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Eur J Cardiothorac Surg 2005;27:1000-1004
© 2005 Elsevier Science NL

Right ventricular disarticulation. An 18-year single centre experience

Joseph Zachariasb, Jonathan Fortyb, James Colin Doiga, John Pius Bourkea, Colin John Hiltonb,*

a Department of Academic Cardiology, Freeman Hospital, Newcastle upon Tyne NE 7 7DN, UK
b Department of Cardiothoracic Surgery, Freeman Hospital, Newcastle upon Tyne, NE 7 7DN, UK

Received 7 October 2004; received in revised form 21 February 2005; accepted 22 February 2005.

* Corresponding author. Tel.: +44 191 233 6161; fax: +44 191 2231175. (E-mail: c.j.hilton{at}ncl.ac.uk).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Surgical details
 4. Results
 5. Discussion
 6. Conclusion
 References
 
Objective: Right ventricular disarticulation (RVD) is an accepted procedure in the treatment of ventricular tachycardia of right ventricular origin. We set out to review the long-term outcomes with RVD at our institution for patients with arrhythmogenic right ventricular dysplasia (ARVD) or refractory tachycardia. A renewed interest in this operation has come about in patients unable to tolerate implantable cardioverter defibrillators. Methods: Seventeen patients had RVD carried out between 1985 and 2003. There were 15 males and 2 females. The age range was 14–72 (median: 34). Six patients had partial RVD and 11 a complete RVD. ARVD was confirmed in 15 patients at histology. Biventricular pacing was used post-operatively in the two most recent patients. Results: The follow-up was complete in 94% (16/17). The median follow-up was 13 years (0–18). The overall hospital mortality was 6% (1/17). Over the follow-up period there were three deaths 9, 11 and 17 years post-surgery. Heart transplantation due to biventricular failure was required in two patients. In the group followed up for more than 10 years the over all event free survival at 10 years was 77% (3/13). Conclusions: In cases of refractory ventricular tachycardia, where multiple antiarrhythmic medication, repeated catheter ablation and ICD insertion are unsuccessful at symptom control, RVD is an excellent antiarrhythmic procedure. In the long term, signs of biventricular failure present, possibly, dependent on the natural history of ARVD. The long-term effect of biventricular pacing on the disarticulated right ventricle is yet to be defined.

Key Words: Right ventricular disarticulation • Arrhythmogenic right ventricular dysplasia • Follow-up


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Surgical details
 4. Results
 5. Discussion
 6. Conclusion
 References
 
Right ventricular disarticulation (RVD) has been described previously as a curative procedure for patients with multifocal ventricular tachycardia arising diffusely from the right ventricular free wall [1]. A large proportion of these patients have arrhythmogenic right ventricular dysplasia (ARVD) a type of cardiomyopathy affecting predominantly the right ventricle and presenting with sudden death or refractory ventricular tachycardia. The short and medium term results of RVD have been described before by Cox et al. and our group [2,3]. At our institution the first of these procedures was done in 1985. A further 16 patients have undergone either a partial or a complete right ventricular disarticulation since. In performing this review we set out to review the long-term results in this patient group and to define the consequences of this procedure in patients late after surgery.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Surgical details
 4. Results
 5. Discussion
 6. Conclusion
 References
 
A retrospective review was carried out of all patients who underwent right ventricular disarticulation between 1985 and 2003. Seventeen patients were identified and a notes review was carried out on all these patients. The current status of all living patients was determined from the case notes. Most patients were referred from out of the region and these patients were contacted directly on the telephone or the referring cardiologists were asked to send details from the last clinic review. The follow-up was complete in 16 patients. One patient was lost to cardiological follow-up alive and well, from the referring hospital 5 years after surgery and, due to multiple changes in address, could not be traced. The survival from surgery was represented using a Kaplan–Meier survival curve (Fig. 1).



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  		Fig. 1. Actuarial survival figure of patients undergoing right ventricular disarticulation represented by a Kaplan–Meier curve.

 

   3. Surgical details
Top
 Abstract
 1. Introduction
 2. Methods
 3. Surgical details
4. Results
 5. Discussion
 6. Conclusion
 References
 
Most patients had a complete disarticulation carried out as described initially by Guiraudon et al. in 1983 [1]. This involved a general anaesthetic and standard cardiopulmonary bypass using bicaval cannulation and returning blood to the ascending aorta. Once on bypass patients were kept normothermic and had an intraoperative electro-physiological study (EPS) to map the area of origin of the right ventricular tachycardia. Once the focus was mapped to the free wall a decision was made to disarticulate the right ventricular free wall. The disarticulation procedure was carried out after cross-clamping of the aorta and cardioplegic arrest of the heart. The incision was started 4–5mm from the left anterior descending artery on the right ventricular side and the full thickness incision carried out along the course of the LAD down to the apex. The incision was then carried over the apex staying close to the vessels and carried on along the inferior surface of the heart parallel and adjacent to the posterior descending artery until the papillary muscles and chordae to the tricuspid valve limit further extension. The incision at the top of the RV near the LAD was then extended across the right ventricular outflow tract along the inferior aspect of the pulmonary valve to the interventricular septum. The papillary muscles arising from the RV free wall were then divided and the RV free wall is opened like a book. At this stage the only connection left between the RV free wall and the rest of the heart was the area under the tricuspid valve annulus. The two ends of the previous incision were joined together under the tricuspid annulus along the atrio-ventricular junction leaving the RV free wall attached only by epicardial fat and the right coronary artery and its ventricular branches. This dissection can be carried out with a knife to control the depth of the myocardial incision until the epicardial fat is visible. Once this dissection is carried out in the cross-clamp was removed and the heart reperfused. A further EPS was carried out and VT induced in the disarticulated RV free wall to demonstrate complete electrical isolation if no cross over to the rest of the heart was seen. In the early cases cryotherapy was used to ensure complete electrical dissociation along the atrio-ventricular ‘hinge’ area. In a further three cases an area on the septum noted to be a separate focus of VT was frozen with a cryotherapy probe at this stage. Non-absorbable 4-0 sutures were then used to reattach the disarticulated segment back together. Pledgetted sutures were used to reattach the papillary muscle head. Once the ventricular suture line was completed and haemostasis secured the patient was weaned from cardiopulmonary bypass with atrio-biventricular pacing if the RV free wall appeared to have contractility. In some patients with advanced ARVD there was little RV contraction and these patients do not benefit from RV pacing.

Seven patients had a partial disarticulation. This was carried out if EPS appeared to identify a small localised area of RV free wall giving rise to the VT. The incision, in these cases, was limited to the acute margin of the RV and parallel to the PDA or LAD depending on the site of origin of the VT. The premise was that this would maintain RV function better while isolating the VT focus.

Post-operative recovery was dependent on the extent of RV failure. They require high right-sided filling pressures in the immediate post-operative period. As most of the patients with ARVD already have some degree of RV dysfunction pre-operatively and little free wall activity post-surgery most of the RV outflow is dependent on the movement of the septum in systole and diastole and right atrial activity. They behave like a Fontan circulation and are very sensitive to anything that might increase pulmonary resistance such as hypoxia and pleural effusions. All patients had a pre-discharge EPS to confirm electrical isolation of the RV free wall. The right ventricle was not captured with pacing despite high voltages in the early patients and hence permanent biventricular pacing was not attempted in the initial 15 patients. The two most recent patients, however, had residual function in the isolated RV and permanent pacing was used in an attempt at maintaining RV function.


   4. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Surgical details
 4. Results
5. Discussion
 6. Conclusion
 References
 
Between 1985 and 2003, 17 patients underwent a right ventricular disarticulation procedure. The age range was 14–72 with a median of 34 years. There were 15 males and 2 females in this group. All patients presented with more than three episodes of VT with the range being 3–9. Syncope was the presenting feature for 12 patients. Intractable VT was the presenting feature in three patients. A mean of 4 antiarrhythmic drugs (range 3–8) had been tried in all the patients. All patients had been treated with antiarrhythmic drugs, which had failed to control the symptoms. An angiogram was done in 12 patients and 14 patients had an echocardiogram to look at the morphology of the RV and LV. None of the patients had significant coronary artery disease.

The diagnosis of ARVD was made by the ECG findings, the abnormality of the RV and the history of recurrent VT. A CT scan was done in two patients and the diagnosis of ARVD was confirmed. Histology at the time of surgery confirmed the diagnosis in 15. A family history was noted in only three patients. As all these patients were referred from other units there was no record of screening of the rest of the family available.

Seventeen patients underwent surgical disarticulation of the RV. One patient died in the post-operative period with complications related to heart failure (6% mortality). A partial disarticulation was done in seven patients while a complete RV disarticulation was carried out in the 10 remaining patients. Three patients also had additional cryotherapy lesions to the septum following intra-operative EPS mapping which was used in all patients.

The post-operative complications occurred in 11 patients (64%). Reoperation for bleeding in four (23%). A tracheostomy was required in two (11%) patients to facilitate their weaning off the ventilator. Renal failure was seen in three patients, which was transient in two. In one patient with pre-operative liver derangement this deteriorated in the post-operative period. All patients showed signs of transient right heart failure in the immediate post-operative period that improved with time. The mean post-operative hospital stay was 17.6 days with a range 9–32 days. All patients had EPS before discharge and two patients had a pacemaker inserted prior to discharge. This added to the post-operative stay. Eight patients (47%) were discharged with no antiarrhythmic medication. The most common drug at discharge was Digoxin in six patients. Three patients were discharged on diuretics. Warfarin was used for anticoagulation in four patients due to the experience with one patient developing a pulmonary embolism after the surgical procedure.

In the post-operative period four patients (23%) developed a further episode of VT. In the group of patients having a partial disarticulation VT episodes were seen in 3 out of 7 patients (42%). One patient with a complete disarticulation presented post-operatively with VT (12%). This patient was noted to have a focus for the VT at the rim of RV at the apex. This procedure was the first done by one of the surgeons and a large rim of RV was left connected to the septum to facilitate suturing at the end and this area needed catheter ablation post-surgery. Another patient with complete disarticulation developed one episode of non-sustained VT that was not inducible on EP studies and did not recur after. In the follow-up period 10 patients have developed supra-ventricular tachycardia and are presently on beta-blocker therapy.

On comparing the patients having partial disarticulation with complete, there was no difference in length of hospital stay post-surgery with the median post-operative stay being 17 days in the seven patients with partial disarticulation while it was 16.5 days in the eight patients that survived complete disarticulation. There were the same number of events (transplantation or death) in both groups (28%) and at last follow-up one patient in each group was on the active transplant waiting list.

We did not have echocardiography details on all patients but the six patients followed up at our institution showed grossly dilated right ventricles with no contraction in the free wall. The right ventricular dilatation appeared to be progressive, with concomitant dilation of the right atrium. The tricuspid valve is widely patent with no coaptation of the leaflet edges. Interestingly, there is no tricuspid regurgitation as the lack of ventricular contraction prevents any active flow in either direction across the open valve. Blood flow patterns from the right atrium to the pulmonary artery is in the form of whorls with the ventricle acting as a passive conduit.

The median follow-up period for this group was 13 years with a range of 0–18 years. At review three patients had died 9, 11 and 17 years post-surgery. A further two patients had undergone successful heart transplantation at our unit for heart failure 3 and 8 years after surgery. Of the 10 patients alive at last review, five patients were doing well and were in NYHA class II or less. Two patients was in NYHA class III and three patients were in NYHA class IV. Of these three patients two were on active heart transplant waiting lists 3 and 14 years after the disarticulation procedure. On looking at the group of 13 patients who had been followed up for a period of 10 years the overall event free survival (transplantation or death) was 77% (3/13). The overall survival of the whole group has been represented in Fig. 1, using a Kaplan–Meier survival graph.


   5. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Surgical details
 4. Results
 5. Discussion
6. Conclusion
 References
 
In ARVD patients the possibility of sudden death is the most worrying aspect to patients and clinicians treating them. This case series documents among the longest follow-up published for patients with ARVD. The median follow-up is more than 12 years. It is promising to note that there were no cases of sudden death in this group post-surgery. The use of ICD devices has certainly reduced the perceived risk [4]. In a review of ARVD patients with ICD implantation there was still a risk of sudden death [5] probably due to disease involvement around the area of lead placement. A recent large review of ARVD patients with ICD [6] implantation as primary therapy the device appeared to be well tolerated in the majority of patients with few complications over the mean follow-up period of 3.5 years. We would hope that our cohort of patients will provide a standard for long-term outcome against which newer therapies can be judged in the prevention of sudden death in ARVD.

ARVD affects young individuals and most will require long-term treatment with antiarrhythmic drugs. Despite ICD devices most patients get more than one antiarrhythmic drug following device discharges [7]. In our patients post-surgery it was noted that a partial disarticulation was not as good an antiarrhythmic procedure as the complete disarticulation [8]. The haemodynamic deterioration appeared to be similar over time with both procedures. Since that time our practise, has been to offer complete disarticulation. Only one patient required antiarrhythmic drugs after a complete disarticulation. This was felt to be due to a slightly larger rim of right ventricle left connected to the septum to suture the myocardium back onto after the procedure. Catheter ablation of the apex was successful in achieving control of the VT.

Heart failure has been the most disappointing aspect of this procedure. The need for transplantation in two patients and a further two patients being on the active transplant list may demonstrate an inevitable progression to this outcome in post-surgical patients. It was interesting to note that some of these patients though in right heart failure managed to maintain an acceptable quality of life. In cases of impairment of left ventricular function transplantation was clearly the only choice. It is uncertain whether the progression to heart failure was purely related to the surgical disarticulation of the right ventricle or whether progression of the natural disease also played a part. A review of ARVD patients over an average of 8 years showed a 20% mortality due to heart failure [8]. Another review of 50 ARVD patients treated with catheter ablation showed a 24% mortality over a mean follow-up of 5.8 years [9]. There is increasing evidence that this disease is not limited to the right ventricle and some involvement of the left ventricle does occur [10,11]. In our group of patients some tolerate right ventricular failure better and for longer than others. We believe, that the patients who tolerate right ventricular disarticulation well in the long term may be those in whom the left ventricle is unaffected by the disease process. In two of our patients heart transplantation was required relatively early after surgery. These patients may have had disease progression to involve the left side. Unfortunately, as this is a retrospective study we did not have the required details to look into these hypotheses in more detail. The two patients who underwent heart transplantation had a good outcome and are alive and well and the previous procedure did not appear to influence outcome in the pre- or post-transplant period. Two patients have been listed on the transplant list for deteriorating left ventricular function. Ventricular arrhythmias have not been a contributing factor in either case.

The impact of ICD electrical storms on the quality of life of patients has not been well documented in the literature. In young patients this event can be very disabling and some patients require anti-psychotic drugs to control their anxiety particularly if electrical storms have followed exertion. Two of the patients referred to us most recently were completely psychologically disabled due to previous exercise related episodes. During electrophysiological studies (EPS) a diffuse origin of the arrhythmia from the right ventricular free wall was noted. This was induced despite drug therapy and was not amenable to catheter RFA. Both these patients got a good result from surgical disarticulation. We believe this may be an indication for surgical treatment of these arrhythmias, although the unpredictability of such storms and the possibility of prolonged remissions [7] between events might make this conclusion controversial. Cognitive behavioural therapy may be useful in helping these unfortunate patients cope with the fear of another episode. In our two patients both these suggestions were met with non-compliance and surgery was undertaken with the long-term possibility of heart transplantation fully discussed with the patients. They both were very keen to prevent the possibility of any further internal cardioversions and following surgery this has been achieved satisfactorily.

Biventricular pacing has been suggested by Damiano et al. [12] as a means of maintaining right ventricular transport despite disarticulation. It initially was noted to improve cardiac output by Jones et al. in 1984 [13]. Early attempts by our group at attempting biventricular pacing were unsuccessful due to an inability to capture the RV free wall despite high pacing voltages. We presumed that this was related partly to the already abnormal myocardium in the RV in most of those patients and possibly in part due to ischaemia induced in the free wall during surgery. We have been successful in biventricular pacing in our two most recent patients but as the follow-up period was inside a year we will need to wait to see if pacing slows the progression to right heart failure after disarticulation. A case report of established right heart failure after surgical disarticulation improving with biventricular pacing holds promise [14]. Over time the disarticulated segment may undergo fibrous changes, which will reduce the potential benefits of pacing. We hope to compare the progress of this small subgroup of patients against our larger group to see if there is any long-term advantage.

We choose to routinely anticoagulate all our patients post-disarticulation due to the risk of thrombus formation within a non-contractile right ventricle. Due to the extensive nature of the dissection and the raw area left behind after cryotherapy we anticoagulate patients for the first few months. We use Warfarin for anticoagulation. It may not be necessary in the longer term if biventricular pacing is found to maintain some ventricular contractility.

Supra-ventricular tachyarrhythmias are a common finding in patients some years after disarticulation surgery. We believe this is related to the progressive dilatation of the right atrium over time. It appears to be well controlled with beta-blocker therapy in most patients. There is a suggestion that ARVD may predispose patients to atrial arrhythmias and that this may be part of the natural history of the disease process [15]. Again both natural history and surgery probably contribute to this regular finding in our patient group.

This study suffers from being a small retrospective case series. Most of the patients were referred to us from other units in recurrent VT with failure of medical management. Their follow-up was then carried out mainly at the referring unit and we were only made aware of the regular yearly follow-up clinic episodes. We did not have a registry of all ARVD patients referred to our institution over this time period. We are aware of a group of patients that have been treated by RFA and AICD insertion during this period. We hope to look at this group, in the future, to compare long-term outcomes with our surgical patients.


   6. Conclusion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Surgical details
 4. Results
 5. Discussion
 6. Conclusion
References
 
We present these findings so that as the large registry of ARVD patients set up by Corrado et al. [16] accumulate details of the progression of this disease and the long-term survival achieved in this group of patients with or without AICD implantation, we will have more of an idea, of the true role of surgery in ARVD. The success of the procedure as an anti-arrhythmic one was offset by the gradual haemodynamic deterioration noted in nearly all patients. We also hope to compare the more recent subset of patients with biventricular pacing and watch their RV function over the coming years to look for a positive impact in maintaining contractility with time.

ARVD patients pose a difficult challenge to physicians who undertake their management, we hope this study adds to the literature available and with time will help establish the precise role of this procedure as an alternative strategy available in selected patients who may be unable to tolerate long-term antiarrhythmic therapy and an AICD.


   Acknowledgments
 
We would like to thank Ms Therese Small for help with creation of the Kaplan–Meier survival figure and Mr Barry Cumberledge for help with echocardiography review.


   Footnotes
 
{star} Presented at the joint 18th Annual Meeting of the European Association for Cardiothoracic Surgery and the 12th Annual Meeting of the European Society of Thoracic Surgeons, Leipzig, Germany, September 12–15, 2004.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Surgical details
 4. Results
 5. Discussion
 6. Conclusion
 References
 

  1. Guiraudon GM, Klein GJ, Gulamhusein SS, Painvin GA, Del Campo C, Gonzales JC, Ko PT. Total disconnection of the right ventricular free wall: surgical treatment of right ventricular tachycardia associated with right ventricular dysplasia. Circulation 1983;67(2):463-470.[Abstract/Free Full Text]
  2. Cox JL, Bardy GH, Damiano Jr RJ, German LD, Fedor JM, Kisslo JA, Packer DL, Gallagher JJ. Right ventricular isolation procedures for nonischemic ventricular tachycardia. J Thorac Cardiovasc Surg 1985;90(2):212-224.[Abstract]
  3. Nimkhedkar K, Hilton CJ, Furniss SS, Bourke JP, Glenville B, McComb JM, Campbell RW. Surgery for ventricular tachycardia associated with right ventricular dysplasia: disarticulation of right ventricle in 9 of 10 cases. J Am Coll Cardiol 1992;19(5):1079-1084.[Abstract]
  4. Marcus FI, Fontaine GH, Frank R, Gallagher JJ, Reiter MJ. Long-term follow-up in patients with arrhythmogenic right ventricular disease. Eur Heart J 1989;10:68-73.
  5. Link MS, Wang PJ, Haugh CJ, Homoud MK, Foote CB, Costeas XB, Estes 3rd NA. Arrhythmogenic right ventricular dysplasia: clinical results with implantable cardioverter defibrillators. J Interv Card Electrophysiol 1997;1(1):41-48.[CrossRef][Medline]
  6. Roguin A, Bomma CS, Nasir K, Tandri H, Tichnell C, James C, Rutberg J, Crosson J, Spevak PJ, Berger RD, Halperin HR, Calkins H. Implantable cardioverter-defibrillators in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy. J Am Coll Cardiol 2004;43(10):1843-1852.[Abstract/Free Full Text]
  7. Blomstrom-Lundqvist C, Sabel KG, Olsson SB. A long term follow up of 15 patients with arrhythmogenic right ventricular dysplasia. Br Heart J 1987;58(5):477-488.[Abstract/Free Full Text]
  8. Doig JC, Nichol IE, McComb JM, Furniss SS, Hilton CJ, Bourke JP, Campbell RW. Right ventricular disarticulation procedures: the role of late potentials in the genesis of postoperative ventricular arrhythmias. Pacing Clin Electrophysiol 1997;20(4 Pt 1):923-929.[CrossRef][Medline]
  9. Fontaine G, Tonet J, Gallais Y, Lascault G, Hidden-Lucet F, Aouate P, Halimi F, Poulain F, Johnson N, Charfeddine H, Frank R. Ventricular tachycardia catheter ablation in arrhythmogenic right ventricular dysplasia: a 16-year experience. Curr Cardiol Rep 2000;2(6):498-506.[Medline]
  10. Atalay S, Imamoglu A, Gumus H, Gurdal M, Ozenci M. Value of the echocardiographic findings of arrhythmogenic right ventricular dysplasia with left ventricular involvement in a child. Pediatr Cardiol 1996;17(1):40-42.[Medline]
  11. Peters S, Peters H, Thierfelder L. Heart failure in arrhythmogenic right ventricular dysplasia-cardiomyopathy. Int J Cardiol 1999;71(3):251-256.[CrossRef][Medline]
  12. Damiano Jr RJ, Asano T, Smith PK, Ferguson TB, Cox JL. Hemodynamic consequences of right ventricular isolation: the contribution of the right ventricular free wall to cardiac performance. Ann Thorac Surg 1988;46(3):324-330.[Abstract]
  13. Jones DL, Guiraudon GM, Klein GJ. Total disconnection of the right ventricular free wall: physiological consequences in the dog. Am Heart J 1984;107(6):1169-1177.[CrossRef][Medline]
  14. Tang C, Klein GJ, Guiraudon GM, Yeung-Lai-Wah JA, Qi A, Kerr CR. Pacing in right ventricular dysplasia after disconnection surgery. J Cardiovasc Electrophysiol 2000;11(2):199-202.[Medline]
  15. Brembilla-Perrot B, Jacquemin L, Houplon P, Houriez P, Beurrier D, Berder V, Terrier de la Chaise A, Louis P. Increased atrial vulnerability in arrhythmogenic right ventricular disease. Am Heart J 1998;135(5 Pt 1):748-754.[CrossRef][Medline]
  16. Corrado D, Fontaine G, Marcus FI, McKenna WJ, Nava A, Thiene G, Wichter T. Arrhythmogenic right ventricular dysplasia/cardiomyopathy: need for an international registry. Study Group on Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy of the Working Groups on Myocardial and Pericardial Disease and Arrhythmias of the European Society of Cardiology and of the Scientific Council on Cardiomyopathies of the World Heart Federation. Circulation 2000;101(11):E101-E106.



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