Surgical treatment of supraventricular tachyarrhythmias

Surgical treatment of supraventricular tachyarrhythmias In this report, we have outlined our experiences with the direct surgical treatment of 16 patients with supraventricular tachyarrhythmias (SVTA). Re-entry supraventricular tachycardia (SVT) was demonstrated by the 4 patients who had retrograde-conducting Kent pathways. The SVT was corrected by the successful division of the Kent bundle in 3 and a partially successful His bundle division in one patient. The remaining 9 patients with re-entry, which included 6 with Kent pathways and WPW, all had His bundle section. The remaining 3 with His interruption had focal tachycardias associated with dysfunction of the atrioventricular (AV) node. Of the 13 His bundle interruptions, nine were successful, three resulted in questionable AV conduction, and one failed. Problems with suture ligation and cautery explained the failures. Cryothermia was the most successful procedure used. However, excision of that portion of the atrium containing the AV node shows promise of being satisfactory. The possibility is discussed of using measures much more precise and less destructive than His bundle interruption for SVTA.

Will C. Sealy, M.D., Robert W. Anderson, M.D., and John J. Gallagher, M.D., Durham, N. C.

Oupraventricular tachyarrhythmias (SVTA) have only recently been considered amenable to treatment by direct operations upon the conduction system. We1, 2 have previously reported on a series of patients with Wolff-Parkinson-White syndrome (WPW) in whom the re-entry supraventricular tachycardia (SVT) was corrected by interrupting the Kent bundle. In another group of our patients with WPW, His bundle division was undertaken, which interrupts the other pathway needed for a re-entry SVT. Other varieties of SVTA, refractory to medical management, have been treated by His bundle division.3' 4 The electrophysiological mechanisms that form the basis for the SVTA may be classified as either focal or re-entrant.5, 6 The focal tachyarrhythmias are due to abnormal firing of cells in the pacemaking and conducting system or in the atrial muscle. Thus they are abnormalities of impulse formation. Focal tachyarrhythmias are of surgical importance only when the From the Divisions of Thoracic Surgery and Cardiovascular Medicine, Duke University Medical Center, Durham, N. C. 27710. Funded partially by National Institutes of Health Grant Nos. HL13920 and HL 15190. This work was done during Dr. John J. Gallagher's tenure as an Established Investigator of the American Heart Association. Read at the Second Annual Meeting of the Samson Thoracic Surgical Society, Banff, Alberta, Canada, June 1-4, 1976.

atrioventricular (AV) node fails to function properly or is bypassed. When normal, the node acts as a protective mechanism preventing a fast ventricular response to a fast atrial rate. Re-entrant SVT occurs when circumstances exist which produce differences in impulse transmission in two pathways in a system; thus it is an abnormality of conduction. The classic example occurs in WPW, in which there is an anomalous second connection, the Kent bundle between the atrium and the ventricle. In this report, we will relate our experience with the direct surgical treatment of 16 patients with SVTA refractory to medical management. Included will be patients in whom re-entrant SVT was corrected by division of one of the dual pathways involved, either the Kent or His bundle. In others, the His bundle was divided to prevent the rapid transmission of atrial impulses through the malfunctioning AV node to the ventricle. In the patients who had His bundle interruption and were left without AV conduction, strict indications were adhered to before surgery was advised. The patient had to have a life-threatening or disabling tacharrhythmia that had been proved to be resistant to medical treatment administered under hospital control. The surgical approach we used to the Kent bundle interruption has been described in other publications. The emphasis in this report will be on the technical problems encountered in His bundle interruption. 51 1

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5 1 2 Sealy, Anderson, Gallagher

Table I Patient Group

Sex

Age (yr.)

Symptoms

Diagnosis

M

19

Tachycardia since 1 yr. of age; congestive failure

Re-entrant SVT by postseptal Kent with only retrograde conduction: fast conduction, AV node, heart rate 160-200/min.

I I I

F M M

40 13 18

Tachycardia; chest pain; syncope Tachycardia Tachycardia; cyanosis

II

F

27

Tachycardia

II

M

15

Tachycardia

Re-entrant SVT by left free wall Kent with retrograde function only Re-entrant SVT by left free wall Kent with retrograde function only Re-entrant SVT by right free wall Kent with retrograde function only: Ebstein's anomaly; patent foramen ovale WPW Re-entrant SVT by postseptal Kent; fast ventricular response to atrial fib./flutter WPW; postseptal Kent

II II II

M F F

68 38 30

II

F

28

Tachycardia; syncope Tachycardia Tachycardia; ventricular fibrillation; syncope Tachycardia; syncope

III III

M F

52 62

III HI

M F

42 42

IV

F

40

Tachycardia; bradycardia Tachycardia; bradycardia; congestive failure Tachycardia; syncope Tachycardia; bradycardia; postop. repair of secundum ASD Tachycardia; syncope

IV

F

36

Tachycardia

WPW; left free wall Kent WPW; two Kent bundles, left free wall WPW; two Kent bundles, postseptal and right free wall; rapid ventricular response to atrial fib./flutter WPW; postseptal Kent; rapid ventricular response to atrial fib./flutter Atrial flutter with fast ventricular response; SA and AV node dysfunction^ James fibers; fast conduction through AV node; atrial fib./flutter; mitral insufficiency Cardiomyopathy; SA and AV node dysfunction; ventricular tachycardiat Sinus node and AV node dysfunction Sinus tachycardia to 200/min.; re-entrant SVT to 300 that progressed to ventricular fibrillation; James fibers Re-entrant SVT probably above AV

Legend: ASD, Atrial septal defect. SVT, Supraventricular tachycardia. AV, Atrioventricular. WPW, Wolff-Parkinson-White syndrome. SA, Sinoatnal.

Clinical material On the basis of electrophysiological abnormalities, our patients were divided into four groups as shown in Table I. Group I. Group I consisted of 4 patients, all of whom had re-entrant SVT because of a Kent bundle, which had the property to conduct only in a retrograde manner (ventricle to atrium). Thus the patients did not have WPW, since there was no antegrade conduction to produce early excitation of the ventricle and a delta wave. The first patient in Group I was a 13-year-old boy who had a life-long history of recurrent episodes of SVT. Control with drugs was not successful. This patient's father had had WPW and died suddenly after starting medication for tachycardia. Electrophysiological studies demonstrated an accessory pathway in the posterior free wall of the left ventricle that would conduct only retrograde. In this patient the retrogradeconducting Kent pathway was identified and successfully divided. He now has normal sinus rhythm with atrial to ventricular conduction by the His bundle. The second patient was 57 years of age. Her problem began 17 years earlier, when she first had SVT as-

sociated with substernal pain and dizziness. Since then, the episodes occurred with increasing frequency associated one time with syncope. Trials with numerous drugs and an overdrive pacemaker did not control the patient's arrhythmia. Electrophysiological studies revealed that the patient had a Kent pathway in the left lateral free wall that would conduct only retrograde. She had successful division of the Kent bundle and has normal atrial to ventricular conduction. The third patient, an 18-year-old man, had had almost constant SVT since birth, with a heart rate that was between 180 to 220 beats per minute. Sinus rhythm had never been noted for more than a few beats. He was tall, muscular, and active in athletics. One year before admission, while he was hiking at an altitude of 12,000 feet, congestive heart failure developed with marked pulmonary edema that was controlled by medical treatment. A year later, while he was again hiking in the mountains, a second episode of failure developed that was much more resistant to treatment. He was observed in our hospital for about 3 weeks, and when his medical program was made less restrictive, congestive failure would again develop. An electrophysiological study demonstrated a posterior septal Kent path-

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Result

Operation

Kent divided Kent divided Kent divided; tricuspid valve replaced.

Marked improvement: tachycardia 120-130/min.; congestive failure controlled; status of His function awaits further study; 12 mo. follow-up; pacemaker No SVT No SVT No SVT

Attempted Kent division; His interrupted by suture and cautery

Sinus rhythm via Kent; no SVT

Attempted Kent division; His interrupted by cautery, suture, and ligation Attempted Kent division; His interrupted by suture Attempted Kent division, one divided; His interrupted by incision Attempted Kent division (right free wall), one divided; His interrupted by excision of AV node Attempted Kent division; His interrupted by suture

Sinus rhythm by Kent; no SVT

His interrupted by excision of AV node

His interrupted with cryothermia His interruption after two attempts with suture and incision; mitral valve replacement His interrupted with cryothermia His interrupted by suture and cautery (oper. 1964) His interrupted by incision, suture, and cautery His interrupted with cryothermia

way that would conduct only retrograde. Owing to the patient's precarious condition and the difficult access to the pathway, the His bundle was interrupted by removal of the A V node. In the postoperative period, the heart rate decreased to 120 per minute, where it has remained. The patient's condition has improved dramatically in the year since his operation. The status of AV conduction and the cardiac pacing focus is uncertain. Another electrophysiological study will be carried out soon. The fourth patient, an 18-year-old man with Ebstein's anomaly associated with severe tricuspid insufficiency and a patent foramen ovale, had almost constant SVT with heart rates of 120 to 140 beats per minute. He was cyanotic and had right heart failure. Electrophysiological studies showed a Kent pathway in the right lateral free wall that would only conduct retrograde. The Kent pathway was successfully divided, the foramen ovale closed, and a prosthetic valve was inserted in the tricuspid position. His condition has been markedly improved since the operation. He no longer has SVT, cyanosis, or right heart failure. Group II. Group II comprised 6 patients, all of whom had WPW and re-entrant SVT (Fig. 1). All in

Sinus rhythm by Kent; no SVT Sinus rhythm by Kent; questionable interruption of His Sinus rhythm by Kent; no SVT; subject to fast ventricular response to atrial fib./flutter Sinus rhythm via Kent; no SVT; subject to fast ventricular response to atrial fib./flutter His rhythm 60/min.; pacemaker His rhythm 40/min.; pacemaker His rhythm 50/min.; pacemaker Failed; SVTA continued; died of multiple pulmonary emboli His rhythm 40-60/min.; pacemaker His rhythm 60/min.; pacemaker

the group had had unsuccessful attempts at division of the Kent bundle. The His bundle was then interrupted. With two exceptions, this group had posterior septal Kent pathways which have been difficult to locate and divide. Two of the patients had a history of syncope. Electrophysiological studies in both showed that a one-toone ventricular response to atrial pacing rates of around 300 beats per minute could be maintained. In addition, both had re-entrant SVT over posterior septal pathways. One of the 2 patients, a 27-year-old woman, had second Kent bundle in the right lateral free wall, in addition to the posterior septal Kent bundle. This condition was of particular interest, since it could be shown that on occasion, during re-entrant tachycardia, the impulse would travel down one Kent pathway and re-enter the atrium by the second Kent bundle. At other times, the impulse would go down the AV node-His bundle system and establish re-entry through the posterior septal Kent pathway. The Kent bundle in the lateral right free wall was divided in this patient, but the posterior septal one was missed. Both of these patients had a successful His bundle division. They are still subject to fast ventricular responses to rapid atrial rates

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— Kent

-Kent

AV NODE ATRIUM

Fig. 1. Diagram showing the pathways in two types of supraventricular tachyarrhythmias that are associated with the presence of dual pathways of atrioventricular conduction. Left, Classic re-entry supraventricular tachycardia with reentry to the atrium by the Kent bundle. This occurred in the patients in Groups I and II. Right, An example of what could be classed as a focal atrial and ventricular tachycardia; In fast atrial flutter, the Kent pathway, which in this instance has a short refractory period, conducts impulses one to one from the atrium to the ventricle bypassing the atrioventricular node. The latter is represented as blocking 3 of the 4 atrial impulses. AVN, Atrioventricular node. H, His bundle.

Table II. Results of His bundle interruption Procedure

No. of pts.

Failure

Questionable

Success

Suture, cautery, incision Excision of AV node Cryothermia

8

1

2

5*

2

0

1

1

3

0

0

3

Totals

13

1

3

9

AV NODE JAMES FIBER

Fig. 2. These two drawings, patterned after those of Childers,6 show re-entry tachycardia occurring in the AV node, so-called dual pathways. The other shows re-entry occurring through a James pathway, which is one that goes directly from the atrium to the His bundle. Similarly, a Mahaim pathway, one that goes from the AV node-His junction or His bundle to the ventricle, bypassing the Purkinge system, can also act as a re-entry pathway.

Table III. Surgical Group: Operation

results

No. of pts.

Failure

Questionable

Success

I Kent His

4 3 1

0 0

0 1

3 0

II His

6 6

0

2

4

III His

4 4

1*

0

3

IV His

2 2

0

0

2

*One patient had two operations.

*Died 10 days postoperatively.

by the Kent pathway, but they no longer have SVT, because the His bundle, the second pathway needed for re-entry, has been ablated. A third patient, a 28-year-old woman with only SVT from a posterior septal Kent bundle, had successful interruption of the His bundle after failure to divide the Kent. Two patients with only SVT underwent attempted interruption of Kent pathways in the left lateral free wall. However, they were treated early in our series, and the operations were failures. One patient, a 43year-old woman, had a Kent pathway in the posterior lateral free wall and a second one in the anterior lateral free wall. The anterior pathway was successfully di-

vided, but the posterior one was not. A second attempt to divide this was not successful, and this patient has had the His bundle interrupted. Although the patient no longer has SVT, we are not certain from the electrocardiogram that the His bundle has been interrupted. The other patient was a 68-year-old man with a Kent bundle in the left lateral free wall who had had repeated episodes of SVT that had proved to be uncontrollable with medical management. At operation, the free-wall Kent bundle was located and temporarily interrupted, but the SVT recurred one week after surgery. He then had successful interruption of the His bundle and insertion of a pacemaker. The sixth patient, who only had SVT, was a 14-

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Fig. 3. Drawing of the interior of the right heart showing the relationship of the A V node (dotted area) and the His bundle to the right fibrous trigone, annulus of tricuspid valve, and membranous septum, which is denoted by the oblique lines. The proximal border of the AV node shows its connections to the surrounding atrium, particularly the atrial septum just as the septum inserts into right fibrous trigone. The His bundle is shown penetrating the right fibrous trigone and the posterior aspect of the membranous ventricular septum. The latter projects into the atrium. The His bundle is a ventricular structure with only the AV node-His junction at the tricuspid ring. (A V node-His bundle junction drawn after Truex.13) year-old boy with a posterior septal pathway that was missed at the first operation. He had a successful His bundle interruption and pacemaker insertion at a second operation. He now has AV conduction by the Kent bundle. All of the patients in this group have demand ventricular pacemakers, which are seldom used because sinus rhythm persists with conduction from the atrium to the ventricle down the Kent bundle. Group III. Group III consisted of 3 patients who had dysfunction of both the AV and sinoatrial (SA) nodes, as well as episodes of focal SVTA. The problem that brought them to surgery was a fast ventricular rate response to SVTA that was impossible to control with medication. Thus the AV node malfunction was the indication for surgery. The first patient was a 52-year-old man with a 30 year history of SVTA that with time became increasingly resistant to medication. Even minimal exercise would precipitate an attack. He had experienced two syncopal episodes. The admission diagnosis was WPW. Electrophysiological studies showed only sinus node and AV nodal dysfunction, as well as a rate-dependent left bundle branch block; a Kent bundle was not dem-

onstrated. During tachycardia, the rate varied from 150 to 160 beats per minute but would be followed occasionally by episodes of bradycardia with rates recorded as low as 40 beats per minute. Sinus node recovery time was markedly prolonged. With provoked atrial fibrillation and flutter, there would occur a rapid ventricular response of more than 200 beats per minute. Owing to failure of drug control and to complete disability, His interruption was carried out successfully by freezing the area where His deflections were found on electrophysiological mapping to —60° C. for 90 seconds with a special cryothermia unit. A pacemaker was inserted, and he has now returned to full activity. The second patient was 61 years old and had a history of rheumatic heart disease that began at the age of 5 years. For the past 17 years, she had had episodes of atrial fibrillation and flutter that had become more frequent and troublesome. On one occasion, the irregular heart rate was associated with syncope. The condition was refractory to careful medical management. An electrophysiological study showed that, during atrial flutter, there was a ventricular response of 180 to 200 betas per minute which, on cessation, was followed by rates as low as 30 beats per minute, indicating dysfunction of both the sinus and AV nodes. Pacing of the His

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Fig. 4. This drawing illustrates a precise surgical method for His bundle interruption and, except for cryothermia, may be the only certain way for safe complete interruption of AV conduction. B, The muscular ventricular septum is shown by the transverse muscle fibers. The left A V junction and left atrial wall can be seen, represented by the muscle bundles at right angles to those on the muscular septum. This is a free space anterior to the coronary sinus. The irregular muscle fibers on the section partially excised are the divided attachments of the atrial septum to the right trigone, which is the small glistening area just above the membranous septum. The atrial septum has to be completely separated from the fibrous trigone. The posterior sinus of Valsalva is exposed and all atrial fibers on it and the trigone must be divided. Exit from the heart may occur here. The rectangle of tissue can be removed and the area easily repaired. bundle caused pre-excitation of the ventricle at rates up to 130 beats per minute by what was thought to be a James fiber, which is a connection from the atrium to the His bundle bypassing the AV node. Cardiac catheterization showed significant mitral insufficiency. This patient had mitral valve replacement followed by an attempted His interruption with multiple sutures. At a second attempt His bundle interruption was successful. An incision was begun above the tricuspid annulus and carried across the insertion of the atrial septum into the right trigone. The ventricular rate is now controlled with a pacemaker and she is back to full activity. The third patient had had attempted His bundle interruption in 1964. Seven years previously, she had an atrial septal defect closed. Although examined before modern electrophysiological studies were possible, she was thought to have both sinus and AV node dysfunction. His bundle interruption was attempted by suture and electrocauterization. Sinus rhythm returned in 24 hours. She died 12 days later from pulmonary emboli. The fourth patient was a 42-year-old man who was well until 1974, when he began to have frequent and severe episodes of SVTA in addition to runs of ven-

tricular tachycardia. The various episodes became more frequent and resistant to medical management. He had to be resuscitated from one episode of ventricular tachycardia associated with syncope. Electrophysiological study showed slow sinus node recovery time, AV node dysfunction, and slow conduction in the His-Purkinje system. The heart was markedly enlarged, and he was thought to have cardiomyopathy. Coronary arteriography showed no abnormalities, but global ventricular dysfunction was noted with increase filling pressures and a depressed ejection fraction. The His bundle was successfully interrupted with a cryothermia unit, and an artificial pacemaker was installed. This has successfully controlled the multiple arrhythmic episodes. Group IV. Group IV consisted of 2 patients who had uncontrollable re-entrant SVT originating above and/or in the AV node refractory to medical management (Fig. 2). The first patient was a 39-year-old woman who began having SVT with increasing frequency in 1963, with rates recorded as high at 250 to 300 beats per minute. She had several episodes of syncope that ac-

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AVNode

bicuspid Valve

\Tricuspid Valve

Fig. 5. Drawings from sections through the septum at a point just before the AV node changes to the His bundle, patterned from our observations and those of James. "Left, Posteriorly at about the beginning of the right trigone. Right, The AV node just before the His bundle emerges from it and penetrates the trigone. The aortic wall is shown here with the A V node adjacent to it. The complications that could follow either cauterization and freezing too deeply are easily understood. A deeply placed suture in this area could transfix the posterior cusp of the aortic wall. companied the fast heart rate. When in sinus rhythm, the rate was still fast, being 160 to 180 beats per minute. With programmed atrial stimulation, the SVT could be induced and reverted. Occasionally, at the end of the SVT, runs of ventricular tachycardia occurred. The time required for an impulse to go from the atrium to the His bundle was short, as was the time required for an impulse to go from the His bundle to the ventricle. It was felt that this patient had dual A V conduction, meaning that there were two parallel pathways in the AV node-His system or that a James pathway was present which bypassed the AV node. She had sinus tachycardia and ventricular fibrillation secondary to SVTA. This patient had His bundle interruption by suture, electrocauterization, and incision. She is now back to full activity with a demand pacemaker. The second patient was a 27-year-old woman with a history of extreme obesity for which she had been treated with an ileojejeunal bypass one year prior to her referral to Duke University. Since the age of 18 years she has had repeated episodes of atrial fibrillation and supraventricular tachycardia. During atrial fibrillation, the ventricular rates were as high as 200 beats per minute, and SVT resulted in rates between 160 and 210 beats per minute. She had frequent syncopal attacks, and during hospitalization she had five or six episodes of SVT per day with rates ranging from 160 to 210 beats per minute. By electrophysiological study, this patient had re-entrant SVT originating above the AV node. Despite vigorous medical management, the SVTA could not be controlled. This patient had a suc-

cessful His bundle interruption with a cryothermia unit followed by insertion of a pacemaker. She is now back to full activity. Surgical treatment In previous reports, we have described the method for interrupting the bundle of Kent. This procedure has been used successfully in our last 25 patients with WPW and was utilized on 3 of 4 patients included in this report who had re-entrant SVT by way of a retrograde-functioning Kent pathway. Division of the His bundle is almost as difficult as division of the Kent (Tables II and III). Although we followed both the laboratory and clinical methods reported by others, we have not always found them to be satisfactory.7-12 For this reason, we investigated this problem in the laboratory. These studies, plus those of Truex and Smythe,13 Walls,14 Widran and Lev,15 Lie's group,16 James,17' 18 Hackel, 19 Titus,20 Anderson and Becker,21'22 and Kistin,23 form the basis for the following description. The AV node is located in the right atrial wall and the atrial septum anterior to the coronary sinus and superior to the tricuspid annulus (Fig. 3). Its length is from 5 to 8 mm., its width 3 mm., and its thickness 1 mm. Its proximal portion, which is in the right atrial wall, has indistinct borders, but at its distal end, where it enters the atrial septum, it becomes more compact. Just as it reaches the right fibrous trigone, it becomes the His bundle (AV bundle). Then the His bundle, which is 2 mm. long, passes through the trigone and

5 1 8 Sealy, Anderson, Gallagher

penetrates or goes behind the membranous ventricular septum where the branches to the left ventricle quickly emerge. The relationship of the AV node-His bundle junction to the surrounding structures has important bearings on the surgical approach. The membranous ventricular septum rides high in the right atrium, and where it inserts into the right fibrous trigone, it is higher than the tricuspid annulus. This explains why an incision through the right atrium above the tricuspid annulus, even when carried to the membranous ventricular septum, may fail to interrupt the His, for the His bundle has already entered the ventricle at this point. The AV node, just before becoming the His bundle, is in the atrial septum. The latter structure, as it inserts into the right fibrous trigone, is less than 1 cm. in width with its anterior portion located underneath the epicardium. The posterior aspect of the atrial septum at its insertion into the right trigone can be exposed by making an incision through the entire thickness of the right atrium, 2 mm. above the tricuspid annulus in front of the coronary sinus (Fig. 4). This gives entry into a triangular space with left atrium on the opposite side and muscular ventricular septum in the floor. The apex is made by the tricuspid and mitral rings joining together at their insertion into the right fibrous trigone. From this position, the atrial septum can be dissected from its insertion into the trigone. Just above the right trigone, the AV node rests upon the central fibrous body and underneath the right atrial endocardium, as shown in Fig. 5. It is obvious that too vigorous cauterization with the electrocautery will damage the aorta, as we have noted in our laboratory, or deep sutures placed blindly for His bundle interruption can transfix the posterior aortic cusp. Because of connections from the anterior part of the atrial septum to the AV node, sutures placed for interruption must include all of the septum just above the fibrous trigone, or they will fail. During the operation, the His bundle can be identified by electrophysiological mapping of the interior of the right atrium.24 Since the His bundle is not an atrial structure, the His deflections obtained are ones on the right trigone and the membranous septum. The AV node, of course, cannot be identified in this way. The point where AV conduction is interrupted determines the eventual heart rate, so that it is important to divide the His bundle just at the AV junction. For example, the His bundle before branching may have a pacing rate of 40 to 60 beats per minute, whereas the bundle branch may have one of 35 to 60 beats per minute.6 The procedures for His bundle interruption used in

The Journal of Thoracic and Cardiovascular Surgery

our patients include the recommended ones of others as well as the one devised at our hospital (Tables II and III). Cardiopulmonary bypass was used, and all patients had electrophysiological mapping to identify the His bundles. Mattress sutures for interruption were used in one patient who had a mitral valve replacement, which gave us easy access to the atrial septum. Five sutures were placed through the atrium just above the mitral annulus, which emerged just above the tricuspid annulus on the opposite side. AV conduction was not interrupted. In retrospect, it was obvious that the sutures had not gone far enough anteriorly in the atrial septum, so that they missed the connection between the atrium and the AV node, just before the AV node changed to the His bundle and the latter penetrated the right fibrous trigone. Finally, an incision through the tricuspid ring and the attachment of the atrial septum to the right fibrous trigone resulted in AV block. Other patients had cauterization of the area in addition to suture placement. An insulated needle with a 1 mm. point was used, with several burns placed in the atrium beginning anteriorly to the coronary sinus and extending up onto the membranous septum. It was surprising how many times cauterization had to be done in addition to suturing before the pathway was successfully interrupted. In 2 of the patients we excised a portion of the right atrium bounded by the coronary sinus and the right trigone and including a portion of the atrial septum. However, we were successful in only one, the result being doubtful in the other. The most success was obtained in 3 patients who had the His bundle frozen with a cryothermia unit devised by Gallagher and Harrison.25 The His bundle was first identified, and all areas where a His electrogram could be demonstrated were frozen to —60° C. for 90 seconds. This included an area from the right fibrous trigone down to the membranous ventricular septum. Usually, the area included two or three circles of about 1 cm. in diameter. If a special cryothermia unit is not available, it is suggested that all of the area containing the AV node be excised as shown in Fig. 4. The incision should begin 2 mm. above the annulus of the tricuspid valve and carried to the membranous ventricular septum. The triangular space is entered on top of the muscular ventricular septum. The incision should then be carried upward at the point where the membranous ventricular septum is reached, so that the right fibrous trigone is exposed. At this point, one can then remove the attachment of the atrial septum to the right fibrous trigone. The rectangle of atrial tissue can be removed

Volume 73 Number 4 April, 1977

and the atrial wall repaired. All atrial fibers should be dissected away from the right fibrous trigone. This should save all of the His bundle and give the highest inherent pacing rate in this structure. AV conduction and ventricular to atrial conduction should be evaluated carefully at the end of the procedure by pacing of both the atrium and ventricle. If an antegrade-functioning Kent bundle is present, the interpretation of the result of His interruption can be difficult, for sinus rhythm may still be present. However, when conduction is by the His bundle, the appearance of the "blocking action" of the AV node will be evident at higher pacing rates. Discussion In this paper, we have reported our experience with the direct surgical treatment of SVTA of both the focal and the re-entrant type. The classic example of the re-entrant SVT was illustrated by the patients with Kent bundles. The presence of a normal and an anomalous pathway, which may have different electrophysiological characteristics, are ideal for a re-entry tachcardia. A premature atrial beat usually starts the SVT. First, the premature impulse travels down the AV node-His bundle system, for the AV node frequently has a shorter refractory period than does the Kent. The Kent bundle, in the meantime, becomes excitable and the impulse re-enters the atrium by the Kent and travels back down the AV node-His system. In the electrophysiology laboratory, an induced premature stimulus will both produce and interrupt the re-entry. The fact that in WPW the two pathways used for reentry are widely separated and can be identified by electrophysiological mapping makes definitive surgery possible. It gives the surgeon two options, for either the Kent or the His bundle may be interrupted. In patients with Kent pathways that conduct antegrade and retrograde, sinus rhythm remains after Kent interruption; however, after His bundle division, a demand pacemaker is still needed, for conduction down the Kent pathway is not completely reliable. SVT's of the re-entrant type that are not associated with Kent connections are less well defined.26'27 They are thought to occur in the SA node and the atrium, in the AV node alone, and in the AV node and His bundle. There were two examples in this series. In one, the mechanism was thought to be located just above the AV node and the second one within the node. Both patients had to have interruption of the bundle of His. SVTA's that are focal in origin are more difficult to delineate by electrophysiological study. A premature stimulus may initiate the tachyarrhythmia but, in con-

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trast to re-entrant SVT, will not interrupt it. It is also very likely that multiple foci are present, a condition which precludes any possibility of a local excision of a focus. If the point of origin of the focal tachycardia is proximal to an A V node with normal filtering function, the SVTA will unlikely be considered for His division. The 4 patients belonging to this group all had AV node dysfunction. Thus, in these patients, the operation was done because of A V node dysfunction during tachycardia rather than for the atrial tachyarrhythmia. Two of our patients with classic WPW had a Kent pathway that transmitted atrial impulses almost one to one during atrial fibrillation and flutter. This, in effect, was a focal tachyarrhythmia involving the atrium and ventricle, for the AV node was completely bypassed with a pathway very likely composed of working myocardium. The His bundle division in these 2 patients did not protect them from a life-threatening arrhythmia that might occur with atrial flutter and fibrillation. Interruption of the His bundle would appear to be a simple surgical procedure. On the basis of the experience of most cardiac surgeons, the His bundle is harder to avoid than to injure. As one becomes more familiar with its location, deep within the fibrous skeleton of the heart, it becomes obvious that the His division by incision or suture ligature will not be successful in all patients, even though in the dog, in which heart is much smaller, this is more frequently successful. Only a small strand of atrial muscle connected to the AV node-His bundle junction is needed to continue AV conduction. Destruction of the His bundle by cautery has been reported and was used by us with varying success. Our laboratory experiences indicate that if the area shown to contain the His bundle by electrogram is cauterized too deeply, the aortic wall over the posterior sinus of Valsalva can be damaged. In this regard, a mattress suture in the same place can transfix an aortic valve leaflet. The use of cyrothermia delivered with a special unit and probe has proved to be an effective method of His destruction in 3 patients. The procedure preserves the strength of the collagen fibers until the area is replaced with scar, and the freezing process does not extend through the aortic wall. The area of block is much larger than can safely be obtained with an electrocautery. Another successful laboratory method for interruption of the His bundle is the excision of the part of the right atrium and the atrial septum that contains the AV node. This approach will save all of the His bundle, so that the patient is left with the highest possible inherent

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His pacing rate. This procedure is uniformly successful in dogs and has been successful in one patient, but with an uncertain result in another. The precise surgical approach to interruption of the His bundle raises the possibility of saving some atrial pacemaking function in certain tachyarrhythmias. As we have demonstrated in our laboratory, the AV node can be excluded along with a small rim of atrium from the remainder of the atrium in dogs by means of inflow occlusion and hypothermia. It should be possible to save even a portion of the AV node. This would seem feasible for tachyarrhythmias that originate above the AV node. The remaining atrial tissue around the node may be inadequate to sustain a tachycardia or a flutterfibrillation pattern. The application of these precise experimental procedures to other tachyarrhythmias can be done only when electrophysiological diagnosis becomes more accurate. However, an operation that will preserve an atrial pacemaker may make the surgical treatment of SVTA more successful and more widely used in the future. Summary In this report, we have outlined our experiences with the direct surgical treatment of 16 patients with SVTA. The re-entry SVT was demonstrated by the 4 patients who had retrograde-conducting Kent pathways. The SVT was corrected by the successful division of the Kent pathway in 3 and a partially successful His bundle division in one. The remaining 9 patients with re-entry, which included 6 with Kent pathways and WPW, all had His bundle section. The remaining 3 with His interruption had focal tachycardias associated with dysfunction of the AV node. Of the 13 His bundle interruptions, nine were successful, three have resulted in questional AV conduction, and one failed. Problems with suture ligation and cautery explained the failures. Cryothermia was the most successful procedure used. However, excision of that portion of the atrium containing the AV node shows promise of being satisfactory. The possibility is discussed of using measures much more precise and less destructive than His interruption for SVTA. Addendum The third patient in Group I had a second operation 17 months after the first. The atrial septum was completely severed from its connection with the right fibrous trigone. He now has complete AV block. REFERENCES 1 Sealy, W. C , and Wallace, A. G.: The Surgical Treatment of the Wolff-Parkinson-White Syndrome, J. THORAC. CARDIOVASC. SURG. 68: 757,

1974.

2 Sealy, W. C , Gallagher, J. J., and Wallace, A. G.: The Surgical Treatment of the Wolff-Parkinson-White Syndrome: Evolution of the Improved Methods of Identification and Interruption of the Kent Bundle, Ann. Thorac. Surg. In press. 3 Garcia, R., and Arciniegas, E.: Recurrent Atrial Flutter: Treatment With a Surgically Induced Atrioventricular Block and Ventricular Pacing, Arch. Intern. Med. 132: 754, 1973. 4 Gooch, A. S., Jan, M. A., Fernandez, J., Fertig, H., Morse, D., and Maranhao, V.: Uncontrolled Tachycardia in Atrial Fibrillation: Management by Surgical Ligature of AV Bundle and Pacemaker, Ann. Thorac. Surg. 17: 181, 1974. 5 Wellens, H. J. J.: Electrical Stimulation of the Heart in the Study and Treatment of Tachycardia, Baltimore, Md., 1971, University Park Press. 6 Childers, R.: Classification of Cardiac Dysrhythmias, Med. Clin. North Am. 60: 3, 1976. 7 Alabaster, C. E.: A Method of Producing Permanent Complete Atrioventricular Block in the Rat, Br. J. Pharmacol. 46: 581-P, 1972. 8 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 AV Bundle, Circulation 38: 1030, 1968. 9 Edmonds, J. H., Jr., Ellison, R. G., and Crews, T. L.: Surgically Induced Atrioventricular Block as Treatment for Recurrent Atrial Tachycardia in Wolff-ParkinsonWhite Syndrome, Circulation 39, 40: 105, 1969 (Suppl. I). 10 Mayer, J. H., Ill, Almond, C. H., Andio, H., Seaber, A. V., and MacKenzie, J. W.: Complete Heart Block: Treatment by Pedicle Grafting of the Sinoauricular Node to the Right Ventricle, Arch. Surg. 94: 90, 1967. 11 Meakins, J.: Experimental Heart Block With Atrioventricular Rhythm, Heart 5: 281, 1914. 12 Starzl, T. E., and Gaertner, R. A.: Chronic Heart Block in Dogs: A Method for Producing Experimental Heart Failure, Circulation 12: 259, 1955. 13 Truex, R. C , and Smythe, M. Q.: Reconstruction of the Human Atrioventricular Node, Anat. Rec. 158: 11, 1967. 14 Walls, E. W.: Dissection of the Atrioventricular Node and Bundle in the Human Heart, J. Anat. 79:46, 1945. 15 Widran, J., and Lev, M.: The Dissection of the Atrioventricular Node, Bundle and Bundle Branches in the Human Heart, Circulation 4: 863, 1951. 16 Lie, J. T., Rosenberg, H. S., and Erickson, E. E.: Histopathology of the Conduction System in the Sudden Infant Death Syndrome, Circulation 53: 3, 1976. 17 James, T. N.: Morphology of the Human Atrioventricular Node, With Remarks Pertinent to its Electrophysiology, Am. Heart J. 62: 756, 1961. 18 James, T. N.: Cardiac Conduction System: Fetal and Postnatal Development, Am. J. Cardiol. 25: 213, 1970. 19 Hackel, D. B.: Anatomy and Pathology of the Cardiac Conducting System, Chap. 11, The Heart, 1974, Interna-

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tional Academy of Pathology, Monograph No. 15, p. 232. Titus, J. L.: Anatomy of the Conduction System, Circulation 47: 170, 1973. Anderson, R. H., Becker, A. E., Brechenmacher, C , Davies, M. J., and Rossi, L.: The Human Atrioventricular Junctional Area: A Morphologic Study of the Atrioventricular Node and Bundle, Eur. J. Cardiol. 3: 11, 1975. Becker, A. E., and Anderson, R. H.: Morphology of the Human Atrioventricular Junctional Area, in Wellens, H. J. J., Lie, K. I., and Janse, M. J., editors: The Conduction System of the Heart, Philadelphia, Pa., 1976, Lea & Febiger, Publishers, p. 263. Kistin, A. D.: Observations on the Anatomy of the Atrioventricular Bundle (Bundle of His) and the Question of Other Muscular Atrioventricular Connections in Normal Human Hearts, Am. Heart J. 37: 849, 1949. Dick, M., II, Krongrad, E., Antar, R. E., Ross, S., Bowman, F. O., Jr., Malm, J. R., and Hoffman, B. F.: Intraoperative Recording of the His Bundle Electrogram in Man: An Assessment of its Precision, Circulation 53: 224, 1976. Gallagher, J. J., and Harrison, L.: Personal communication. Bigger, J. T., Jr., and Goldreyer, B. N.: The Mechanism of Supraventricular Tachycardia, Circulation 52: 673, 1970. Moe, G. K., Preston, J. B., and Burlington, H.: Physiologic Evidence for a Dual AV Transmission System, Circ. Res. 4: 357, 1956.

Discussion D R . R O G E R R. E C K E R Oakland, Calif.

Ordinarily, we ask our authors to find a discusser. However, since Dr. Sealy is far from our area and was not able to find one who would be at the meeting, he suggested Dr. William Bloomer. I am going to read to you the discussion that Dr. Bloomer was able to forward to me. I asked numerous surgeons in our area what they did when they had a patient with these arrhythmias, and they all said they sent them back to North Carolina. Very few people in our area are doing this kind of work. The excellence of the electrophysiological studies that the cardiac catheterization technicians do in Durham, along with the surgical expertise of Dr. Sealy and his group, has attracted patients from across the country.

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trollable with the usual medications. The patient was 65 years old and had had episodes of substernal pressure with pain radiating into the left arm associated with episodes of tachycardia. She had required an average of four to six hospitalizations per year for the preceding 3 to 4 years. A diagnosis of idiopathic hypertrophic cardiomyopathy had been made after an endocardial biopsy at Stanford, and superimposed upon this were tachy-bradyarrhythmias. An Omni Stanicor endocardial pacemaker was placed in the right ventricle in June of 1974 in the hope that the atrial arrhythmias could be suppressed by drugs. However, despite the administration of digoxin to levels of near toxicity, and although all combinations of the usual medications were used, these were found to be of no avail. Supraventricular tachycardia developed despite a combination of 240 mg. of Inderal daily plus Dilantin and Quinaglute. At this point, we then decided to follow Dr. Sealy's lead and to produce AV block surgically. At the time of operation, performed in April 1975, Dr. Messenger scrubbed in after we had opened the right atrium, to determine whether a His bundle recording catheter would be of help in identifying the bundle. He found it was possible to obtain His bundle recordings on the ventricular side, but this technique did not appear helpful on the atrial side, where Dr. Sealy had told us it was preferable to section the AV bundle. Accordingly, an incision was made in what was taken to be anatomically the appropriate place. The incision began approximately halfway between the coronary sinus and the central fibrous body, a few millimeters proximal to the tricuspid annulus, and continued toward the central fibrous body turning up toward it in a hockey-stick fashion. At this point, as we approached the central fibrous body, the electrocardiogram showed the development of total A V block. Stimulating electrodes were then applied to the right atrium to produce atrial tachycardia. The ventricle was shown to continue its idioventricular rhythm as dictated by the cardiac pacing lead that was already present. Postoperatively, the patient has done well over the past 22 months since the operation. For the first time in 10 years, she has been free of cardiac symptoms and has not required any hospitalization. We have been quite impressed by this one example of the potential value of this approach that Dr. Sealy has described for certain selected cases that otherwise defy management with a combination of medication and pacemakers. We believe this approach will have an increasingly important place in the thoracic surgeon's armamentarium. DR. J A M E S W. C A L V I N

DR. W I L L I A M E. B L O O M E R Long Beach. Calif.

[Discussion read by Dr. Ecker.] We have had experience with a case that indicates how effective Dr. Sealy's approach can be. In June of 1974, I was asked by Dr. John Messenger at Long Beach Memorial Hospital to examine a patient who had sick sinus syndrome with tachycardias that had been uncon-

Ventura, Calif.

[Slide] Another surgical technique, an indirect one, to be considered for some medically resistant atrial and nodal tachycardias uses pacing equipment to accomplish overdrive suppression of re-entrant pathways by rapid pacing of the atrium, not the ventricle, via the induction technique. Although this maneuver does not directly attack the pathological anatomy, as Dr. Sealy has shown us how to do,

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it is nonetheless clinically effective. Kahn and Citron have recorded success in 17 of their group of 18 closely followed patients, which includes my personal series. [Slide] Easy application of the necessary stimulating voltages to the atrial chambers has only recently been made possible by the development of new leads. One of these is an experimental "pinch-on" electrode, which is easily applied with the aid of a simple plastic applicator tool and a standard right-angle surgical clamp. My experience is with the epicardial approach, for which a 2 inch skin incision and a limited mediastinotomy provide sufficient intrapericardial exposure. [Slide] Of course, elaborate preliminary testing of atrial pacing with confirmation of noncapture of the ventricle at these rapid rates and perhaps with His bundle electrograms are necessary to select appropriate candidates. However, results such as these [slide] can be obtained. In this instance, 3 or 4 seconds of stimulation at 300 beats per minute with sudden cessation converted paroxysmal atrial tachycardia to atrial fibrillation; the latter is a dysrhythmia of lesser consequence and is usually self-limiting. More often, there is immediate restoration to normal sinus rhythm with dramatic clinical relief. [Slide] This patient's history was similar to that of the patient just described by Dr. Ecker. Now that easy-to-apply electrodes are available, and a simple surgical technique has been developed, intermittent, rapid atrial pacing with a radiofrequency pacemaker, with sudden cessation for refractory supraventricular tachycardias, deserves further clinical trials. DR. PAT O. D A I L Y San Diego, Calif.

I would like to congratulate Dr. Sealy for his very significant, basic contribution in dealing with this very difficult and relatively rare problem. His very lucid descriptions and delineation of the electrophysiological concepts involved, the anatomy of this area, and the surgical approaches have perhaps made it possible for some of us on the West Coast to stop sending our patients to Durham, North Carolina. His operative experience with 64 patients now certainly qualifies him as the pioneer for ablative surgery for patients with supraventricular tachycardia refractory to medical management. My first, rather frustrating, experience with this kind of surgery was observing an experienced cardiac surgeon 8 or 9 years ago attempting to perform this procedure, that is, interruption of the His bundle. After a considerable period of time, during which the surgeon made numerous incisions in a variety of locations in the right atrium, the patient persisted in having normal sinus rhythm. For some reason, though, I have not really had much trouble myself with this. I recall a patient who had bacterial endocarditis of the aortic valve in whom I decided to position the aortic valve a bit lower than usual. Perfect AV block resulted.

The Journal of Thoracic and Cardiovascular Surgery

My only experience with a different kind of surgery related to this problem was much like that just described by Dr. Calvin—the use of radiofrequency pacemakers which the patient controls for overdrive pacing to break these supraventricular tachycardias. My experience along with Dr. John Ross in San Diego, California, has been limited, but it has been very effective in terms of dealing with this problem. I would like to ask Dr. Sealy if this approach was used in any of his patients prior to his technique of ablative surgery or whether it has been used as an alternate approach in some patients. Also, I would like to ask if he has attempted to approach the conducting system through the aortic root in the area of the membranous septum that lies beneath the commissure between the right and noncoronary leaflets of the aortic valve. It seems that this would be a relatively easy place to approach this area, certainly in my prior experience. The question would involve whether or not the incision would be too low in the conducting system. However, this might be another approach, since at least for some people the atrial approach has not been terribly easy. D R . S E A L Y (Closing) I appreciate very much Dr. Ecker and Dr. Bloomer's discussion. Our last patient treated by His bundle interruption had almost exactly the same history summarized by Dr. Ecker. Among the approximately 150 to 160 patients with WPW examined at Duke University, pacemakers for the control of the tachycardia have been used on 7. Most of them were treated several years ago before we were confident that we could interrupt the Kent bundle on the left side. The rationale for use of pacemakers is based on one of the diagnostic measures used for determining whether a patient has re-entrant tachycardia. A characteristic of a re-entrant tachycardia is the ability to produce it or revert it by an extra stimulus. In patients with re-entrant SVT, the pacemaker is used to put in a random atrial stimulus which interrupts the re-entrant tachycardia. Either a demand ventricular pacemaker or radiofrequency-activated atrial pacemaker can be used in patients with WPW. We have placed the radiofrequency-activity pacemaker in 6 patients. Dr. Daily's suggestion that we approach the His bundle from the aorta is interesting. The left bundle is supposed to have an anterior and posterior fascicle. However, it really emerges from the common bundle like the bristles on a brush. Thus, there are no demonstrable common bundles or fascicles on the left side, and one would have difficulty in dividing the His bundle from this approach. The use of freezing with a cryothermic probe for His division has been successful, but the instrument is a special one. Therefore, unless this particular instrument is available, it will be necessary to excise the A V node-His bundle junction.