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Surgical treatment of Wolff-Parkinson-White syndrome
Surgical treatment of Wolff-Parkinson-White syndrome Wolff-Parkinson-White (WPW) syndrome can be associated with disabling and life-threatening dysrhythmias that are resistant to medical treatment yet are amenable to surgical treatment. This report relates our experience with 10 Type A and 10 Type B patients who have been treated by surgery. The operation has evolved from one procedure, applicable to only a few patients, to a new procedure which allows the chance for cure for nearly all patients. By the old method, the Kent bundle was sectioned from the ventricular side; now it is divided from the atrial side, an approach which allows access to the septal tracts. There have been twelve cures, four partially successful operations, and four failures. In one failure, correction of a Type B lesion in the septal area was attempted via the old operation. In a second failure, WPW was associated with Ebstein's anomaly. In the other two failures, the Kent bundle entered the left side of the ventricular septum from the atrial septum at a point adjacent to the atrioventricular (A V) node and His bundle. This group, atrial septal Type A, may require His bundle division as well as Kent bundle division. All other patients with WPW can be cured by properly planned and performed operations.
Will C. Sealy, M.D., and Andrew G. Wallace, M.D. (by invitation), Durham, N. C.
h e Wolff-Parkinson-White (WPW) syndrome ' may be associated with both lifethreatening and disabling disturbances in cardiac rhythm that are refractory to medical management. Pre-excitation or early depolarization of the ventricles, the characteristic of this abnormality on the electrocardiogram, lacked a plausible explanation until Holzmann and Scherf" and later Wolferth and Wood" suggested that it was caused by the bundle of Kent, which is an anomalous connection between the atrium and the ventricle. Later, Wood and co-workers! described the case of a boy with WPW syndrome who died suddenly. At autopsy, they found an anomalous connection from the right lateral atrium to the ventricle simiFrom the Divisions of Thoracic Surgery and Cardiovascular Medicine, Duke University School of Medicine, Durham, N. C. 27710. Supported by U. S. Public Health Service Grants HL13920-03 and HL1519D-01. Read at the Fifty-fourth Annual Meeting of The American Association for Thoracic Surgery, Las Vegas, Nevada, April 22, 23, and 24, 1974.
lar to that described by Kent. 5-8 This theory, however, has until just recently remained open to question, chiefly because there is still an inadequate amount of anatomic material" available to corroborate the physiological evidence accumulated by many observers. 1 0 - 1 6 By identifying the anomalous tract at surgery with electrophysiological methods and then dividing it, we": 18 have furnished unequivocal proof that this tract is the cause of the WPW syndrome. This disorder, which is both disabling and life threatening, has assumed surgical importance now that the cause is known and a definitive operation for its correction has been devised. In this report we will relate our experience with 20 patients, selected from 45 with the WPW syndrome, who had surgical correction of their anomaly. A description will be given of how the operative procedure has evolved from our" initial approach in the first successful correction of this disorder to the present technique, which offers an excellent chance for complete cor-
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Delta Wave
\
t Short PR Normal PJ Fig. 1. An electrocardiogram of a patient with Wolff-Parkinson-White syndrome shows the typical alterations of the QRS by pre-excitation causing a delta wave, a short PR interval, but a normal PI time.
Table I. Experience with Wolff-Parkinson-White syndrome No. of patients
Total No. Type A Type B Medical treatment Deaths Pacemaker Surgical treatment Type A Type B Deaths
45 33 12
20
5 20 10 10 1
rection in nearly all patients with the WPW syndrome. Clinical experience
In this discussion, Type A WPW syndrome will be used to denote a Kent bundle that crosses the annulus fibrosus at the mitral ring or that enters the left side of the ventricular septum from the atrial septum. The latter we will designate as atrial septal Type A. Type B will denote any bundle traversing the right annulus fibrosus. The electrocardiogram in pre-excitation, though it may vary considerably depending upon the location of the bundle of Kent, does provide evidence for the classification of patients with the WPW syndrome into Type A and Type B
as noted by Rosenbaum," and Boineau," and their colleagues. As the term pre-excitation implies, the characteristic of the electrocardiogram is the early activation of some or all of the ventricular muscle by pathways other than the normal atrioventricular (AV) node-His pathway. Thus the interval between the P wave and the QRS becomes shorter than normal, yet the P-J time is normal (Fig. I). The QRS is distorted by the appearance of a delta wave. Although there are exceptions, Type A usually has an upright delta wave in the precordial Leads V, and V 2 with the remaining QRS forces directed anteriorly. In Type B, the delta wave is negative in Leads V,and V 2 with the QRS vector directed predominantly posteriorly. In Type A the QRS may suggest right bundle branch block, whereas in Type B it may suggest left bundle branch block. Although helpful, the electrocardiogram cannot always be relied upon to localize the side involved. During the past 5 years, 45 patients have been referred to our hospital for consideration for surgery for WPW syndrome (Table I). The group was composed of 33 females and 12 males varying in age from 8 to 61 years. In this group, 27 were classified by electrocardiography as having Type A WPW syndrome and 18 as having Type B. Thirtythree were disabled before the age of 20 years from the arrhythmias associated with WPW syndrome. Thirty-nine had supraventricular tachycardia, whereas 15 had atrial flutter-fibrillation. Five had recorded episodes of ventricular fibrillation. Three patients had Ebstein's anomaly, 1 had an atrial septal defect, and 5 had a balloon mitral valve. Twenty patients were treated by medical measures. There was one death, that of an 18-year-old boy with a Type A anomaly. This occurred 6 months after we first saw him, presumably due to a cardiac conduction disturbance. Four patients had demand ventricular pacemakers implanted, and 1 other patient had a left atrial pacer installed that was activated by a radio-frequency device. In all patients, the rationale for employing a pace-
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Wolff-Parkinson-White syndrome
Number 5
759
November, 1974
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Fig. 2. This is an example of a supraventricular tachycardia occurring in a patient with WPW syndrome. The episode was induced by a paced premature atrial beat (AP). The absence of the delta wave during the tachycardia indicated the impulse was conducted antegrade down the AV node-His system and retrograde by the Kent bundle.
Fig. 3. During preoperative evaluation, the patient, a 14-year-old boy, developed atrial flutterfibrillation that was conducted one-to-one to the ventricle, finally degenerating into ventricular tachycardia-fibrillation. The patient had atrial septal Type A WPW syndrome.
maker was to use it to induce a random extrasystole, either in the ventricle or the atrium, which would interrupt the circus movement that causes supraventricular tachycardia. One patient had advanced coronary artery disease and died of a myocardial infarction a year later. Another patient had severe emphysema. Neither the patients treated medically nor 3 of the 5 patients with pacemakers were offered a definitive operation at the time we examined them, because they all had Type A anomalies and we were not satisfied with our method of handling this type at that time. The 20 patients on whom we attempted a complete operative correction varied in age from 12 to 56 years. Fourteen were males and 6 were females. The indications for surgery were repetitive episodes of supraventricular tachycardia in 13 patients and
atrial fibrillation-flutter accompanied by syncope in 7 patients (Figs. 2 and 3). In the first group there were 3 patients who had such prolonged episodes of tachycardia that cardiac failure developed. One patient with heart failure caused by the tachycardia also had an unknown type of myocarditis, which eventually led to his death approximately 3 years after the operation. However, the supraventricular tachycardia never recurred. Two patients, both with Type B anomaly, had Ebstein's anomaly, though only 1 had an insufficient tricuspid valve and required tricuspid valve replacement. One patient (Type A anomaly) had a balloon mitral valve. The group of patients, 7 in all, who had syncope were "surgical emergencies" in light of our current knowledge about WPW. For example, I patient, a 28-year-old woman with Type B disease, required defibrillation
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Sealy and Wallace
--r-
Rel
--Y-Kent(45J
~(49J f---}OO----i
msec Fig. 4. This drawing shows the method for epicardial mapping of the ventricles in a patient with Type B WPW syndrome. The ventricular electrode is the point of reference, whereas the exploring bipolar electrode, shown here in two positions, is tracked over the ventricle. The arbitrary grid is used as a guide. The area of the Kent bundle (45) records an electrogram earlier than the reference, whereas the second electrode (49) appears later. The atrial pacer can be used to induce pre-excitation. This is sometimes useful, particularly on the left side.
on three occasions because of syncope resulting from ventricular tachycardia and fibrillation. Another such life-threatening dysrhythmia, shown in Fig. 3, occurred in a 14-year-old boy. Studies before surgery, in addition to surface electrocardiography, have consisted of His bundle evaluations, intracardiac pressure and shunt measurements and, in some instances, cineangiography. By means of these evaluations it has been possible to confirm the presence of the anomalous tract and to exclude other associated disorders. Determination of the refractory period of the anomalous tract was made in most patients by both antegrade stimulation from the atrium and retrograde stimulation from the ventricle. It is our impression that patients who have a Kent bundle with a short refractory period and no block are liable to have ventricular tachycardia and fibrillation when they have atrial fibrillation and flutter. The patients in whom the refractory period of the Kent bundle is prolonged are more liable to get supraventricular tachycardia from circus movement. In these latter pa-
tients, during the tachycardia the impulse passes down the AV node-His system and then goes retrograde through the tract, the whole sequence of events being initiated by a premature auricular contraction (Fig. 3). In carrying out the operation for complete correction of the WPW syndrome, the surgeon must first locate the bundle of Kent. This is done entirely by electrophysiological techniques, for there are no anatomic changes that point to the anomalous tract. Epicardial mapping of the ventricles, which has been described in detail elsewhere by our group as well as by Durrer'" and Burchell,!' can be expressed in the simplest terms as the determination of the point on the surface of the ventricle where depolarization occurs first. With our current method, we use as a point of reference a ventricular electrode sutured as close as possible to the area where we suspect the anomalous tract to be located (Fig. 4). Then, with a search bipolar electrode, the ventricular epicardial activation times are determined; for orientation, arbitrary grids on diagrammatic drawings on the surfaces of the heart are used. It
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is the earliest area of ventricular depolarization that points to the anomalous tract. As expected, the location is at the AV ring. In addition, we place an atrial pacing electrode on the side where we suspect the tract to be located, for in some patients, usually the ones with Type A disease, the WPW complex does not occur on the electrocardiogram at all times. In that case it is possible to use the atrial pacing electrode to induce conduction through the .Kent bundle. With these observations it is possible to relate the earliest area of ventricular activation to the appearance of the delta wave. This can be important, for in 6 patients with Type Band 3 with Type A anomalies, we have noted a delay in the area of earliest epicardial activation of the ventricle, when this is related to the delta wave. Those patients had Kent bundles in the septal area. In 1969, when we performed the first successful correction of this anomaly, the principle we followed required that we divide the bundle of Kent at the annulus fibrosus (Fig. 5). Judging from the descriptions available, it was evident that the tracts have a wide span both above and below the annulus but have a narrow neck where the tract crosses the annulus. Another point we considered important was the possibility that there might be more than one tract in the immediate area, as noted by Wood and colleagues.' In the first operation and in the next nine, we divided the attachment of the ventricle to the annulus fibrosus, approaching it externally through the AV groove. Exposure had to be obtained by displacing the coronary artery and vein out of the groove. This procedure has been abandoned because we encountered two serious problems. On the left, it was difficult to expose the AV ring because of problems with the control of bleeding from the coronary veins. The second difficulty occurred because the external approach did not permit access to the tracts located along the septal area. We now expose the annulus fibrosus through the atrium and then make an incision through the atrial muscle at its attachment to the annulus fibrosus (Figs. 6 to 8). The fat that
Fig. S. This is a diagrammatic drawing of the connections of the atrium and the ventricle to the annulus fibrosus. The division of the Kent bundle, based on the few anatomic descriptions available, must be made just as it crosses .the annulus fibrosus. The upper sketch shows the division of the atrium as we now do it, and the lower sketch shows the division at the ventricle as used in the old operation. TR, Tricuspid.
surrounds the coronary vessels is next identified. By staying within this dissection plane, we can separate from the annulus the atrial muscle that includes the bundle of Kent. On the left side, the incision along the annulus can be extended anteriorly from the insertion of the mitral valve to the left trigone, which is the anterior part of the fibrous skeleton of the heart. The incision is further extended posteriorly to the insertion of the valve into the central fibrous body, which is called the right trigone. Between these two trigones the mitral valve is continuous with the aorta; thus there is no connection in this area between the atrium and the ventricle. On the right side, the incision can be "made in this same way; it is begun just anterior to the membranous septum and is extended around to the His bundle, which is at the posterior edge of the membranous septum
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Fig. 6. This drawing shows the relat ionship of the left atrium to the annulus fibrosus and the coronary fat pad and vessels. With an incision made from the inside of the atrium, the surgeon can identify the fat pad and make a wide incision yet still remain within the heart.
As the incision is extended from the anterior free wall of the ventricle toward the septum, a plane is still present that is filled with fat. This is between the aorta and the right atrial wall. Posteriorly, in the septal area , there is also a fat pad in the groove between the right and left atria just above the ventricular septum . The only problem that we encountered with the new operation has been with those tracts that course through the portion of the atrial septum that is immediately above the ventricular septum. At this level, the septum is only 4 or 5 mm. wide. The AV node-His bundle is also in this location. Since all the patients have had Type A anomalies, we believe that the tracts must have entered the left side of the ventricular septum and emerged posteriorly at the AV ring just to the left of the ventricular septum. Although the anatomy in these cases was Type A by epicardial studies and electrocardiography, the Kent bundle did not cross the left annulus fibrosus. The epicardial maps of these hearts also showed that the earliest area of ventricular depolarization occurred after the onset of the delta wave. In order to divide a bundle in this location in the future, we probably will have to divide the
His bundle as well. The Type B tracts that emerge on the right, adjacent to the ventricular septum in this same relative location, have been successfully interrupted; there has been one exception, however, a patient with an associated Ebstein's anomaly. On the right, the tract may be just underneath the coronary sinus yet still in the right atrial wall. The exposure for the operation for an anomalous bundle on the right side (Type B) is obtained through a median sternotomy incision. Since the atrium is usually small, the inferior vena cava is cannulated through the saphenous bulb and femoral vein. After the establishment of cardiopulmonary bypass, the right atrium is opened, and the area along the annulus fibrosus that corresponds to the point of early activation along the AV groove is defined. We next fibrillate the heart in order to find more easily the dissection plane between the atrial wall externally and the internal surface of the coronary fat pad. At this point, the heart can be defibrillated and the electrocardiogram monitored as the incision is lengthened. Then the incision through the atrial wall at its insertion into the annulus is closed. Finally, we close the atriotomy incision and stop the extra-
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Wolff-Parkinson-White syndrome
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Fig. 7. The approach to the left or Type A WPW, made through a left lateral thoracotomy, is illustrated in this figure. The incision is shown beginning at the left trigone. This is the point where the mitral valve is continuous with the aorta. Going in a clock-wise direction from this point, there are no more connections between the atrium and the ventricle until the right trigone (central fibrous body) and base of the atrial septum are reached.
corporeal circulation. We believe that mapping should again be done after bypass but before the cannulas to the extracorporeal device are removed. In the new operative technique for a bundle of Kent on the left side, we use a left lateral thoracotomy. We have found that exposure to the interior of such a small atrium is best obtained through the fourth rib or third intercostal space. The venous return to the pump oxygenator is accomplished by putting one outflow catheter in the right ventricular outflow tract and the other in the femoral vein. The approach to the junction of the atrium with the annulus
fibrosus is the same as on the right side. Mapping should be done before the incision in the heart is closed. The results of surgery are summarized in Table II and Fig. 9. We have divided the anomalies on the right (Type B) into three classes: lateral, corresponding to Kent's description; anterior to the membranous septum; and posterior to the membranous septum. We have classified those on the left (Type A) as atrial septal Type A, lateral, and posterior. The posterior bundles are located along the free wall of the ventricle. A good result is considered one in which the electrocardiogram has reverted to nor-
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Fig. 8. This figure illustrates the approach to a right or Type B WPW through a median sternotomy incision. The incision in the atrium, as shown here, is posterior and extends toward the coronary sinus level. It can be carried to the level of the anterior lip of the coronary sinus. At this point the atrial septum would be reached and thus the incision would be at the AV node-His bundle. As we have done, an incision can be started in this same relative position anteriorly and then extended to the opposite or anterior margin of the membranous septum by means of the same plane of dissection.
mal and the patient no longer has supraventricular tachycardia. If atrial flutter-fibrillation was present and should then recur, it must be conducted to the ventricle through the AV node-His system. A fair result is defined as one in which (1) the WPW complex is still present on the electrocardiogram but the patient no longer has episodes of supraventricular tachycardia or (2) there is absence of one-to-one conduction to the ventricle with atrial fibrillation-flutter. A
poor result is defined as one in which there is evidence that the aberrant tract was not divided. Not only is the WPW complex evident on the electrocardiogram, but also the patient still has episodes of dysrhythmia. In our earlier operation, we approached the bundle through the AV groove; with the new operation, the approach is through the atrium . In the former, the ventricle was separated from the annulus; in the latter, the atrium is separated from it.
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* Foilure,newoperalion
A Success
o Failure,old operation • Ebstein's, failure e WPW on EKG clinicol cure
TYPE A, 7 patients Atrial septal, 3 patients Fig. 9. In this diagrammatic drawing of the heart, the location of the Kent bundle for each of our surgically treated patients is shown. We believe the bundles in the septal area along the left annulus fibrosus were in the atrial septum and entered the left side of the ventricular septum, probably following the course of the AV node and His bundle. Thus these tracts did not cross the left annulus fibrosus, as this drawing might indicate.
Table II. Summary of data on patients operated upon for
Wolff-Parkinson-White syndrome Location of tract
No. of patients
Result
Operation Old
New
Cure
Fair
Failure
4 1 2
o
0
Type B
Lateral Anterior septal Posterior septal
4 3 3
2 2 1
Lateral Posterior Atrial septal
5 2
2 2
3
1
2 1 2 Type A 3 0 2
1
1* It
o
5 2 1
2
• Patient died 18 hours postoperatively (old operation). tEbstein's anomaly (new operation).
We were successful in treating 7 of the 10 patients with Type B anomalies. In 1 patient the result was fair, and in 2 patients the operation was a failure. One of the patients with a poor result and the 1 patient with a fair result belonged to the anterior
septal subgroup. With the old operative technique, in spite of wide division of the right lateral ventricular wall at its insertion into the annulus, the bundle was missed in 1 patient; in the other, the bundle must have been partially damaged. From a subsequent
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successful operation via the new approach, we now believe the tracts were close to or adjacent to the anterior part of the membranous septum. The I patient with a poor result in the anterior septal group was the only one to die in this series. The patient was a 39-year-old woman who died 18 hours after the operation from an uncontrollable tachyarrhythmia. Another possible failure occurred in 1 of the 2 patients who had Ebstein's anomaly. The electrocardiogram showed no delta wave for 12 hours after surgery, but subsequently the wave returned. The patient is improved due to insertion of a tricuspid valve to correct valvular insufficiency, but she still has episodes of dysrhythmia. We obtained good results in 5 patients from the Type A group. The bundles were located laterally in all. Results were fair in 2 patients in whom the bundles were in a posterior location and who were operated upon via the old technique. The patients in the atrial septal Type A group have thus far not had correction of the WPW syndrome. Two of the patients in this group had poor operative results and 1 had a fair result, although his follow-up period is short. The latter patient deserves special comment. We thought there was a chance that the Kent bundle might have entered the ventricular septum on the right and surfaced on the left posteriorly, for the distance is such that this could have occurred. At operation, an incision in the right annulus fibrosus was made to a point beneath the middle of the coronary sinus. This did not cause the electrocardiogram to revert to normal. Next the left atrium was exposed through the atrial septum, and the atrium was incised at the annulus all the way to the right trigone, a procedure which likewise failed to obliterate the delta wave. As a last resort, an area in the superior muscular ventricular septum on the left was cauterized with the electrocautery. At our preoperative study, an atrial impulse was conducted one-to-one at well above 200 beats per minute across the anomalous tract with atrial fibrillation and flutter (Fig. 3).
Postoperatively, although the WPW complex was still present, the Kent bundle blocked when a pacing rate of 180 was exceeded. This extensive dissection left undivided only the narrow atrial septum that contained the AV node and His bundle. One group of patients, those in whom the arrhythmias have been prevented but in whom the WPW complexes remain, is a difficult group to explain. However, this situation has been reported by others. Iwa" has noted this in 2 of his 9 patients, and a similar experience in I patient has been reported both by Cole':' and by Lindsay." This type of result could have occurred because the connection was either partially divided or because other smaller connections were present and missed. In regard to the first explanation, it is possible that with only one or two remaining connections of the anomalous bundle to the ventricular muscle, the electrophysiological characteristics may have been so changed that retrograde transmission could not occur. Therefore, circus movement that goes down the AV node and retrograde to the Kent bundle would no longer be possible. It is also of interest that 1 patient (Type A) had a WPW complex in the immediate postoperative period but never had recurrent tachycardia. He was seen by us about 2 years postoperatively. At this time the electrocardiogram was normal, and pre-excitation was ruled out by a His bundle and intracardiac pacing study. In regard to the possibility of other connections, it is well known that there are patients with electrocardiographic evidence of the WPW complex who rarely or never have tachycardia.s- 23 Discussion
From this clinical study we believe we have accumulated undeniable evidence which indicates that the WPW syndrome is caused by a physiologically demonstrable anomalous conduction pathway coursing from the atrium to the ventricle. Although we do not have morphologic evidence to confirm our findings, the clear-cut change in the electrocardiogram and the relief of the patient's
Volume 68 Number 5 November, 1974
symptoms permit this conclusion. Our operative experience confirms the fact that the tract can occur anywhere in the area of the AV junction. Thus the observations of Kent-:" and others are correct in that lateral connections or, expressed another way, freewall connections as well as septal ones do occur. In addition to the presence of the tracts around the annulus fibrosus, the anomalous connections can course from the atrium to the ventricle about the area where the atrial septum is adjacent to the membranous septum of the ventricle. By following this pathway, the tract can get to the left side of the ventricular septum without traversing the left annulus. This places the tract adjacent to the AV node. Levu and James" have offered evidence that the pathway for preexcitation may be in this position. Although mapping of the epicardial surfaces has been successful in indicating the location ot' the anomalous tracts, the absence of many good anatomic studies of the bundle of Kent has hampered the planning and execution of the operative procedure. The embryologic abnormality that explains the development of the anomalous tracts is related to the annulus fibrosus." This structure separates the atria from the ventricles. As it develops, it lays down thick connective tissue to form the ring. When the annulus finally becomes fully developed, it obliterates the muscle connections between the atria and the ventricle which are present in the embryo and leaves only the His bundle hiatus intact. If this mechanism is the explanation for the presence of the anomalous tracts, then the possibility exists that there could be more than one tract. Lunel" has presented evidence that this may occur. Wood" also found three tracts in a 1 em. area of the right annulus fibrosus. Boineau-' noted a tract on the right and left in a squirrel monkey. Logically, one would suspect that anomalous tracts would occur along the atrial septum and ventricular septum, the only place where the annulus fibrosus is normally pierced by the AV connections. As has been pointed out, we have found the tracts located anterior to the membranous
Wolff-Parkinson-White syndrome
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septum and just posterior to the His bundle on the right side. We believe also that a number of these, as found in 3 of our patients, will be adjacent to the AV node and His bundle. Other congenital defects involving the AV valves also occur in conjunction with the WPW syndrome. One patient with a Type A anomaly had a balloon mitral valve. Two other patients in our series of operations had Ebstein's anomaly. The procedure now followed for surgical treatment of WPW requires a large number of highly trained people plus expensive and delicate equipment. In addition, the mapping prolongs the already lengthy procedure. However, the accuracy of surface electrocardiography is such that we cannot completely rely upon it for localization of the side involved. If the latter method were accurate, it would be tempting to proceed directly to the appropriate annulus fibrosus, develop the proper plane, and then extend the incision around until the electrocardiogram became normal. There are several reports, beginning with the ones by Edmonds," Dreifus," and their colleagues, which suggest that this disorder might be palliated by dividing the His bundle and implanting a demand pacemaker. Recently, Hatcher" and Dunaway" have reported the use of this procedure on 3 patients. This is a simple method of controlling the supraventricular tachycardia and can actually be done with a cautery, as Ellison did, without extracorporeal circulation. On the other hand, it is indicated only in a few instances, such as, we believe, in patients with atrial septal Type A anomalies. From information based on our studies of the e1ectrophysiological characteristics of some of the bundles of Kent, we have been concerned about dividing the His bundle yet leaving the Kent bundle, for fear that the patients might stilI be liable to ventricular tachycardia and fibrillation. This possibility exists because patients may have Kent bundles with short refractory periods, which thus can conduct one-to-one when atrial fibrillation occurs. The implications are obvious. We have outlined our experience with
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pacemakers used to induce an extra beat to break the cycle causing the supraventricular tachycardia. This is at best a poor method of treatment and is only indicated in patients with problems that preclude a thoracotomy. Others have had success in locating and either dividing or partially dividing the Kent bundle. Lindsay and colleagues" reported their treatment of 1 patient with a Type B WPW complex located posteriorly. The patient also had mitral valve disease and required valve replacement. The incision was made through the annulus area. The WPW complex recurred temporarily after surgery but later disappeared. The patient has had no further problems with arrhythmias, and a recent electrocardiogram no longer showed the WPW complex. Cole':' has reported his group's experience with 2 patients who had Type B anomalies. In 1 the bundle was in a right lateral position. A wide incision through the ventricular and atrial walls failed to correct the electrocardiographic abnormality, and an attempt to divide the His bundle also failed to produce heart block. This patient, as in some of Iwa's-" and some of our patients, still has the delta wave on the electrocardiogram but no longer has tachycardia. Iwa's second patient had an anterior area of early activation. Interruption of the Kent bundle occurred when the area of the His bundle was manipulated. This suggests, as in our experience, that early ventricular depolarization on the right anterior side may indicate a septal tract. Burchell and associates" made an attempt to divide a right lateral bundle after localizing it with surface mapping. The incision was made away from the annulus. Iwa'" has attempted to correct the WPW syndrome in 9 patients. In 4 patients with Type B disease, the tracts were divided successfully by means of an incision in the region of the AV ring. The operation failed in 4 Type B patients. In the 1 Type A patient, the electrocardiogram was not changed but the number of episodes of tachycardia has decreased. Although there have been failures in the complete correction of the WPW syndrome both in our experience and in that of others,
information and methods are now available to offer nearly all patients with this syndrome a chance for cure. The surgical principles we have learned in treating these patients are stated as follows: 1. Careful electrophysiologic localization at the AV ring ot the earliest area of ventricular depolarization is essential. This is the guide to the bundle of Kent. 2. Early activation of the ventricle, either anteriorly on the right or posteriorly at the septum on the', right and left, may indicate that the Kent bundle is in the septal area. 3. The incision at the annulus fibrosus should be at least 2 em. in length in order to divide any other bundles of Kent that might be in the same area. 4. The surgical incision in the atrium should be adjacent to and against the annulus fibrosus in order to divide the bundle of Kent at its narrowest point. REFERENCES Wolff, L., Parkinson, J., and White, P. D.: Bundle-Branch Block With Short P-R Interval in Healthy Young People Prone to Paroxysmal Tachycardia, Am. Heart J. 5: 685, 1930. 2 Holzmann, M., and Scherf, D.: Uber Elektrokardiogramme Mit Verkurzter Vorhof-Krammer-Distanz und Positiven P-Zacken, Z. Klin. Med. 121: 404, 1932. 3 Wolferth, C. C, and Wood, F. C.: The Mechanism of Production of Short P-R Intervals and Prolonged QRS Complexes in Patients With Presumably Undamaged Hearts: Hypothesis of an Accessory Pathway of Auriculoventricular Conduction (Bundle of Kent), Am. Heart J. 8: 297, 1933. 4 Wood, F. C., Wolferth, C. C, and Geckeler, G. D.: Histologic Demonstration of Accessory Muscular Connections Between Auricle and Ventricle in a Case of Short P-R Interval and Prolonged QRS Complex, Am. Heart J. 25: 454, 1943. 5 Kent, A. F.: Researches on the Structure and Function of the Mammalian Heart, J. Physiol. 14: 233, 1893. 6 Kent, A. F. S.: The Right Lateral Auriculoventricular Junction of the Heart, J. Physiol. 48: 22, 1914. 7 Kent, A. F. S.: Illustrations of the Right Lateral Auriculo-ventricular Junction in the Heart, J. Physiol. 48: 63, 1914. 8 Kent, A. F. S.: A Conducting Path Between the Right Auricle and the External Wall of the Right Ventricle in the Heart of the Mammal, J. Physiol. 48: 57, 1914.
Volume 68 Number 5 November, 1974
9 Mann, R. B., Fisher, R. S., Scherlis, S., and Hutchins, G. M.: Accessory Left Atrioventricular Connection in Type A Wolff-ParkinsonWhite Syndrome, Johns Hopkins Med. J. 132: 242, 1973. 10 Durrer, D., and Roos, J. P.: Epicardial Excitation of the Ventricles in a Patient With WolffParkinson-White Syndrome (Type B), Circulation 35: 15, 1967. 11 Burchell, H. B., Frye, R. L., Anderson, M. W., and McGoon, D. C.: Atrioventricular and Ventriculoatrial Excitation in Wolff-ParkinsonWhite Syndrome (Type B), Circulation 36: 663, 1967. 12 Dreifus, L. S., Nichols, H., Morse, D., Watanabe, Y., and Truex, R.: Control of Recurrent Tachycardia of Wolff-Parkinson-White Syndrome by Surgical Ligature of the A-V Bundle, Circulation 38: 1030, 1968. 13 Lindsay, A. E., Nelson, R. M., Abildskov, J. A., and Wyatt, R.: Attempted Surgical Division of the Pre-excitation Pathway in the Wolff-Parkinson-White Syndrome, Am. J. Cardio!. 28: 581, 1971. 14 Cole, J. S., Wills, R. E., Winterscheid, L. C., Reichenbach, D. D., and Blackmon, J. R.: The Wolff-Parkinson-White Syndrome: Problems in Evaluation and Surgical Therapy, Clin. Res. 18: 113, 1970. 15 Dunaway, M. C., King, S. B., Hatcher, C. R., Jr., and Logue, R. B.: Disabling Supraventricular Tachycardia of Wolff-Parkinson-White Syndrome (Type A) Controlled by Surgical A-V Block and a Demand Pacemaker After Epicardial Mapping Studies, Circulation 45: 522, 1972. 16 Iwa, T., Kazui, T., Sugii, S., and Wada, J.: Wolff-Parkinson-White: Surgical Treatment, Jap. J. Thorac. Surg. 23: 513, 1970. 17 Sealy, W. c., HaUler, B. G., Jr., Blumenschein, S. D., and Cobb, F. R.: Surgical Treatment of Wolff-Parkinson-White Syndrome, Ann. Thorac. Surg, 8: 1, 1969. 18 Wallace, A. G., Boineau, J. P., Davidson, R. M., and Sealy, W. c.: Wolff-Parkinson-White Syndrome: A New Look, Am. J. Cardio!. 28: 509, 1971. 19 Cobb, F. R., Blumenschein, S. D., Sealy, W. C., Boineau, J. P., Wagner, G. S., and Wallace, A. G.: Successful Surgical Interruption of the Bundle of Kent in a Patient With Wolff-Parkinson-White Syndrome, Circulation 38: 1018, 1968. 20 Rosenbaum, F. F., Hecht, H. H., Wilson, F. N., and Johnston, F. D.: The Potential Variations of the Thorax and the Esophagus in Anomalous Atrioventricular Excitation (Wolff-Parkinson-White Syndrome), Am. Heart J. 29: 281, 1945. 21 Boineau, J. P., Moore, E. N., Spear, J. F., and Sealy, W. C.: Basis of Static and Dynamic
Wolff-Parkinson-White syndrome
22
23 24
25 26
27
28
29
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Electrocardiographic Variations in Wolff-Parkinson-White Syndrome, Am. J. Cardio!. 32: 32, 1973. Giardina, A. C. V., Ehlers, K. H., and Engle, M. A.: Wolff-Parkinson-White Syndrome in Infants and Children: A Long-Term Follow-up Study, Br. Heart J. 34: 839, 1972. Flensted-Jensen, E.: Wolff-Parkinson-White Syndrome: A Long-Term Follow-up of 47 Cases, Acta Med. Scand. 186: 65, 1969. Lev, M., and Lerner, R.: The Theory of Kent: A Histologic Study of the Normal Atrioventricular Communications of the Human Heart, Circulation 12: 176, 1955. James, T. N.: The Wolff-Parkinson-White Syndrome: Evolving Concepts of its Pathogenesis, Progr, Cardiovasc. Dis. 13: 159, 1970. Truex, R. C., Bishof, J. K., and Hoffman, E. L.: Accessory Atrioventricular Muscle Bundles of the Developing Human Heart, Anat. Rec. 131: 45, 1958. Lunel, A. A. V.: Significance of Annulus Fibrosus of Heart in Relation to AV Conduction and Ventricular Activation in Cases of Wolff-Parkinson-White Syndrome, Br. Heart J. 34: 1263, 1972. Edmonds, 1. H., Ellison, R. G., and Crews, T. L.: Surgically Induced Atrioventricular Block as Treatment for Recurrent Atrial Tachycardia in Wolff-Parkinson-White Syndrome, Circulation 39: 105, 1969 (Supp!. I). Hatcher, C. R., Jr.: Personal communication, 1974.
Discussion DR. TAKASHI IWA Kanazawa, Japan
Dr. Sealy is certainly a pioneer in this particular field of cardiac surgery. [Slide] I operated upon my first patient with WPW syndrome in July, 1969. Since then I have accumulated 9 cases altogether, including 8 cases of Type Band 1 case of Type A. Among many preoperative examinations, epicardial mapping was the most reliable and indispensable to determine the exact location of the accessory pathway. [Slide] However, we have found in our most recent case that the electrical potential of the accessory conduction pathway can be detected by a bipolar electrode, which is applied along the tricuspid annulus ring in the right atrium. A sharp deflection is recorded between the P and delta waves. It indicates precisely the localization of the accessory conduction pathway passed by beneath the atrial endocardium. A very small incision of this area, 2 em. in length in this case, was enough to cure the disease. [Slide] In the serial sections of specimens resected from incised areas, a special muscle bundle was found in 2 cases studied. It is believed that
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this is a Kent bundle because of its localization, running course, and appearance. [Slide] As there are many theories and controversial facts, the WPW syndrome cannot be explained by only a lateral bundle. I must admit that radical surgery is not always satisfactory. Therefore, as an adjunct method, I developed an inductive radio-frequency atrial pacemaker in 1969. Its receiver, of which there are a button type and a catheter type, has been implanted in 12 patients with refractory supraventricular tachycardia. Three of these patients have WPW syndrome. The patients could terminate the tachycardias by applying batterylized transceiver by themselves from outside their bodies anytime and anywhere tachycardia occurred. The applied electrical stimulation rate was between 250 and 500 times per minute and lasted several seconds. This method is more physiological and safer than creation of AV block and implantation of a demand pacemaker. [Slide] With my own experience, along with Dr. Sealy's high rate of success, I am now more inclined to believe that most of the patients with WPW syndrome, in whom medical treatment is not feasible, can be cured by a rather simple operation. The surgical management of arrhythmias, of which WPW syndrome is one, will be a new field in cardiac surgery. DR. SIDNEY LEVITSKY Chicago, 1Il.
I would like to compliment the Duke group on a fine presentation. Recently we had the opportunity to treat a 15-year-old boy at the University of Illinois with severe symptomatic WPW syndrome, Type B. Before operating on this young man, we visited Dr. Sealy in Durham, North Carolina, to observe his operative approach. [Slide] We employed an epicardial mapping system similar to that described by Drs. Sealy and Wallace. The incision across the bundle of Kent occurred at the point of the arrow noted on the slide. Prior to that point, there was a positive delta wave in Lead I and a negative delta wave in Lead II. After the incision, the delta wave disappeared. The month prior to the operation, the patient had over twenty syncopal episodes secondary to tachyarrhythmias. The patient has been totally asymptomatic for 2 months postoperatively. DR. RUSSELL M. NELSON Salt Lake City, Utah
I too would like to express gratitude to Dr. Sealy for this among his many contributions to our specialty. I would like to make a comment about the terminology that is used in this particular area. There is a difference between the electrocardiographic pattern of pre-excitation and the WPW
syndrome. Pre-excitation is the electrocardiographic pattern without tachycardia. When the pre-excitation pattern is coupled with tachycardia, then the name Wolff-Parkinson-White syndrome may be applied. Not everyone with pre-excitation pattern has WPW syndrome, and not everyone with WPW syndrome needs an operation, as has been pointed out in Dr. Sealy's comments. However, for those who intend to perform such an operation, J would suggest that not only Dr. Sealy's work be studied in detail, but also that of Dr. Dirk Durrer of Amsterdam, who has been a pioneer in epicardial mapping. I would like to ask Dr. Sealy one question. In many of these patients, the appearance of the tachyarrhythmias and even of the pre-excitation pattern is intermittent. Is there a way of stimulating the pre-excitation pattern in the operating room? If the heart reverts to the non-pre-excitation pattern at the time of the proposed division of the Kent bundle, the target will have disappeared before the incision is made. DR. SEALY (Closing) I thank the discussers very much. I particularly appreciate Dr. Iwa's contribution to this discussion. He made a special trip from his country to participate. The intermittent nature of the WPW complex on the electrocardiogram is a problem and may be particularly so with Type A WPW. That is why we use an atrial pacer during trapping. I would like to also comment about the incidence of clinical symptoms with this disorder. It has been estimated that between 40 and 60 per cent of patients with a WPA complex will have symptoms. The next problem is determining how many symptoms or how severe the symptoms have to be for the patient to need an operation. For this reason, extensive preoperative studies of the His bundle and of pacing are necessary. I think now that any patient who has had an episode of tachycardia and who, on study, shows evidence of one-to-one conduction across the Kent bundle probably should have an operation. Perhaps in another 20 cases we can be more certain about this. [Slide] There are important problems with the atrial septal Type A anomaly. The conduction tract comes down with AV node-His system. On the right side, these tracts cross the AV valve, and we have been able to divide them in this location. On the left side, the tracts do not cross the annulus of the valve, but rather go along with the AV nodeHis system. We hope that we can separate the AV nodeHis system from the Kent bundle in this group. Once that is accomplished, we can leave the AV node-His system intact and then divide only that part of the septum which contains the Kent bundle.
Will C. Sealy, M.D., and Andrew G. Wallace, M.D. (by invitation), Durham, N. C.
h e Wolff-Parkinson-White (WPW) syndrome ' may be associated with both lifethreatening and disabling disturbances in cardiac rhythm that are refractory to medical management. Pre-excitation or early depolarization of the ventricles, the characteristic of this abnormality on the electrocardiogram, lacked a plausible explanation until Holzmann and Scherf" and later Wolferth and Wood" suggested that it was caused by the bundle of Kent, which is an anomalous connection between the atrium and the ventricle. Later, Wood and co-workers! described the case of a boy with WPW syndrome who died suddenly. At autopsy, they found an anomalous connection from the right lateral atrium to the ventricle simiFrom the Divisions of Thoracic Surgery and Cardiovascular Medicine, Duke University School of Medicine, Durham, N. C. 27710. Supported by U. S. Public Health Service Grants HL13920-03 and HL1519D-01. Read at the Fifty-fourth Annual Meeting of The American Association for Thoracic Surgery, Las Vegas, Nevada, April 22, 23, and 24, 1974.
lar to that described by Kent. 5-8 This theory, however, has until just recently remained open to question, chiefly because there is still an inadequate amount of anatomic material" available to corroborate the physiological evidence accumulated by many observers. 1 0 - 1 6 By identifying the anomalous tract at surgery with electrophysiological methods and then dividing it, we": 18 have furnished unequivocal proof that this tract is the cause of the WPW syndrome. This disorder, which is both disabling and life threatening, has assumed surgical importance now that the cause is known and a definitive operation for its correction has been devised. In this report we will relate our experience with 20 patients, selected from 45 with the WPW syndrome, who had surgical correction of their anomaly. A description will be given of how the operative procedure has evolved from our" initial approach in the first successful correction of this disorder to the present technique, which offers an excellent chance for complete cor-
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Delta Wave
\
t Short PR Normal PJ Fig. 1. An electrocardiogram of a patient with Wolff-Parkinson-White syndrome shows the typical alterations of the QRS by pre-excitation causing a delta wave, a short PR interval, but a normal PI time.
Table I. Experience with Wolff-Parkinson-White syndrome No. of patients
Total No. Type A Type B Medical treatment Deaths Pacemaker Surgical treatment Type A Type B Deaths
45 33 12
20
5 20 10 10 1
rection in nearly all patients with the WPW syndrome. Clinical experience
In this discussion, Type A WPW syndrome will be used to denote a Kent bundle that crosses the annulus fibrosus at the mitral ring or that enters the left side of the ventricular septum from the atrial septum. The latter we will designate as atrial septal Type A. Type B will denote any bundle traversing the right annulus fibrosus. The electrocardiogram in pre-excitation, though it may vary considerably depending upon the location of the bundle of Kent, does provide evidence for the classification of patients with the WPW syndrome into Type A and Type B
as noted by Rosenbaum," and Boineau," and their colleagues. As the term pre-excitation implies, the characteristic of the electrocardiogram is the early activation of some or all of the ventricular muscle by pathways other than the normal atrioventricular (AV) node-His pathway. Thus the interval between the P wave and the QRS becomes shorter than normal, yet the P-J time is normal (Fig. I). The QRS is distorted by the appearance of a delta wave. Although there are exceptions, Type A usually has an upright delta wave in the precordial Leads V, and V 2 with the remaining QRS forces directed anteriorly. In Type B, the delta wave is negative in Leads V,and V 2 with the QRS vector directed predominantly posteriorly. In Type A the QRS may suggest right bundle branch block, whereas in Type B it may suggest left bundle branch block. Although helpful, the electrocardiogram cannot always be relied upon to localize the side involved. During the past 5 years, 45 patients have been referred to our hospital for consideration for surgery for WPW syndrome (Table I). The group was composed of 33 females and 12 males varying in age from 8 to 61 years. In this group, 27 were classified by electrocardiography as having Type A WPW syndrome and 18 as having Type B. Thirtythree were disabled before the age of 20 years from the arrhythmias associated with WPW syndrome. Thirty-nine had supraventricular tachycardia, whereas 15 had atrial flutter-fibrillation. Five had recorded episodes of ventricular fibrillation. Three patients had Ebstein's anomaly, 1 had an atrial septal defect, and 5 had a balloon mitral valve. Twenty patients were treated by medical measures. There was one death, that of an 18-year-old boy with a Type A anomaly. This occurred 6 months after we first saw him, presumably due to a cardiac conduction disturbance. Four patients had demand ventricular pacemakers implanted, and 1 other patient had a left atrial pacer installed that was activated by a radio-frequency device. In all patients, the rationale for employing a pace-
Volume 68
Wolff-Parkinson-White syndrome
Number 5
759
November, 1974
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Fig. 2. This is an example of a supraventricular tachycardia occurring in a patient with WPW syndrome. The episode was induced by a paced premature atrial beat (AP). The absence of the delta wave during the tachycardia indicated the impulse was conducted antegrade down the AV node-His system and retrograde by the Kent bundle.
Fig. 3. During preoperative evaluation, the patient, a 14-year-old boy, developed atrial flutterfibrillation that was conducted one-to-one to the ventricle, finally degenerating into ventricular tachycardia-fibrillation. The patient had atrial septal Type A WPW syndrome.
maker was to use it to induce a random extrasystole, either in the ventricle or the atrium, which would interrupt the circus movement that causes supraventricular tachycardia. One patient had advanced coronary artery disease and died of a myocardial infarction a year later. Another patient had severe emphysema. Neither the patients treated medically nor 3 of the 5 patients with pacemakers were offered a definitive operation at the time we examined them, because they all had Type A anomalies and we were not satisfied with our method of handling this type at that time. The 20 patients on whom we attempted a complete operative correction varied in age from 12 to 56 years. Fourteen were males and 6 were females. The indications for surgery were repetitive episodes of supraventricular tachycardia in 13 patients and
atrial fibrillation-flutter accompanied by syncope in 7 patients (Figs. 2 and 3). In the first group there were 3 patients who had such prolonged episodes of tachycardia that cardiac failure developed. One patient with heart failure caused by the tachycardia also had an unknown type of myocarditis, which eventually led to his death approximately 3 years after the operation. However, the supraventricular tachycardia never recurred. Two patients, both with Type B anomaly, had Ebstein's anomaly, though only 1 had an insufficient tricuspid valve and required tricuspid valve replacement. One patient (Type A anomaly) had a balloon mitral valve. The group of patients, 7 in all, who had syncope were "surgical emergencies" in light of our current knowledge about WPW. For example, I patient, a 28-year-old woman with Type B disease, required defibrillation
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--r-
Rel
--Y-Kent(45J
~(49J f---}OO----i
msec Fig. 4. This drawing shows the method for epicardial mapping of the ventricles in a patient with Type B WPW syndrome. The ventricular electrode is the point of reference, whereas the exploring bipolar electrode, shown here in two positions, is tracked over the ventricle. The arbitrary grid is used as a guide. The area of the Kent bundle (45) records an electrogram earlier than the reference, whereas the second electrode (49) appears later. The atrial pacer can be used to induce pre-excitation. This is sometimes useful, particularly on the left side.
on three occasions because of syncope resulting from ventricular tachycardia and fibrillation. Another such life-threatening dysrhythmia, shown in Fig. 3, occurred in a 14-year-old boy. Studies before surgery, in addition to surface electrocardiography, have consisted of His bundle evaluations, intracardiac pressure and shunt measurements and, in some instances, cineangiography. By means of these evaluations it has been possible to confirm the presence of the anomalous tract and to exclude other associated disorders. Determination of the refractory period of the anomalous tract was made in most patients by both antegrade stimulation from the atrium and retrograde stimulation from the ventricle. It is our impression that patients who have a Kent bundle with a short refractory period and no block are liable to have ventricular tachycardia and fibrillation when they have atrial fibrillation and flutter. The patients in whom the refractory period of the Kent bundle is prolonged are more liable to get supraventricular tachycardia from circus movement. In these latter pa-
tients, during the tachycardia the impulse passes down the AV node-His system and then goes retrograde through the tract, the whole sequence of events being initiated by a premature auricular contraction (Fig. 3). In carrying out the operation for complete correction of the WPW syndrome, the surgeon must first locate the bundle of Kent. This is done entirely by electrophysiological techniques, for there are no anatomic changes that point to the anomalous tract. Epicardial mapping of the ventricles, which has been described in detail elsewhere by our group as well as by Durrer'" and Burchell,!' can be expressed in the simplest terms as the determination of the point on the surface of the ventricle where depolarization occurs first. With our current method, we use as a point of reference a ventricular electrode sutured as close as possible to the area where we suspect the anomalous tract to be located (Fig. 4). Then, with a search bipolar electrode, the ventricular epicardial activation times are determined; for orientation, arbitrary grids on diagrammatic drawings on the surfaces of the heart are used. It
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is the earliest area of ventricular depolarization that points to the anomalous tract. As expected, the location is at the AV ring. In addition, we place an atrial pacing electrode on the side where we suspect the tract to be located, for in some patients, usually the ones with Type A disease, the WPW complex does not occur on the electrocardiogram at all times. In that case it is possible to use the atrial pacing electrode to induce conduction through the .Kent bundle. With these observations it is possible to relate the earliest area of ventricular activation to the appearance of the delta wave. This can be important, for in 6 patients with Type Band 3 with Type A anomalies, we have noted a delay in the area of earliest epicardial activation of the ventricle, when this is related to the delta wave. Those patients had Kent bundles in the septal area. In 1969, when we performed the first successful correction of this anomaly, the principle we followed required that we divide the bundle of Kent at the annulus fibrosus (Fig. 5). Judging from the descriptions available, it was evident that the tracts have a wide span both above and below the annulus but have a narrow neck where the tract crosses the annulus. Another point we considered important was the possibility that there might be more than one tract in the immediate area, as noted by Wood and colleagues.' In the first operation and in the next nine, we divided the attachment of the ventricle to the annulus fibrosus, approaching it externally through the AV groove. Exposure had to be obtained by displacing the coronary artery and vein out of the groove. This procedure has been abandoned because we encountered two serious problems. On the left, it was difficult to expose the AV ring because of problems with the control of bleeding from the coronary veins. The second difficulty occurred because the external approach did not permit access to the tracts located along the septal area. We now expose the annulus fibrosus through the atrium and then make an incision through the atrial muscle at its attachment to the annulus fibrosus (Figs. 6 to 8). The fat that
Fig. S. This is a diagrammatic drawing of the connections of the atrium and the ventricle to the annulus fibrosus. The division of the Kent bundle, based on the few anatomic descriptions available, must be made just as it crosses .the annulus fibrosus. The upper sketch shows the division of the atrium as we now do it, and the lower sketch shows the division at the ventricle as used in the old operation. TR, Tricuspid.
surrounds the coronary vessels is next identified. By staying within this dissection plane, we can separate from the annulus the atrial muscle that includes the bundle of Kent. On the left side, the incision along the annulus can be extended anteriorly from the insertion of the mitral valve to the left trigone, which is the anterior part of the fibrous skeleton of the heart. The incision is further extended posteriorly to the insertion of the valve into the central fibrous body, which is called the right trigone. Between these two trigones the mitral valve is continuous with the aorta; thus there is no connection in this area between the atrium and the ventricle. On the right side, the incision can be "made in this same way; it is begun just anterior to the membranous septum and is extended around to the His bundle, which is at the posterior edge of the membranous septum
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Fig. 6. This drawing shows the relat ionship of the left atrium to the annulus fibrosus and the coronary fat pad and vessels. With an incision made from the inside of the atrium, the surgeon can identify the fat pad and make a wide incision yet still remain within the heart.
As the incision is extended from the anterior free wall of the ventricle toward the septum, a plane is still present that is filled with fat. This is between the aorta and the right atrial wall. Posteriorly, in the septal area , there is also a fat pad in the groove between the right and left atria just above the ventricular septum . The only problem that we encountered with the new operation has been with those tracts that course through the portion of the atrial septum that is immediately above the ventricular septum. At this level, the septum is only 4 or 5 mm. wide. The AV node-His bundle is also in this location. Since all the patients have had Type A anomalies, we believe that the tracts must have entered the left side of the ventricular septum and emerged posteriorly at the AV ring just to the left of the ventricular septum. Although the anatomy in these cases was Type A by epicardial studies and electrocardiography, the Kent bundle did not cross the left annulus fibrosus. The epicardial maps of these hearts also showed that the earliest area of ventricular depolarization occurred after the onset of the delta wave. In order to divide a bundle in this location in the future, we probably will have to divide the
His bundle as well. The Type B tracts that emerge on the right, adjacent to the ventricular septum in this same relative location, have been successfully interrupted; there has been one exception, however, a patient with an associated Ebstein's anomaly. On the right, the tract may be just underneath the coronary sinus yet still in the right atrial wall. The exposure for the operation for an anomalous bundle on the right side (Type B) is obtained through a median sternotomy incision. Since the atrium is usually small, the inferior vena cava is cannulated through the saphenous bulb and femoral vein. After the establishment of cardiopulmonary bypass, the right atrium is opened, and the area along the annulus fibrosus that corresponds to the point of early activation along the AV groove is defined. We next fibrillate the heart in order to find more easily the dissection plane between the atrial wall externally and the internal surface of the coronary fat pad. At this point, the heart can be defibrillated and the electrocardiogram monitored as the incision is lengthened. Then the incision through the atrial wall at its insertion into the annulus is closed. Finally, we close the atriotomy incision and stop the extra-
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Fig. 7. The approach to the left or Type A WPW, made through a left lateral thoracotomy, is illustrated in this figure. The incision is shown beginning at the left trigone. This is the point where the mitral valve is continuous with the aorta. Going in a clock-wise direction from this point, there are no more connections between the atrium and the ventricle until the right trigone (central fibrous body) and base of the atrial septum are reached.
corporeal circulation. We believe that mapping should again be done after bypass but before the cannulas to the extracorporeal device are removed. In the new operative technique for a bundle of Kent on the left side, we use a left lateral thoracotomy. We have found that exposure to the interior of such a small atrium is best obtained through the fourth rib or third intercostal space. The venous return to the pump oxygenator is accomplished by putting one outflow catheter in the right ventricular outflow tract and the other in the femoral vein. The approach to the junction of the atrium with the annulus
fibrosus is the same as on the right side. Mapping should be done before the incision in the heart is closed. The results of surgery are summarized in Table II and Fig. 9. We have divided the anomalies on the right (Type B) into three classes: lateral, corresponding to Kent's description; anterior to the membranous septum; and posterior to the membranous septum. We have classified those on the left (Type A) as atrial septal Type A, lateral, and posterior. The posterior bundles are located along the free wall of the ventricle. A good result is considered one in which the electrocardiogram has reverted to nor-
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Fig. 8. This figure illustrates the approach to a right or Type B WPW through a median sternotomy incision. The incision in the atrium, as shown here, is posterior and extends toward the coronary sinus level. It can be carried to the level of the anterior lip of the coronary sinus. At this point the atrial septum would be reached and thus the incision would be at the AV node-His bundle. As we have done, an incision can be started in this same relative position anteriorly and then extended to the opposite or anterior margin of the membranous septum by means of the same plane of dissection.
mal and the patient no longer has supraventricular tachycardia. If atrial flutter-fibrillation was present and should then recur, it must be conducted to the ventricle through the AV node-His system. A fair result is defined as one in which (1) the WPW complex is still present on the electrocardiogram but the patient no longer has episodes of supraventricular tachycardia or (2) there is absence of one-to-one conduction to the ventricle with atrial fibrillation-flutter. A
poor result is defined as one in which there is evidence that the aberrant tract was not divided. Not only is the WPW complex evident on the electrocardiogram, but also the patient still has episodes of dysrhythmia. In our earlier operation, we approached the bundle through the AV groove; with the new operation, the approach is through the atrium . In the former, the ventricle was separated from the annulus; in the latter, the atrium is separated from it.
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* Foilure,newoperalion
A Success
o Failure,old operation • Ebstein's, failure e WPW on EKG clinicol cure
TYPE A, 7 patients Atrial septal, 3 patients Fig. 9. In this diagrammatic drawing of the heart, the location of the Kent bundle for each of our surgically treated patients is shown. We believe the bundles in the septal area along the left annulus fibrosus were in the atrial septum and entered the left side of the ventricular septum, probably following the course of the AV node and His bundle. Thus these tracts did not cross the left annulus fibrosus, as this drawing might indicate.
Table II. Summary of data on patients operated upon for
Wolff-Parkinson-White syndrome Location of tract
No. of patients
Result
Operation Old
New
Cure
Fair
Failure
4 1 2
o
0
Type B
Lateral Anterior septal Posterior septal
4 3 3
2 2 1
Lateral Posterior Atrial septal
5 2
2 2
3
1
2 1 2 Type A 3 0 2
1
1* It
o
5 2 1
2
• Patient died 18 hours postoperatively (old operation). tEbstein's anomaly (new operation).
We were successful in treating 7 of the 10 patients with Type B anomalies. In 1 patient the result was fair, and in 2 patients the operation was a failure. One of the patients with a poor result and the 1 patient with a fair result belonged to the anterior
septal subgroup. With the old operative technique, in spite of wide division of the right lateral ventricular wall at its insertion into the annulus, the bundle was missed in 1 patient; in the other, the bundle must have been partially damaged. From a subsequent
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successful operation via the new approach, we now believe the tracts were close to or adjacent to the anterior part of the membranous septum. The I patient with a poor result in the anterior septal group was the only one to die in this series. The patient was a 39-year-old woman who died 18 hours after the operation from an uncontrollable tachyarrhythmia. Another possible failure occurred in 1 of the 2 patients who had Ebstein's anomaly. The electrocardiogram showed no delta wave for 12 hours after surgery, but subsequently the wave returned. The patient is improved due to insertion of a tricuspid valve to correct valvular insufficiency, but she still has episodes of dysrhythmia. We obtained good results in 5 patients from the Type A group. The bundles were located laterally in all. Results were fair in 2 patients in whom the bundles were in a posterior location and who were operated upon via the old technique. The patients in the atrial septal Type A group have thus far not had correction of the WPW syndrome. Two of the patients in this group had poor operative results and 1 had a fair result, although his follow-up period is short. The latter patient deserves special comment. We thought there was a chance that the Kent bundle might have entered the ventricular septum on the right and surfaced on the left posteriorly, for the distance is such that this could have occurred. At operation, an incision in the right annulus fibrosus was made to a point beneath the middle of the coronary sinus. This did not cause the electrocardiogram to revert to normal. Next the left atrium was exposed through the atrial septum, and the atrium was incised at the annulus all the way to the right trigone, a procedure which likewise failed to obliterate the delta wave. As a last resort, an area in the superior muscular ventricular septum on the left was cauterized with the electrocautery. At our preoperative study, an atrial impulse was conducted one-to-one at well above 200 beats per minute across the anomalous tract with atrial fibrillation and flutter (Fig. 3).
Postoperatively, although the WPW complex was still present, the Kent bundle blocked when a pacing rate of 180 was exceeded. This extensive dissection left undivided only the narrow atrial septum that contained the AV node and His bundle. One group of patients, those in whom the arrhythmias have been prevented but in whom the WPW complexes remain, is a difficult group to explain. However, this situation has been reported by others. Iwa" has noted this in 2 of his 9 patients, and a similar experience in I patient has been reported both by Cole':' and by Lindsay." This type of result could have occurred because the connection was either partially divided or because other smaller connections were present and missed. In regard to the first explanation, it is possible that with only one or two remaining connections of the anomalous bundle to the ventricular muscle, the electrophysiological characteristics may have been so changed that retrograde transmission could not occur. Therefore, circus movement that goes down the AV node and retrograde to the Kent bundle would no longer be possible. It is also of interest that 1 patient (Type A) had a WPW complex in the immediate postoperative period but never had recurrent tachycardia. He was seen by us about 2 years postoperatively. At this time the electrocardiogram was normal, and pre-excitation was ruled out by a His bundle and intracardiac pacing study. In regard to the possibility of other connections, it is well known that there are patients with electrocardiographic evidence of the WPW complex who rarely or never have tachycardia.s- 23 Discussion
From this clinical study we believe we have accumulated undeniable evidence which indicates that the WPW syndrome is caused by a physiologically demonstrable anomalous conduction pathway coursing from the atrium to the ventricle. Although we do not have morphologic evidence to confirm our findings, the clear-cut change in the electrocardiogram and the relief of the patient's
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symptoms permit this conclusion. Our operative experience confirms the fact that the tract can occur anywhere in the area of the AV junction. Thus the observations of Kent-:" and others are correct in that lateral connections or, expressed another way, freewall connections as well as septal ones do occur. In addition to the presence of the tracts around the annulus fibrosus, the anomalous connections can course from the atrium to the ventricle about the area where the atrial septum is adjacent to the membranous septum of the ventricle. By following this pathway, the tract can get to the left side of the ventricular septum without traversing the left annulus. This places the tract adjacent to the AV node. Levu and James" have offered evidence that the pathway for preexcitation may be in this position. Although mapping of the epicardial surfaces has been successful in indicating the location ot' the anomalous tracts, the absence of many good anatomic studies of the bundle of Kent has hampered the planning and execution of the operative procedure. The embryologic abnormality that explains the development of the anomalous tracts is related to the annulus fibrosus." This structure separates the atria from the ventricles. As it develops, it lays down thick connective tissue to form the ring. When the annulus finally becomes fully developed, it obliterates the muscle connections between the atria and the ventricle which are present in the embryo and leaves only the His bundle hiatus intact. If this mechanism is the explanation for the presence of the anomalous tracts, then the possibility exists that there could be more than one tract. Lunel" has presented evidence that this may occur. Wood" also found three tracts in a 1 em. area of the right annulus fibrosus. Boineau-' noted a tract on the right and left in a squirrel monkey. Logically, one would suspect that anomalous tracts would occur along the atrial septum and ventricular septum, the only place where the annulus fibrosus is normally pierced by the AV connections. As has been pointed out, we have found the tracts located anterior to the membranous
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septum and just posterior to the His bundle on the right side. We believe also that a number of these, as found in 3 of our patients, will be adjacent to the AV node and His bundle. Other congenital defects involving the AV valves also occur in conjunction with the WPW syndrome. One patient with a Type A anomaly had a balloon mitral valve. Two other patients in our series of operations had Ebstein's anomaly. The procedure now followed for surgical treatment of WPW requires a large number of highly trained people plus expensive and delicate equipment. In addition, the mapping prolongs the already lengthy procedure. However, the accuracy of surface electrocardiography is such that we cannot completely rely upon it for localization of the side involved. If the latter method were accurate, it would be tempting to proceed directly to the appropriate annulus fibrosus, develop the proper plane, and then extend the incision around until the electrocardiogram became normal. There are several reports, beginning with the ones by Edmonds," Dreifus," and their colleagues, which suggest that this disorder might be palliated by dividing the His bundle and implanting a demand pacemaker. Recently, Hatcher" and Dunaway" have reported the use of this procedure on 3 patients. This is a simple method of controlling the supraventricular tachycardia and can actually be done with a cautery, as Ellison did, without extracorporeal circulation. On the other hand, it is indicated only in a few instances, such as, we believe, in patients with atrial septal Type A anomalies. From information based on our studies of the e1ectrophysiological characteristics of some of the bundles of Kent, we have been concerned about dividing the His bundle yet leaving the Kent bundle, for fear that the patients might stilI be liable to ventricular tachycardia and fibrillation. This possibility exists because patients may have Kent bundles with short refractory periods, which thus can conduct one-to-one when atrial fibrillation occurs. The implications are obvious. We have outlined our experience with
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pacemakers used to induce an extra beat to break the cycle causing the supraventricular tachycardia. This is at best a poor method of treatment and is only indicated in patients with problems that preclude a thoracotomy. Others have had success in locating and either dividing or partially dividing the Kent bundle. Lindsay and colleagues" reported their treatment of 1 patient with a Type B WPW complex located posteriorly. The patient also had mitral valve disease and required valve replacement. The incision was made through the annulus area. The WPW complex recurred temporarily after surgery but later disappeared. The patient has had no further problems with arrhythmias, and a recent electrocardiogram no longer showed the WPW complex. Cole':' has reported his group's experience with 2 patients who had Type B anomalies. In 1 the bundle was in a right lateral position. A wide incision through the ventricular and atrial walls failed to correct the electrocardiographic abnormality, and an attempt to divide the His bundle also failed to produce heart block. This patient, as in some of Iwa's-" and some of our patients, still has the delta wave on the electrocardiogram but no longer has tachycardia. Iwa's second patient had an anterior area of early activation. Interruption of the Kent bundle occurred when the area of the His bundle was manipulated. This suggests, as in our experience, that early ventricular depolarization on the right anterior side may indicate a septal tract. Burchell and associates" made an attempt to divide a right lateral bundle after localizing it with surface mapping. The incision was made away from the annulus. Iwa'" has attempted to correct the WPW syndrome in 9 patients. In 4 patients with Type B disease, the tracts were divided successfully by means of an incision in the region of the AV ring. The operation failed in 4 Type B patients. In the 1 Type A patient, the electrocardiogram was not changed but the number of episodes of tachycardia has decreased. Although there have been failures in the complete correction of the WPW syndrome both in our experience and in that of others,
information and methods are now available to offer nearly all patients with this syndrome a chance for cure. The surgical principles we have learned in treating these patients are stated as follows: 1. Careful electrophysiologic localization at the AV ring ot the earliest area of ventricular depolarization is essential. This is the guide to the bundle of Kent. 2. Early activation of the ventricle, either anteriorly on the right or posteriorly at the septum on the', right and left, may indicate that the Kent bundle is in the septal area. 3. The incision at the annulus fibrosus should be at least 2 em. in length in order to divide any other bundles of Kent that might be in the same area. 4. The surgical incision in the atrium should be adjacent to and against the annulus fibrosus in order to divide the bundle of Kent at its narrowest point. REFERENCES Wolff, L., Parkinson, J., and White, P. D.: Bundle-Branch Block With Short P-R Interval in Healthy Young People Prone to Paroxysmal Tachycardia, Am. Heart J. 5: 685, 1930. 2 Holzmann, M., and Scherf, D.: Uber Elektrokardiogramme Mit Verkurzter Vorhof-Krammer-Distanz und Positiven P-Zacken, Z. Klin. Med. 121: 404, 1932. 3 Wolferth, C. C, and Wood, F. C.: The Mechanism of Production of Short P-R Intervals and Prolonged QRS Complexes in Patients With Presumably Undamaged Hearts: Hypothesis of an Accessory Pathway of Auriculoventricular Conduction (Bundle of Kent), Am. Heart J. 8: 297, 1933. 4 Wood, F. C., Wolferth, C. C, and Geckeler, G. D.: Histologic Demonstration of Accessory Muscular Connections Between Auricle and Ventricle in a Case of Short P-R Interval and Prolonged QRS Complex, Am. Heart J. 25: 454, 1943. 5 Kent, A. F.: Researches on the Structure and Function of the Mammalian Heart, J. Physiol. 14: 233, 1893. 6 Kent, A. F. S.: The Right Lateral Auriculoventricular Junction of the Heart, J. Physiol. 48: 22, 1914. 7 Kent, A. F. S.: Illustrations of the Right Lateral Auriculo-ventricular Junction in the Heart, J. Physiol. 48: 63, 1914. 8 Kent, A. F. S.: A Conducting Path Between the Right Auricle and the External Wall of the Right Ventricle in the Heart of the Mammal, J. Physiol. 48: 57, 1914.
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9 Mann, R. B., Fisher, R. S., Scherlis, S., and Hutchins, G. M.: Accessory Left Atrioventricular Connection in Type A Wolff-ParkinsonWhite Syndrome, Johns Hopkins Med. J. 132: 242, 1973. 10 Durrer, D., and Roos, J. P.: Epicardial Excitation of the Ventricles in a Patient With WolffParkinson-White Syndrome (Type B), Circulation 35: 15, 1967. 11 Burchell, H. B., Frye, R. L., Anderson, M. W., and McGoon, D. C.: Atrioventricular and Ventriculoatrial Excitation in Wolff-ParkinsonWhite Syndrome (Type B), Circulation 36: 663, 1967. 12 Dreifus, L. S., Nichols, H., Morse, D., Watanabe, Y., and Truex, R.: Control of Recurrent Tachycardia of Wolff-Parkinson-White Syndrome by Surgical Ligature of the A-V Bundle, Circulation 38: 1030, 1968. 13 Lindsay, A. E., Nelson, R. M., Abildskov, J. A., and Wyatt, R.: Attempted Surgical Division of the Pre-excitation Pathway in the Wolff-Parkinson-White Syndrome, Am. J. Cardio!. 28: 581, 1971. 14 Cole, J. S., Wills, R. E., Winterscheid, L. C., Reichenbach, D. D., and Blackmon, J. R.: The Wolff-Parkinson-White Syndrome: Problems in Evaluation and Surgical Therapy, Clin. Res. 18: 113, 1970. 15 Dunaway, M. C., King, S. B., Hatcher, C. R., Jr., and Logue, R. B.: Disabling Supraventricular Tachycardia of Wolff-Parkinson-White Syndrome (Type A) Controlled by Surgical A-V Block and a Demand Pacemaker After Epicardial Mapping Studies, Circulation 45: 522, 1972. 16 Iwa, T., Kazui, T., Sugii, S., and Wada, J.: Wolff-Parkinson-White: Surgical Treatment, Jap. J. Thorac. Surg. 23: 513, 1970. 17 Sealy, W. c., HaUler, B. G., Jr., Blumenschein, S. D., and Cobb, F. R.: Surgical Treatment of Wolff-Parkinson-White Syndrome, Ann. Thorac. Surg, 8: 1, 1969. 18 Wallace, A. G., Boineau, J. P., Davidson, R. M., and Sealy, W. c.: Wolff-Parkinson-White Syndrome: A New Look, Am. J. Cardio!. 28: 509, 1971. 19 Cobb, F. R., Blumenschein, S. D., Sealy, W. C., Boineau, J. P., Wagner, G. S., and Wallace, A. G.: Successful Surgical Interruption of the Bundle of Kent in a Patient With Wolff-Parkinson-White Syndrome, Circulation 38: 1018, 1968. 20 Rosenbaum, F. F., Hecht, H. H., Wilson, F. N., and Johnston, F. D.: The Potential Variations of the Thorax and the Esophagus in Anomalous Atrioventricular Excitation (Wolff-Parkinson-White Syndrome), Am. Heart J. 29: 281, 1945. 21 Boineau, J. P., Moore, E. N., Spear, J. F., and Sealy, W. C.: Basis of Static and Dynamic
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23 24
25 26
27
28
29
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Electrocardiographic Variations in Wolff-Parkinson-White Syndrome, Am. J. Cardio!. 32: 32, 1973. Giardina, A. C. V., Ehlers, K. H., and Engle, M. A.: Wolff-Parkinson-White Syndrome in Infants and Children: A Long-Term Follow-up Study, Br. Heart J. 34: 839, 1972. Flensted-Jensen, E.: Wolff-Parkinson-White Syndrome: A Long-Term Follow-up of 47 Cases, Acta Med. Scand. 186: 65, 1969. Lev, M., and Lerner, R.: The Theory of Kent: A Histologic Study of the Normal Atrioventricular Communications of the Human Heart, Circulation 12: 176, 1955. James, T. N.: The Wolff-Parkinson-White Syndrome: Evolving Concepts of its Pathogenesis, Progr, Cardiovasc. Dis. 13: 159, 1970. Truex, R. C., Bishof, J. K., and Hoffman, E. L.: Accessory Atrioventricular Muscle Bundles of the Developing Human Heart, Anat. Rec. 131: 45, 1958. Lunel, A. A. V.: Significance of Annulus Fibrosus of Heart in Relation to AV Conduction and Ventricular Activation in Cases of Wolff-Parkinson-White Syndrome, Br. Heart J. 34: 1263, 1972. Edmonds, 1. H., Ellison, R. G., and Crews, T. L.: Surgically Induced Atrioventricular Block as Treatment for Recurrent Atrial Tachycardia in Wolff-Parkinson-White Syndrome, Circulation 39: 105, 1969 (Supp!. I). Hatcher, C. R., Jr.: Personal communication, 1974.
Discussion DR. TAKASHI IWA Kanazawa, Japan
Dr. Sealy is certainly a pioneer in this particular field of cardiac surgery. [Slide] I operated upon my first patient with WPW syndrome in July, 1969. Since then I have accumulated 9 cases altogether, including 8 cases of Type Band 1 case of Type A. Among many preoperative examinations, epicardial mapping was the most reliable and indispensable to determine the exact location of the accessory pathway. [Slide] However, we have found in our most recent case that the electrical potential of the accessory conduction pathway can be detected by a bipolar electrode, which is applied along the tricuspid annulus ring in the right atrium. A sharp deflection is recorded between the P and delta waves. It indicates precisely the localization of the accessory conduction pathway passed by beneath the atrial endocardium. A very small incision of this area, 2 em. in length in this case, was enough to cure the disease. [Slide] In the serial sections of specimens resected from incised areas, a special muscle bundle was found in 2 cases studied. It is believed that
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this is a Kent bundle because of its localization, running course, and appearance. [Slide] As there are many theories and controversial facts, the WPW syndrome cannot be explained by only a lateral bundle. I must admit that radical surgery is not always satisfactory. Therefore, as an adjunct method, I developed an inductive radio-frequency atrial pacemaker in 1969. Its receiver, of which there are a button type and a catheter type, has been implanted in 12 patients with refractory supraventricular tachycardia. Three of these patients have WPW syndrome. The patients could terminate the tachycardias by applying batterylized transceiver by themselves from outside their bodies anytime and anywhere tachycardia occurred. The applied electrical stimulation rate was between 250 and 500 times per minute and lasted several seconds. This method is more physiological and safer than creation of AV block and implantation of a demand pacemaker. [Slide] With my own experience, along with Dr. Sealy's high rate of success, I am now more inclined to believe that most of the patients with WPW syndrome, in whom medical treatment is not feasible, can be cured by a rather simple operation. The surgical management of arrhythmias, of which WPW syndrome is one, will be a new field in cardiac surgery. DR. SIDNEY LEVITSKY Chicago, 1Il.
I would like to compliment the Duke group on a fine presentation. Recently we had the opportunity to treat a 15-year-old boy at the University of Illinois with severe symptomatic WPW syndrome, Type B. Before operating on this young man, we visited Dr. Sealy in Durham, North Carolina, to observe his operative approach. [Slide] We employed an epicardial mapping system similar to that described by Drs. Sealy and Wallace. The incision across the bundle of Kent occurred at the point of the arrow noted on the slide. Prior to that point, there was a positive delta wave in Lead I and a negative delta wave in Lead II. After the incision, the delta wave disappeared. The month prior to the operation, the patient had over twenty syncopal episodes secondary to tachyarrhythmias. The patient has been totally asymptomatic for 2 months postoperatively. DR. RUSSELL M. NELSON Salt Lake City, Utah
I too would like to express gratitude to Dr. Sealy for this among his many contributions to our specialty. I would like to make a comment about the terminology that is used in this particular area. There is a difference between the electrocardiographic pattern of pre-excitation and the WPW
syndrome. Pre-excitation is the electrocardiographic pattern without tachycardia. When the pre-excitation pattern is coupled with tachycardia, then the name Wolff-Parkinson-White syndrome may be applied. Not everyone with pre-excitation pattern has WPW syndrome, and not everyone with WPW syndrome needs an operation, as has been pointed out in Dr. Sealy's comments. However, for those who intend to perform such an operation, J would suggest that not only Dr. Sealy's work be studied in detail, but also that of Dr. Dirk Durrer of Amsterdam, who has been a pioneer in epicardial mapping. I would like to ask Dr. Sealy one question. In many of these patients, the appearance of the tachyarrhythmias and even of the pre-excitation pattern is intermittent. Is there a way of stimulating the pre-excitation pattern in the operating room? If the heart reverts to the non-pre-excitation pattern at the time of the proposed division of the Kent bundle, the target will have disappeared before the incision is made. DR. SEALY (Closing) I thank the discussers very much. I particularly appreciate Dr. Iwa's contribution to this discussion. He made a special trip from his country to participate. The intermittent nature of the WPW complex on the electrocardiogram is a problem and may be particularly so with Type A WPW. That is why we use an atrial pacer during trapping. I would like to also comment about the incidence of clinical symptoms with this disorder. It has been estimated that between 40 and 60 per cent of patients with a WPA complex will have symptoms. The next problem is determining how many symptoms or how severe the symptoms have to be for the patient to need an operation. For this reason, extensive preoperative studies of the His bundle and of pacing are necessary. I think now that any patient who has had an episode of tachycardia and who, on study, shows evidence of one-to-one conduction across the Kent bundle probably should have an operation. Perhaps in another 20 cases we can be more certain about this. [Slide] There are important problems with the atrial septal Type A anomaly. The conduction tract comes down with AV node-His system. On the right side, these tracts cross the AV valve, and we have been able to divide them in this location. On the left side, the tracts do not cross the annulus of the valve, but rather go along with the AV nodeHis system. We hope that we can separate the AV nodeHis system from the Kent bundle in this group. Once that is accomplished, we can leave the AV node-His system intact and then divide only that part of the septum which contains the Kent bundle.