It appears too early for definitive assessment. of the long-term effectiveness of these various approaches, and further investigation

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1 arrhythmias were not associated with coronary artery disease. The pathophysiological concepts elaborated from this clinical setting were later extended to ventricular tachycardia that complicated myocardial infarction. The method has demonstrated two principal types of findings: (1) the presence of unexpectedly abnormal delayed activity in localized areas of the heart, which favor the concept of intramyocardial reentry, and (2) the epicardial activation pattern of the heart during the arrhythmia. Consequently, the first surgical procedure consisted of a full-thickness incision of the myocardial wall at the point of earliest activation during ventricular tachycardia. This procedure, which proved useful in some idiopathic ventricular tachycardias, was then attempted for use in ventricular tachycardias complicating myocardial ischemia. With this technique, however, treatment was successful in only one case. The explanation for the failures appears to be based on both experimental and clinical data, demonstrating that most ventricular tachycardias after myocardial infarction originate in the subendocardial layers and in the septum, areas generally distant to the epicardial breakthrough of the arrhythmia. Subsequently, we developed the "endocardial encircling ventriculotomy" to exclude the possibility that diseased myocardium at the ischemic border zone could be responsible for the genesis of the arrhythmia. Investigators in Pennsylvania demonstrated an endocardial origin of arrhythmias through preoperative endocardial mapping and used a new procedure incorporating a subendocardial resection. Both of the latter procedures have led to interesting and beneficial results; most patients, previously incapacitated, have had no recurrence and are not on antiarrhythmic drugs. Despite the spontaneous evolution of the disease process, however, it is our opinion that the main problem at present seems to be related to cardiac contractility. Some patients have progressed to intractable cardiac failure and others have tolerated the operation poorly. Experimental studies at Duke University suggest that a new technique, employing cryosurgery, may be less deleterious. It appears too early for definitive assessment of the long-term effectiveness of these various approaches, and further investigation in this field is certain to be forthcoming. Surgical Treatment of Tachycardias in Preexcitation Syndromes Will C. Sealy, M.D., Professor of Thoracic Surgery, Division of Thoracic Surgery, Duke University Medical Center, Durham, U.S.A. T HE SURGICAL correction of patients with tachycardias accompanying the preexcitation syndromes occupies a unique position in the evolution of the direct surgical treatment of arrhythmias. This story begins with Kent, who was the first to recognize that atrioventricular conduction in mammals was myogenic. However, instead of one connection, as described a short time later by His, Kent believed other normal pathways were present. Wood and Wolferth used the theory of Kent to explain the preexcitation of the Wolff-Parkinson-White (WPW) syndrome; Texas Heart Institute Journal 451

2 and, unquestionably guided by the clarity of Kent's illustrations, they focused their attention to the right free wall in the postmortem study of the heart of a boy known to have had the WPW syndrome. They discovered a pathway in the right free wall. In 1968, when it was necessary to interrupt an accessory connection in a man with uncontrollable supraventricular tachycardia due to a type B Kent bundle, the guide to a successful operation was the accurate observations of Wood, based on the misconception of Kent. From a morphologic and thus a surgeon's viewpoint, the preexcitation syndromes can be divided into three groups. The first have a proven anatomic abnormality as found in the WPW syndrome. The second group comprises those that result from a suspected anatomic abnormality, e.g., Mahaim fibers that cause ventricular preexcitation, or James fibers that bypass the atrioventricular (AV) node. The third group consists of those caused by a physiologic abnormality of the normal AV conduction system and, for lack of a better term, is called enhanced conduction through the AV node. Where a clearly demonstrated anatomic structure is involved, as in the first and third groups, surgical intervention has been successful. The second group is awaiting an enlightened but aggressive approach by the surgeon and the electrophysiologist. If these obscure pathways can be identified and localized more definitely, the surgeon should be able to divide them selectively with a precisely placed incision, yet avoid the normal conduction system. Enhanced conduction through a normal anatomic AV node involving the third group is a difficult concept to fully appreciate. Enhanced conduction is defined as: (1) A-to-H interval in sinus rhythm of 60 msec or less, (2) one-to-one conduction from the atrium to the ventricle - 200B/ min, and (3) atrium-to-his-bundle-interval that does not last more than 100 msec at the fastest rate that conduction occurs oneto-one. The experience reported includes 19 patients. In 17 of the patients the arrhythmias were atrial fibrillation and 452 flutter. All attempts to slow the ventricular rates with medication had failed. At operation, the His bundle was identified and then destroyed by area freezing. This procedure will now likely be superseded by a closed procedure where an electrode catheter, passed transvenously, is used to identify the bundle of His. This electrode can then be used to cauterize the node with the direct current defibrillator used as an energy source. The closed procedure is done in the laboratory by the electrophysiologist. Complete heart block follows both the open and closed procedures, thus requiring the placement of a demand ventricular pacemaker. If pacemaker failure occurs, some protection from bradycardia deteriorating to ventricular fibrillation is afforded by the junctional rhythm and early appearance of an escape rhythm. This leaves a hemodynamic situation of a regular ventricular rhythm but without atrial augmentation. Improvement upon these crude procedures eventually would seem possible when interventions are devised where the conduction characteristics of the node can be altered, yet AV conduction retained. Partial division of the AV node, of course, would _~ AS RFW IPS LFW Fig. 1 The classification of Kent bundles based on observations at surgery. AS = anterior septal, RFW = right free-wall, PS = posterior septal, LFW = left free-wall. Vol. 9, No. 4, December 1982

3 be more applicable to patients with AV nodal reentry tachycardia. The surgical experience gained in dividing a bundle of Kent, the first group, has been more extensive and gratifying. The operation is well established now. The remainder of this discussion will be concerned primarily with the unusual problems observed in 190 patients with accessory pathways of AV conduction. The distribution of the pathways in 190 patients was 39 right free-wall, 93 left free wall, 58 posterior septal, and 21 anterior septal, for a total of 21 1 pathways. The location of the pathways is shown in Figure 1. Among the accompanying cardiac disorders observed in this series were cardiomyopathies in six patients, believed to have been caused by what was almost incessant tachycardia. All patients survived. None had a left atriotomy. Three had His bundle interruption because of the lower risk associated with the operation. The two children in the group underwent division of posterior septal pathways, while the sixth patient had division of a right free-wall pathway. Among the interesting subsets, 22 patients had pathways which would conduct retrograde only. As a group, they appeared to have greater difficulty with control of their reentry tachycardia than patients with bidirectional pathways. In this group, six had posterior septal pathways with what Coumel calls incessant junctional tachycardia. The accessory pathways had the conduction characteristics of the AV node. Tachycardia in one patient was corrected by His bundle interruption. The patient still has ventricular-to-atrial conduction. The others were corrected by Kent bundle division, sparing the AV node-his bundle. Right and left free-wall pathways in this series were identified and interrupted by comparable surgical methods, including detailed preoperative studies and intraoperative mapping followed by dissection. In selected patients with pathways in both locations, interruption might now be possible with cryothermia (Figs. 2 and 3). In case of the right, this was done in such a way as to avoid cardiopulmonary bypass. On the left, an atriotomy might be eliminated. The effective application of cryothermia requires precise localization and clear exposure of areas to be destroyed. The free-wall of the right ventricle is ideal, for /.kxc * ;n i- Y/ z, T "IT.10. Fig. 2 Drawing shows beginning exposure of the right atrioventricular junction through the epicardium for interruption of a right free-wall pathway. The crossing point of the pathway is marked by the crosses. These are the earliest areas of atrioventricular conduction. Fig. 3 (Left) Application of the cryothermia probe to the crossing point of the pathway with an ice ball at the tip. ('Middle) The pattern of freezing points is shown by the oxerlapping circles, includling the ventricle, atrium and the annulus. (Right) Epicardlial closure. This method avoids cardiopulmonary bypass. Texas Heart Institute Journal 453

4 the approach to the coronary artery can be easily displaced downward, exposing the right atrium, the annulus fibrosis, and the right ventricle. Application of cryothermia from the epicardial side of the heart eliminates an atriotomy and can be done without cardiopulmonary bypass. In this series, one successful left free-wall pathway interruption was accomplished by applying cryothermia to the epicardium; however, many other attempts have not been successful. This method would be possible in patients with left posterior section free-wall pathways with a right dominant coronary artery, providing exposure is obtained of the ventricular and atrial myocardium. After the pericardium is divided and the coronary sinus is exposed, the crossing of the pathway can be exposed to permit successful cryothermia. In case of injury to this vessel, preservation of the pericardium beneath the coronary sinus provides a layer for securely closing the coronary sinus. Cardiopulmonary bypass would be needed, but an atriotomy could be avoided. As the surgical treatment evolved, problems have emanated from the posterior septal pathways because of the anatomic characteristics of this area. This has led me to look upon the area as a three-sided pyramid with the right fibrous trigone as its apex and the epicardium and coronary sinus as its base (Fig. 4). The right and left atria make up two sides. The third side is the posterior/superior process of the left ventricle and the muscular ventricular septum. This is a large expanse of cardiac tissue. Thus, in addition to originating in the two atrial walls, pathways can originate in the atrial septum or coronary sinus. From these three structures, the pathways can traverse the fat in the space and enter the ventricular septum or posterior/superior process of the left ventricle. Likewise, at the apex of the pyramid, pathways can course from the atrial septum to the ventricle adjacent to the His bundle, as described by Truex. Using these anatomic facts, I will present the plan for the extensive dissection needed for interruption, emphasizing some of the points gained from experience with the last 16 patients. The result of direct surgery in the preexcitation syndrome for the arrhythmia caused by Kent bundles is now well established. The surgeon has proved he can operate in unusual areas of the heart-in the so-called "no man's land," searching for a structure that is neither visible nor palpable. This search has opened new vistas to the surgeon. He now knows more about the location of the components of the normal conduction system-not only how to avoid, but perhaps, how to alter them. The funneling of AV conduction traffic through a small, accessible and identifiable passageway that has unique anatomical and physio- PSPI Fig. 4 Diagrammatic representation of the pyramidal space in the posterior septal area. The top drawing shows the atria removed. The right fibrous trigone (RFT) is the apex. The floor is the posterior/superior process of the left ventricle (PSPLV) and the muscular ventricular septum (Musc. VS). Note in lower drawing the coronary sinus (CS) crosses the space at the base of the pyramid, and this structure and the epicardium make up the base. The right atrium (RA) overlaps the left (LA). The crux is really not a cross because of the atrial relationship. The right atrioventricularjunction is lower than the left. AS = atrial septum, IVC = inferior vena cava, RV = right ventricle, LV = left ventricle. 454 Vol. 9, No. 4, December 1982

5 logical characteristics portends new surgical opportunities as well as pharmacological opportunities to which we have been accustomed in the past. The time is overdue for expansion of surgery. It has been over 15 years since the first AV node-his interruption attempts and 14 years since a successful Kent bundle interruption. (Dr. Sealy's complete article, with references and figures, may be found on page 415.) Tachydysrhythmias in the Pediatric Population Paul C. Gillette, M.D., Director of Clinical Electrophysiology, Texas Children's Hospital; Professor of Pediatrics and Associate Professor of Experimental Medicine, Baylor College of Medicine, Houston, U.S.A. M AJOR ADVANCES have been made in recent years in the diagnosis and treatment of children with tachydysrhythmias. It is now possible to classify tachydysrhythmias clinically, based not only on the site of origin, i.e., supraventricular versus ventricular, but also on the mechanism. Reentrant tachydysrhythmias are those which can be induced and are terminated by programmed stimulation, while automatic focus tachydysrhythmias are unaltered by such maneuvers. Based on these criteria, 14% of pediatric supraventricular tachycardias are due to automatic foci, while the remaining 86% are due to reentry circuits. In the reentry group, half involve an accessory atrial ventricular connection as part of the reentry circuit. The remainder are caused by reentry within the atrioventricular node, atrial muscle or sinoatrial node. This classification, according to the mechanism, assumes importance in medical or surgical treatment. Patients with supraventricular tachycardias due to accessory atrioventricular connections may be definitively treated surgically by division of the accessory connection. Patients who have reentry within the atrioventricular node frequently respond to the combination of digoxin and verapamil. Patients who have supraventricular tachycardias due to an automatic focus can have definitive surgical treatment by removal or cryoablation of the automatic focus. Drug treatment is unsatisfactory in this group. Most ventricular tachycardias in pediatric patients who have had cardiac surgery are caused by reentry mechanisms. Phenytoin is effective in treating most postoperative patients with reentrant ventricular tachycardia. Surgical treatment of patients in this group with ventricular tachycardias is possible, using either division or cryoablation of the reentry circuit. In pediatric patients who have not had cardiac surgery, the mechanism of ventricular tachycardia is often an automatic focus. The rate of automatic discharge usually is not extremely rapid and often does not require treatment. When treatment is required, betablockers are frequently effective. Infants with ventricular tachycardia almost always have some underlying cardiac abnormality, even if it is not apparent. Ventricular myocardial tumors and other lesions can be removed or cryoablated successfully, curing the patient with ventricular tachycardia. Texas Heart Institute Journal 455