| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Eur J Cardiothorac Surg 2001;19:448-454
© 2001 Elsevier Science NL
a Department of Cardio-thoracic Surgery, Heart Lung Institute, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht, The Netherlands
b Department of Cardiology, Heart Lung Institute, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht, The Netherlands
c Department of Experimental Cardiology, University Medical Center, Amsterdam, The Netherlands
Received 10 November 2000; received in revised form 12 February 2001; accepted 14 February 2001.
Corresponding author. Tel.: +31-30-250-6179; fax: +31-30-254-2155
e-mail: p.f.a.bakker{at}hli.azu.nl
 |
Abstract |
|---|
 Top Abstract 1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
Key Words: Ventricular tachyarrhythmias • Surgery • Left ventricular aneurysm
|
1. Introduction |
|---|
|
TopAbstract1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
The lack of (reliable) intraoperative evaluation of treatment efficacy probably plays a role in persistent postoperative inducibility of ventricular tachyarrhythmias, and in spontaneous arrhythmia recurrences as well as sudden death [1]. From this perspective, endocardial resection on the beating heart, using a sequential technique of mapping and resection, may present a major advantage [6]. A limitation to this technique is the inability to ablate arrhythmogenic substrates which are located deep intramurally or subepicardially. In addition, endocardial resection has a limited applicability to the papillary muscles. These limitations can be overcome by the application of cryolesions.
A potential drawback may be that repetitive mapping-ablation cycles are time-consuming and prolonge cardiopulmonary bypass and aortic cross-clamp times. This may increase early and late morbidity and mortality. Also, there is an ongoing debate on the usefulness of intraoperative mapping to guide surgical ablation [7].
The objective of this study was to examine our results of sequential map-guided endocardial resection at normothermia in patients with ventricular tachyarrhythmias late after myocardial infarction to assess the efficacy of this technique as well as the early and long-term outcome.
|
2. Methods |
|---|
|
TopAbstract1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
2.2. Preoperative evaluation
All patients underwent selective coronary angiography, biplane ventriculography, as well as a two-dimensional and Doppler echocardiographic study by standard techniques. Multiple gated acquisition radionuclide angiography with technetium-99 m-labeled red blood cells was performed at rest to measure left ventricular ejection fraction (LVEF). A baseline electrophysiologic study was performed in the fasting non-sedated state, after antiarrhythmic drugs had been discontinued for at least five drug half-lives, whenever possible. Three quadripolar, 6F electrode catheters were inserted percutaneously into the femoral vein and positioned in the high right atrium, across the tricuspid valve close to the His bundle, and the right ventricular apex. The latter catheter was later repositioned for stimulation at the right ventricular outflow tract. The stimulation protocol included delivery of single, double and triple premature ventricular extrastimuli from both right ventricular sites after an eight-beat drive at three paced basic cycle lengths and burst pacing. The stimulation protocol was repeated under isoproterenol (maximal dose 4 mcg/min) if no monomorphic VT could be induced. Endocardial catheter mapping and or body surface mapping were used to localize the arrhythmogenic substrate, whenever possible. Exercise testing was performed for assessment of ischemia and induction of arrhythmias.
2.3. Surgical techniques
A median sternotomy approach was used and a pericardial patch was harvested for endocavitary patch plasty of the left ventricle. The heart was cannulated for cardiopulmonary bypass and epicardial electrodes were attached to the right atrium and to one or both ventricles as timing references and for programmed electrical stimulation. In patients with inferior myocardial infarction, epicardial activation sequence mapping during ventricular tachycardia was performed with a multi-electrode array where possible off-pump. Endocardial mapping under normothermic cardiopulmonary bypass was accomplished in all patients using a multi-electrode balloon introduced through an incision in the aneurysm or myocardial infarct scar. A computerized mapping system was employed for analysis of the mapping data. Essential parts of the re-entry circuit were localized to areas of diastolic potentials and sites of earliest activation (exit sites) during ventricular tachycardia. In some instances, the entire circuit could be localized. Extensive endocardial resection was performed removing all the endocardially visible scarred endocardial and subendocardial layer, sparing the papillary muscles. Normothermia was maintained for repetitive intraoperative electrophysiologic testing and mapping (sequential technique) aiming to map and eradicate all inducible VT morphologies also if they had not been observed clinically. Ventricular tachycardias with deep intramural or subepicardial substrates were ablated by cryosurgery following aortic cross-clamping and cold blood induced cardioplegic arrest. Thereafter, electrophysiologic testing was not repeated. Cryolesions were applied with a 15-mm probe (Frigitronics Inc., Shelton, CT) cooled to -70°C for 2–3 min depending on wall thickness and proximity of left bundle branches and coronary arteries. Concomitant cardiac surgical procedures were performed after treatment of ventricular tachycardias had been accomplished. These procedures were performed under continuous retrograde blood cardioplegia at 34°C. Proximal coronary artery anastomoses were completed during single aortic cross-clamping. Left ventricular geometry was reconstructed applying the technique described by Dor and colleagues [5], with the modification that a two-layered patch consisting of an internal layer of autologous pericardial tissue and an outer layer of Vascutek patch was used. The ventriculotomy was closed over two strips of autologous pericardium or by direct suture. The temporary epicardial electrodes were left in situ for postoperative electrophysiologic testing. All patients received warfarin derivatives after operation.
2.4. Postoperative evaluation
During the postoperative period, patients were continuously monitored by telemetry. Postoperative electrophysiologic and exercise testing were generally done 10 to 14 days after operation. In case sustained monomorphic or polymorphic VT, or 
10 complexes monomorphic or polymorphic VT were inducible, patients were treated with sotalol orally, and the electrophysiologic study was repeated. An implantable defibrillator was inserted in patients in whom inducibility of VT persisted or who did not tolerate drug treatment. Polymorphic VT or ventricular fibrillation induced by three premature ventricular extrastimuli in patients in whom the presenting arrhythmia was monomorphic VT, was considered a non-specific response and consequently did not require further treatment.
Patients were followed-up at our out-patient clinic at 1, 3, 6, and 12 months after discharge from the hospital. Additional follow-up data were obtained from their referring physicians.
2.5. Definitions
Sustained ventricular tachycardia. Ventricular tachycardia lasting more than 30 s or requiring intervention because of hemodynamic deterioration.
Distinct ventricular tachycardia morphologies. Ventricular tachycardia morphologies were considered different if there was a distinctive bundle branch configuration or if the frontal plane QRS-axis differed 90° with the same bundle branch configuration.
Sudden death. Death occurring within 1 h of onset of symptoms in an otherwise clinically stable patient.
Significant coronary artery stenosis. A significant coronary artery stenosis was defined as 50% visual cross-sectional narrowing in any angiographic view.
Left ventricular aneurysm. A left ventricular aneurysm was defined by an infarcted area of the left ventricle with loss of trabeculations producing a diastolic deformity with dyskinetic movement during systole.
Operative mortality. Death before discharge from the hospital or within 30 days after surgery.
2.6. Statistical analysis
Continuous variables are presented as mean values±SD. Kaplan–Meyer life-table analysis was used to obtain cumulative survival probability±standard error.
To assess the additive value of intraoperative mapping, the inducibility of sustained monomorphic VT after the initial mapping-resection sequence was taken as a substitute of postoperative inducibility after non-map-guided extensive endocardial resection to calculate expected failure rate without sequential mapping and resection. Comparisons of failure to eradicate VT substrates at four different anatomic locations were made with the Fisher exact test. A P value <0.05 was considered statistically significant.
|
3. Results |
|---|
|
TopAbstract1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
|
|
|
Six patients required additional cryoablation under hypothermic cardioplegic arrest because of deep myocardial or subepicardial substrates to preserve structural tissue integrity. In one patient, the posteromedial papillary muscle was resected and the mitral valve replaced due to extensive scarring, the papillary muscle being situated in the center of a large aneurysm involving the posteroinferior wall, and being part of the VT substrate.
Additional coronary bypass grafting was performed in 15 patients. The number of distal anastomosis was 2.8±1.4. Restoration of LV geometry with an endocavitary patch was performed in 21 patients. Cardiopulmonary bypass time was 212±96 min and aortic cross-clamp time 96±57 min. One patient required intra-aortic balloon counterpulsation for weaning from extracorporeal circulation.
3.3. Operative mortality and complications
There was one operative death (4.5%). This patient died from pneumonia and sepsis 28 days after operation, and telemetry did not show recurrent VT. One patient underwent percutaneous pericardial drainage because of tamponade. Atrial fibrillation occurred in ten patients and was associated with a transient ischemic attack in one of them.
At postoperative electrophysiologic testing, sustained polymorphic VT was induced with three extrastimuli in one patient who had presented with out-of-hospital cardiac arrest. Sotalol was not tolerated and a defibrillator was implanted. In five patients non-sustained monomorphic VT of 10 or more complexes was induced. These patients were treated with sotalol and subsequently VT became non-inducible.
3.4. Long-term results
During a median follow-up of 26 months (range 1 to 62) there were neither VT recurrences nor cardiac mortality including sudden death. Follow-up data were complete in all patients. At 1 and 2 years, freedom from sudden cardiac death, cardiac mortality, and all-cause mortality were 100, 100, and 91%, respectively. Percentages at 5 years were 100, 100 and 83%. Two patients died from non-cardiac causes at 2 and 25 months respectively. One of these patients was admitted from home to another hospital with acute symptoms of cholecystitis and peritonitis, 2 months postoperatively. He was operated 4 days later and died in hospital. Post-mortem examination was not performed. The second patient died from hepatorenal syndrome due to liver metastases, diagnosed 25 months after operation for ventricular tachycardia. Post-mortem examination revealed an undifferentiated small cell carcinoma which had diffusely metastasized. Cumulative survival probability over a 5-year follow-up period is shown in Fig. 1
. One patient had recurrent angina pectoris, 11 months postoperatively. Coronary angiography revealed a newly developed significant coronary artery stenosis in the left anterior descending coronary artery and patency of the coronary artery bypass grafts. Percutaneous transluminal angioplasty was successfully completed and relieved angina symptoms. There were no recurrent myocardial infarctions.
|
|
4. Discussion |
|---|
|
TopAbstract1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
4.1. Pre- and intraoperative factors affecting early and late mortality
The most important risk factor for operative death and late mortality is myocardial dysfunction [8–10].
Low operative mortality and absence of cardiac mortality from congestive heart failure in the present study is probably mainly due to patient selection based on the presence of 4 normokinetic left ventricular wall segments. It is acknowledged that global left ventricular ejection fraction is not a reliable parameter for the assessment of left ventricular function in the presence of a large left ventricular aneurysm [8]. Left ventricular wall motion score derived from a total of nine segments on the left ventricular angiogram in both the right and left oblique projections or derived from regional wall motion analysis by a centerline chord motion method has been shown to be a significant independent predictor of operative and long-term survival and mortality from congestive heart failure after map-guided subendocardial resection [8,10].
Other contributing factors to early and late survival are summarized underneath. Coronary artery bypass grafting and reversed left ventricular remodeling by geometric reconstruction of the left ventricle improve long-term outcome in patients with ischemic heart disease and significant left ventricular dysfunction [3–5]. The administration of continuous retrograde blood cardioplegia is particularly useful to improve myocardial preservation in patients with extensive coronary artery disease in whom antegrade delivery frequently results in inadequate distribution of cardioplegia [11].
Neither the present study nor previous studies provide evidence that performing extensive intraoperative mapping in these patients increases their operative risk [1,12].
4.2. Pre- and intraoperative factors affecting arrhythmia cure
The inducibility of multiple VT morphologies has found to be a preoperative predictor of surgical failure to ablate arrhythmogenic substrates in other studies [1,13,14].
Despite the fact that different VT morphologies in our study outnumber those in previous series, only one patient had postoperative inducible sustained VT, and spontaneous VT recurrences and sudden death were absent.
In the present study, location of the arrhythmogenic substrate was not associated with failure to eradicate VT with a single extensive endocardial resection. The large numerical differences which suggested that particularly substrates in the interventricular septum were difficult to ablate, did not reach statistical significance. This is possibly related to sample size. Several authors have shown that VT substrates in the inferior left ventricular wall and the interventricular septum negatively affect arrhythmia cure [1,15].
The application of sequential map-guided extensive endocardial resection allowing intraoperative verification of treatment efficacy, and the ability to induce monomorphic VT after ventriculotomy in all our patients are probably the main factors contributing to arrhythmia cure.
Firstly, in about half of the patients, sustained monomorphic VT was still inducible after the initial mapping-resection cycle. Arrhythmogenic substrates appeared to have a more deep intramural location or to be localized outside the visible scar. These observations are in accordance with those described by Kaltenbrunner et al. [16]. It is likely that these VTs would also have been induced at postoperative electrophysiologic testing and would have accounted for a failure rate to ablate VT of 45%. Van Hemel and colleagues [17], recently reported their results with map-guided extensive endocardial resection, not using the sequential technique. In 30 patients, an inducibility rate of sustained VT of 13%, a spontaneous VT recurrence rate of 17%, and a sudden death rate of 13% was found during a mean follow-up of 17.9 months. The same results were obtained by Lee and associates [18], applying map-guided regional endocardial resection and supplemental cryoablation. These data support the validity of sequential map-guided extensive endocardial resection at normothermia.
Secondly, non-inducibility of monomorphic VT after ventriculotomy was not encountered in the present study, allowing localization of arrhythmogenic substrates. Other series [1], reported non-inducibility rates up to 45%, which can explain higher postoperative VT inducibility rates, spontaneous VT recurrences and sudden death.
In most series, postoperative induction of sustained monomorphic VT is considered an indication for adjunctive therapy, being antiarrhythmic drugs or defibrillator implantation. By contrast, we also considered the induction of 10 complexes non-sustained VT an indication for medical therapy. This may have contributed to the absence of VT recurrence and sudden death.
It has been suggested that map-guided procedures do not have an outcome advantage over non-map-guided procedures, as measured by operative and long-term mortality [7,19]. However, valid comparison of the results of VT surgery is hampered by differing patient characteristics, stimulation protocols for electrophysiologic studies, intraoperative mapping systems, surgical techniques and conditions, indications for postoperative antiarrhythmic drug treatment, and length of follow-up. Sample sizes are frequently too small to distinguish statistically significant differences.
Whether mapping and repetitive intraoperative electrophysiologic testing add to effectively treating the arrhythmia is probably dependent on the employed surgical technique. As demonstrated in the present study, extended endocardial resection without mapping and without using the sequential technique can be only be performed without failure to ablate VT substrates as long as the arrhythmogenic substrate is located in the resected superficial endocardial and subendocardial layers. The contribution of mapping to successful ablation of VT by encircling endocardial cryoablation can be expected to be much less, since transmural cryolesions exclude the entire infarct scar from endocardium to epicardium or transseptally. The two pitfalls for failure of this technique are arrhythmogenic substrates located outside the endocardially visible scar and the failure to create a transmural or transseptal lesion [15]. Repetitive cycles of mapping-ablation and programmed electrical stimulation are more cumbersome and probably also less helpful. Cryolesions are preferably applied during cold cardioplegic arrest to enhance lesion size and create a transmural lesion. A sequential technique would require repetitive induction of cold cardioplegic arrest and rewarming. Moreover, myocardial cooling by cryoablation or cold cardioplegia, has been reported to result in false negative intraoperative electrophysiologic test results [1]. From the above it is suggested that location of the arrhythmogenic substrate in combination with the surgical technique of ablation or isolation and the use of map-guidance and repetitive electrophysiologic testing determine arrhythmia cure.
Extensive endocardial resection, only sparsely removing healthy myocardium, is less likely to result in left ventricular pump failure than encircling endocardial cryoablation, particularly in patients with >1 and/or extensive myocardial infarction. The potential negative effect on left ventricular function can be expected to negatively affect survival. In one series [7] employing the latter technique, seven out of 33 patients needed postoperative intra-aortic balloon counter pulsation. Four patients died from congestive heart failure, and two underwent cardiac transplantation over 6-year follow-up. In another series of 38 patients [19], freedom from sudden death was 91% at 5 years, and overall actuarial survival 63%. The majority of patients (n=10) died from congestive heart failure and two patients underwent cardiac transplantation.
A limitation to the present study is that it does not have a prospective randomized design to compare efficacy of treating the arrhythmia by extensive endocardial resection with and without the sequential map-guided approach. In addition, the sample size presents a limitation to perform statistical analysis and detect statistically significant differences.
The early and long-term outcome of this study suggest a continuing role for sequential map-guided extensive endocardial resection at normothermia as a curative treatment of ventricular tachyarrhythmias in selected patients with ventricular tachyarrhythmias late after myocardial infarction.
|
Footnotes |
|---|
|
Appendix A. Conference discussion |
|---|
|
TopAbstract1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
I think there are two large series in the literature from Frapier and also from Guiraudon of more than 50 patients where he is demonstrating that the peroperative mapping has no influence at all in the therapeutic strategy.
Dr Bakker: Our previous series included map-guided extensive endocardial resection, as well as visually guided, during cardioplegic arrest. Of the 43 patients 14 patients were inducible, 12 with monomorphic sustained VT and two with sustained polymorphic VT. For that reason we changed our policy to sequential map-guided extensive endocardial resection in normothermic perfused hearts.
The St. Antonius Hospital in Nieuwegein, also reported their results in 1996 using map-guided extensive endocardial resection under cardioplegic arrest, also with a postoperative freedom from arrhythmia recurrence of 53%, which is comparable to our previous experience.
Dr A. Revishvili (Moscow, Russia): Do you have a fourth type of VT morphology during epistudy in the operating room? How many morphologies of VT do you induce during endocardial study, same type morphology you had before?
Dr Bakker: Both the same morphologies as well as new types.
Dr Revishvili: Same four types?
Dr Bakker: Yes.
Dr Revishvili: Because you are pacing the left side during open heart surgery and you are pacing the right side during open heart surgery?
Dr Bakker: No. We do stimulation from the right ventricular apex and right ventricular outflow tract at operation.
Dr Revishvili: I just would like to be the same opinion with the previous speaker. We are doing extensive resection and probably we have the same results.
Mr T. Treasure (London, UK): I think that is an interesting dilemma. There is one way in which that can occur and that is the experience gained through mapping. Then you can refine your technique and no longer need to map. Could that be the reason you are now getting good results and that you didn't?
Dr Bakker: We performed endocardial resection, particularly on the septum, relatively deep. In several patients diastolic potentials were recorded after the first endocardial resection sequence. This implies that the arrhythmogenic substrates were deeper in the septum, and in these patients cryoablation was performed in addition to resection. In my opinion successful treatment could never have been achieved using endocardial resection alone because of the risk of septal perforation.
Mr S. Large (Cambridge, UK): I think that the one thing you haven't put into your conclusions is that this surgery is still available. It is an operation that of course was described a long time ago, but our cardiological friends would tell us with thrombolysis that we don't need to do this anymore, along with aneurysmectomy. We surgeons who are interested in this area seem to stumble across it still! So it should be there. It is of course curative, unlike ICD placement.
Your description is focused just on mortality. The morbidity of subendocardial resections is a bit of a problem, and the big failing of subendocardial resection is the subsequent development of heart failure. How many of your patients are struggling with heart failure?
Dr Bakker: We used to have problems with heart failure, but following a change in technique, instead of aneurysm resection performing endoventricular patch repair, as well as myocardial protection with continuous retrograde blood cardioplegia, we have not had problems in this area. In our previous series one patient went onto heart transplantation. In this series we did not encounter that problem of congestive heart failure, which is illustrated by the absence of cardiac mortality during follow-up.
Mr Large: The subendocardial resection is smaller?
Dr Bakker: No, I would say they are even more extensive.
Dr J. Melo (Carnaxide, Portugal): You are bringing to our attention new tools that will allow us to really enlarge some of our therapeutic methods. With map-guided resection we can be more precise to make less damage to the myocardium, and I think that in the percutaneous field it has been shown this is feasible, mostly in patients with a concomitant ventricular aneurysm. In your series there was one patient without an aneurysm.
Dr Bakker: That's right.
Dr Melo: Does it mean that you are enlarging your indications beyond patients who have aneurysms, and, in your endocardial resections, do you have the need to go also epicardially to get deeper lesions since you are not transmural?
Dr Bakker: Yes, indeed, particularly in inferior myocardial infarcts. In two patients we needed cryoablation for that very reason.
Dr Melo: And the first question is the patient without an aneurysm.
Dr Bakker: Yes. Well, I think it is also a matter of definition. Some call an aneurysm a dyskinetic area on the left ventricular angiogram, whereas others add not only a diastolic bulge but also the absence of trabeculation. In these patients there is not a transmural scar as evidenced at surgery where ventriculotomy reveals 7 to 8 mm of myocardium.
Dr L. Bockeria (Moscow, Russia): I would like to make a very short comment and not a question, because I agree totally with the chairman that in case we have the possibility to make precise cooling, we should do that, and maybe this is one of the reasons that this type of surgery disappeared in general, talking generally. If you go back 10, 15 years ago, you know many hospitals were doing this very impressive surgery, and now we have this very clear trend to give this type of treatment to the cardiologists, and I think that in the case when the hospital has the possibility to do this type of investigation intraoperatively, it should be done, definitely.
Dr Bakker: Yes, I agree, surgery significantly improves the results when compared to other treatment modalities.
|
References |
|---|
|
TopAbstract1. Introduction2. Methods3. Results4. DiscussionAppendix A. Conference...References |
|---|
This article has been cited by other articles:
|
|
 |
|
  M. Mukaddirov, R. G. Demaria, L. P. Perrault, J.-M. Frapier, and B. Albat Reconstructive surgery of postinfarction left ventricular aneurysms: techniques and unsolved problems. Eur. J. Cardiothorac. Surg., August 1, 2008; 34(2): 256 - 261. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Mukaddirov, J.-M. Frapier, R. G. Demaria, and B. Albat Surgical treatment of postinfarction anterior left ventricular aneurysms: linear vs. patch plasty repair Interactive CardioVascular and Thoracic Surgery, April 1, 2008; 7(2): 256 - 261. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Pirk, J. Bytesnik, J. Kautzner, P. Peichl, V. Vancura, K. Lefflerova, I. Skalsky, and V. Vinduska Surgical ablation of post-infarction ventricular tachycardia guided by mapping in sinus rhythm: long term results Eur. J. Cardiothorac. Surg., August 1, 2004; 26(2): 323 - 329. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. L. Mickleborough Surgical Treatment of Ventricular Arrhythmias Card. Surg. Adult, January 1, 2003; 2(2003): 1287 - 1292. [Full Text]
|
|
|
|
|
|
F. Wellens, P. Geelen, E. Demirsoy, F. Van Praet, R. De Geest, I. Degrieck, H. Vanermen, and P. Brugada Surgical treatment of tachyarrhythmias due to postinfarction left ventricular aneurysm with endoaneurysmorrhaphy and cryoablation Eur. J. Cardiothorac. Surg., November 1, 2002; 22(5): 771 - 776. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |
