window]
[in a new window]
  		Fig 1. (A) Detachment of the anterior leaflet and section of the muscular bands in order to individualize the lateral papillary muscle. Dashed lines indicate the limits of the atrialized chamber. (B) Longitudinal plication of the atrialized chamber from the apex of the right ventricle to the tricuspid annulus. Subsequently, the tricuspid annulus is reduced. (C) Reattachment of the anterior leaflet on the true annulus with a clockwise rotation.

 
Valve repair was accomplished in 96% of patients and valve replacement with a bioprosthesis, in 4% (2/45). Longitudinal plication of the right ventricular chamber was required in 41 patients (91%). Annuloplasty using a prosthetic Carpentier ring was performed in 78% (35 patients). A bidirectional cavopulmonary shunt was added in 12 patients at high risk of early right ventricular failure [12]. Closure of an associated atrial septal defect or patent foramen ovale was performed in 21 patients. Cryoablation of an accessory pathway was performed perioperatively in 2 patients (patients 1 and 24) early in our experience.

Follow-up data were collected at consultations every 6 months, and a 12-lead electrocardiogram was obtained. When clinical symptoms were present or when electrocardiographic abnormalities persisted, a 24-hour recording was made (Holter monitoring).

Statistical analysis
Data are expressed as the mean ± the standard deviation. Differences between preoperative and postoperative data were analyzed using {chi}2 contingency tables for discrete variables and Student’s t test for continuous variables. The Kaplan-Meier method was used to calculate actuarial survival. A p value of less than 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
The hospital mortality rate for the 45 patients with preoperative arrhythmias was 9% (4 patients). The causes of death were right ventricular failure in 3 patients and postoperative hyperthermia in the other. All 4 had severe disease (type C) and an atrialized right chamber. In a previous study [12] we defined patients to be at high risk when one or more of the following elements were present: massive tricuspid insufficiency, a long history of tricuspid valve disease, New York Heart Association functional class IV, or permanent atrial fibrillation. Reoperation for residual tricuspid insufficiency was performed in 3 patients with a second repair in 2 and valve replacement in the other.

Postoperative arrhythmias
In the early postoperative period, 42% (17 of 41) of the patients were in permanent sinus rhythm, and only 7 patients (17%) had supraventricular tachyarrhythmia (Table 2). Atrial fibrillation was seen in 8 patients (19.5%). Implantation of a pacemaker to treat AV dissociation was necessary in 5 patients (12%). The other 3 patients with junctional rhythm immediately after operation regained sinus rhythm with normal AV conduction during the hospital stay. The surgical procedure significantly reduced the incidence of early postoperative arrhythmias: sinus rhythm was present in 17 of the 41 early survivors.


View this table:
[in this window]
[in a new window]
  		Table 2. Clinical Features and Follow-up Data on 45 Patients With Preoperative Arrhythmiasa

 
Follow-up
Follow-up assessment was available for 39 of the 41 patients who survived the operation and the perioperative period (Table 3). The mean follow-up was 58 ± 50 months (range, 4 to 226 months). During this period, there were six deaths. Three patients died suddenly, 2 died of right ventricular failure, and 1 patient died of pulmonary infection. Actuarial survival was 88% ± 5% at 1 year and 76% ± 8% at 5 years and 10 years (Fig 2). Functional status was assessed using the New York Heart Association classification; 38% were in class I, 55% in class II, 5% in class III, and 2% in class IV. Twelve of the surviving 33 patients continued to have arrhythmias (4 had paroxysmal supraventricular tachycardia, 5 had atrial fibrillation, and 3 had WPW), but 15 (45%) patients reported no arrhythmia (see Table 3).


View this table:
[in this window]
[in a new window]
  		Table 3. Baseline Data for 45 Patients in Preoperative and Follow-up Period

 


View larger version (10K):
[in this window]
[in a new window]
  		Fig 2. Actuarial survival curve at 1 year, 5 years, and 10 years.

 
Nineteen of the 24 patients with documented preoperative paroxysmal supraventricular tachycardia were followed up for a mean of 44 ± 39 months. Four died in the hospital, and 1 was lost to follow-up. Nine had no further episodes of palpitation, syncope or near syncope, or electrocardiographic signs of arrhythmia. Two patients died suddenly at a mean 21 ± 3.5 months after operation (patients 18 and 34) while still receiving flecainide acetate therapy for symptomatic tachycardias. Four patients continued to have symptomatic tachycardia, and 2 (patients 19 and 39) had development of atrial fibrillation, and 2 others had permanent pacemaker implantation, 1 of whom (patient 35) had complete AV block.

The 12 patients with preoperative atrial fibrillation were followed up for a mean 74 ± 68 months. There were no hospital deaths in this group, and 1 patient was lost to follow-up. When last seen, 3 were in permanent sinus rhythm. Of the remaining 8 patients, 3 died while on a regimen of digoxin therapy (patients 26, 32, and 43), 1 had development of AV block with subsequent pacemaker implantation, and 3 continued to have chronic atrial fibrillation. One patient had had a pacemaker implanted early postoperatively.

The 8 patients with Wolff-Parkinson-White syndrome were followed up for a mean of 63 ± 44 months. 2 were in sinus rhythm. Of the remaining 6 patients, 1 died 56 months after operation (patient 3), 2 had development of AV block immediately after operation and had a pacemaker implanted (patients 24 and 31), and 3 continued to have WPW, but only 1 has symptoms requiring medications. The patient with preoperative ventricular arrhythmias was free from symptomatic tachycardia at 99 months of follow-up (patient 38).

Quality of life
The number of patients on a regimen of antiarrhythmic therapy decreased significantly from 100% (45 patients) preoperatively to 44% (18 of 41 patients) postoperatively and to 24% (8 of 33 patients) during follow-up (p < 0.01). Seven patients underwent treatment, 2 with SVT, 4 with AF, and 1 with WPW. Two patients with persistent paroxysmal supraventricular tachycardias were on a regimen of propranolol hydrochloride, and 4 patients in atrial fibrillation continued therapy with digoxin and an anticoagulant. The patient with WPW (patient 8) who continued to experience paroxysmal tachycardia was considerably less symptomatic than preoperatively on a regimen of propafenone hydrochloride therapy. New York Heart Association functional status improved significantly during follow-up. In conclusion, of 45 patients with preoperative documented arrhythmias, only 13 patients (39% of the 33 patients available for follow-up) had persisting arrhythmia.


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Patients with Ebstein’s anomaly frequently have troublesome and occasionally fatal cardiac arrhythmias. This anomaly is the most common congenital cardiac defect associated with WPW syndrome. Some arrhythmias such as paroxysmal supraventricular tachycardia with WPW syndrome are explained by the presence of accessory pathways, whereas atrial fibrillation is related to right atrial enlargement caused by tricuspid insufficiency. This finding is consistent with the hypothesis that Ebstein’s anomaly originates from the incomplete separation of the right atrium and the right ventricle [13]. Therefore it is possible that any part of the atrialized ventricle can be connected to the right atrium across the annulus. The accessory AV connections usually are located on the same side as the malformed valve, and in more than 50% of patients, multiple accessory pathways have been found [14–16]. Pressley and coworkers [17] reported that 50% of 38 patients with Ebstein’s anomaly and WPW syndrome had multiple pathways. Cappato and associates [14] described an adult population undergoing radiofrequency ablation for Ebstein’s associated arrhythmia and found 62% of patients had multiple accessory pathways.

The preponderance of right posterior and right posteroseptal accessory pathways [14, 16–19] and the morphological abnormalities of the atrialized ventricle [13] could explain the arrhythmogenic role of this chamber. Thus, we suggest that plication of the right atrialized ventricle permits the interruption of accessory pathways across this region, and, on the other hand, excludes this chamber that causes arrhythmogenic circuits or foci [20].

Our hypothesis is that by means of muscular strands, accessory pathways cross the tricuspid annulus in the place where the anterosuperior leaflet is located. This leaflet, as reported by Anderson and coauthors [1], is always abnormal anatomically. Usually, "it is large and has abnormal fibrous strands running through it. These strands sometimes become muscularized, and attach the leaflet at the right ventricle wall". In some hearts the attachment is by means of these abnormal muscularized chordae, whereas in others the attachment is continuous and can incorporate the anterolateral papillary muscle. The tricuspid valve is "muscularized" in Ebstein’s anomaly, and in 11 of our patients during operation, it was noticed in the presence of continuous muscular bands. Therefore, detachment of the anterosuperior leaflet and incision of all the muscular trabeculations provide not only leaflet mobilization, but also interruption of accessory pathways.

The goals of the various surgical procedures are to reduce the structural and functional anomaly. However, the major unsolved problem is the high incidence of atrial arrhythmias, which exist preoperatively and postoperatively [21]. In a study of cardiac arrhythmias in patients undergoing surgical repair of Ebstein’s anomaly, Oh and associates [3] found that 33% of patients with preoperative arrhythmias continued to have symptomatic tachycardia after operation. For this reason, in patients with a "wide complex," Danielson and co-workers [5] reported prophylactic intravenous administration of lidocaine hydrochloride 48 hours before operation and use of procainamide hydrochloride for 3 months postoperatively once oral intake has begun. In no patient in our series did we use the maze procedure because of the lack of published data favoring a reduction in atrial fibrillation in right-sided lesions. Map-directed ablation of accessory pathways is time-consuming, and according to the Mayo clinic experience [5], the incidence of recurrent rhythmic disturbances is still a problem with this procedure.

With our technique, we were able to reestablish sinus rhythm in about 30% of patients with preoperative cardiac arrhythmias, and fewer than one sixth continued to have symptomatic tachycardias after operation. There was a more marked decrease in the occurrence of supraventricular tachycardia compared with atrial fibrillation. This suggests that the etiology of supraventricular tachycardia in many of these patients may be related more to the presence of the accessory pathways than to primary or secondary myocardial abnormalities seen with Ebstein’s anomaly. These observations correlate with those in previous reports [17, 22] in which the authors observed that patients in atrial fibrillation with surgical ablation of the accessory pathways in Ebstein’s anomaly had a twofold to threefold increased risk of a new atrial fibrillation developing postoperatively compared with patients without Ebstein’s anomaly. This fact demonstrates that the etiology of atrial fibrillation in patients with Ebstein’s anomaly is due overall to right atrial enlargement. In summary, interruption of accessory pathways, whatever the technique used, is not efficient when atrial fibrillation is present. On the basis of the good results of conservative surgical procedures, we advise discussion about an operation before the onset of atrial enlargement.

The significant decreases in the frequency and severity of arrhythmias, in the need of antiarrhythmic drugs, and in activity limitations as demonstrated by a better New York Heart Association class after operation appear to have greatly improved the quality of life of patients with Ebstein’s anomaly. Our study does have limitations. It is a retrospective study, and it was not possible to demonstrate electrophysiologically the presence of accessory pathways in the anterior leaflet of the tricuspid valve. Nevertheless, our study reveals that arrhythmia can be found in nearly 1 of every 2 Ebstein’s patients referred for surgical correction. Detachment of the anterosuperior leaflet and plication of the right ventricular chamber reduce the incidence of postoperative arrhythmias. The technique is not as effective for arrhythmias secondary to atrial enlargement; therefore, we suggest the operation be performed earlier before atrial enlargement occurs.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Anderson K.R., Zuberbuhler J.R., Anderson R., Becker A., Lie J.T. Morphologic spectrum of Ebstein’s anomaly of the heart. Mayo Clin Proc 1979;54:174-180.[Medline]
  2. Schiebler G.L., Gravenstein J.S., Van Mierop L.H. Ebstein’s anomaly of the tricuspid valve. Translation of original description with comments. Am J Cardiol 1968;22:867-873.[Medline]
  3. Oh J.K., Holmes D.R., Hayes D.L., Porter C.B., Danielson G.K. Cardiac arrhythmias in patients with surgical repair of Ebstein’ anomaly. J Am Coll Cardiol 1985;6:1351-1357.[Abstract]
  4. Danielson G.K. Ebstein’s anomaly: editorial comments and personal observations. Ann Thorac Surg 1982;34:396-400.[Abstract]
  5. Danielson G.K., Driscoll D.J., Mair D.D., Warnes C.A., Oliver W.C. Operative treatment of Ebstein’s anomaly. J Thorac Cardiovasc Surg 1992;104:1195-1202.[Abstract]
  6. Hardy K.L., Roge B.B. Ebstein’s anomaly. Further experience with definitive repair. J Thorac Cardiovasc Surg 1969;58:553-561.[Medline]
  7. Quaegebeur J., Sreeram N., Fraser A.G., et al. Surgery for Ebstein’s anomaly: the clinical and echocardiographic evaluation of a new technique. J Am Coll Cardiol 1991;17:722-728.[Abstract]
  8. Lillehei C.W., Kalke B.R., Carlson R.G. Evolution of corrective surgery for Ebstein’s anomaly. Circulation 1967;35,36(Suppl 1):111-118.
  9. Hardy K.L., May I.A., Webster C.A., et al. Ebstein’s anomaly: a functional concept and successful definitive repair. J Thorac Cardiovasc Surg 1964;48:927-932.
  10. Carpentier A., Chauvaud S., Mace L., et al. A new reconstructive operation for Ebstein’s anomaly of the tricuspid valve. J Thorac Cardiovasc Surg 1988;96:92-101.[Abstract]
  11. Chauvaud S., Mihaileanu S., Gaer J., Carpentier A. Surgical treatment of Ebstein’s malformation. The ‘Hôpital Broussais’ experience. Cardiol Young 1996;6:4-11.
  12. Chauvaud S., Fuzellier J.F., Berrebi A., et al. Bi-directional cavopulmonary shunt associated with ventriculo and valvuloplasty in Ebstein’s anomaly: benefits in high risk patients. Eur J Cardio-thorac Surg 1998;13:514-519.[Abstract/Free Full Text]
  13. Anderson K.R., Lie J.T. The right ventricular myocardium in Ebstein’s anomaly. A morphometric histopathologic study. Mayo Clin Proc 1979;54:181-184.[Medline]
  14. Cappato R., Schluter M., Weiss C., et al. Radiofrequency current catheter ablation of accessory atrioventricular pathways in Ebstein’s anomaly. Circulation 1996;94:376-383.[Abstract/Free Full Text]
  15. Reich J.D., Auld D., Hulse E., Sullivan K., Campbell R. The Pediatric Radiofrequency Ablation Registry’s experience with Ebstein’s anomaly. Pediatric Electrophysiology Society. J Cardiovasc Electrophysiol 1998;9:1370-1377.[Medline]
  16. Smith W.M., Gallagher J.J., Kerr C.R., et al. The electrophysiologic basis and management of symptomatic recurrent tachycardia in patients with Ebstein’s anomaly of the tricuspid valve. Am J Cardiol 1982;49:1223-1233.[Medline]
  17. Pressley J.C., Wharton J.M., Tang A.S., Lowe J.E., Gallagher J.J., Prystowsky E.N. Effect of Ebstein’s anomaly on short- and long-term outcome of surgically treated patients with Wolff-Parkinson-White syndrome. Circulation 1992;86:1147-1155.[Abstract/Free Full Text]
  18. Sealy W.C., Gallagher J.J., Pritchett E.L., Wallace A.G. Surgical treatment of tachyarrhythmias in patients with both an Ebstein anomaly and a Kent bundle. J Thorac Cardiovasc Surg 1978;75:847-853.[Abstract]
  19. Kastor J.A., Goldreyer B.N., Josephson M.E., et al. Electrophysiologic characteristics of Ebstein’s anomaly of the tricuspid valve. Circulation 1975;52:987-995.[Abstract/Free Full Text]
  20. Lo H.M., Lin F.Y., Jong Y.S., Tseng Y.Z., Wu T.L. Ebstein’s anomaly with ventricular tachycardia: evidence for the arrhythmogenic role of the atrialized ventricle. Am Heart J 1989;117:959-962.[Medline]
  21. Westaby S., Karp R.B., Kirklin J.W., Waldo A.L., Blackstone E.H. Surgical treatment in Ebstein’s malformation. Ann Thorac Surg 1982;34:388-395.[Abstract]
  22. Misaki T., Watanabe G., Iwa T., et al. Surgical treatment of patients with Wolff-Parkinson-White syndrome and associated Ebstein’s anomaly. J Thorac Cardiovasc Surg 1995;110:1702-1707.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
K. S. Al-Najashi, O. H. Balint, E. Oechslin, W. G. Williams, and C. K. Silversides
Mid-term outcomes in adults with ebstein anomaly and cavopulmonary shunts.
Ann. Thorac. Surg., July 1, 2009; 88(1): 131 - 136.
[Abstract] [Full Text] [PDF]

Home page
 MMCTSHome page
S. Chauvaud and A. Carpentier
Ebstein's anomaly: the Broussais approach
MMCTS, June 26, 2008; 2008(0626): 3038.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
J. M. Chen, R. S. Mosca, K. Altmann, B. F. Printz, K. Targoff, P. A. Mazzeo, and J. M. Quaegebeur
Early and medium-term results for repair of Ebstein anomaly
J. Thorac. Cardiovasc. Surg., April 1, 2004; 127(4): 990 - 999.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Alain F. Carpentier
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chauvaud, S. M.
Right arrow Articles by Carpentier, A. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chauvaud, S. M.
Right arrow Articles by Carpentier, A. F.
Related Collections
Right arrow Congenital - cyanotic

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS