Catheterization and Cardiovascular Diagnosis 2:113-124 11976)
Comprehensive Review THE WOLFF-PARKINSON-WHITE SYNDROME: The Value of the HIS Bundle Electrogram Jacob I. Haft, M.D., and Joseph Anthony C. Gomes, M.D. The HIS bundle electrogram has led to the aquisition of additional information on the physiology of the WPW syndrome and has become a useful technique for its dlagnosis. The findings on the HBE and their interpretation in WPW are reviewed. Key words: HIS bundle electrogram, Wolff-Parkinson-White syndrome, supraventricular tachycardia, atrioventricular conduction, atrial pacing.
In 1930, Wolff, Parkinson, and White ( 1 ) described a group of patients who had recurrent paroxysmal tachycardias, the absence of abnormal cardiac physical findings when not in tachycardia, and a peculiar ECG pattern with a short PR interval and a slurred, prolonged QRS that could occasionally be reverted to normal by exercise or by the administration of atropine (Fig. I ) . Wilson had published a similar case in 1915 (2), but the importance of his findings was not realized until the work of Wolff et al (I). Since the original description of the WPW syndrome there have been numerous investigations performed and theories suggested to explain the mechanism of the syndrome and to establish criteriafor its diagnosis. Until recently the diagnosis of WPW has depended almost solely on the recognition of the characteristic ECG or VCG pattern (3). With the advent of the HIS bundle electrogram, electrophysiological studies on AV conduction in man have been made possible, and more objective criteria for the diagnosis of WPW are now available. HIS bundle studies in conjunction with atrial pacing have lead to further elucidation of the mechanism of the syndrome and its associated tachycardias. Results of these studies have supported much of the previous theoretical work and have allowed the delineation of the electrophysiological properties of the abnormal conduction pathways (4-7). It is the purpose of this communication to review the information on the physiology of WPW derived from the HBE, to demonstrate HIS bundle electrographic findings in patients with WPW and to discuss the value of HIS bundle electrogram in confirming the diagnosis of the syndrome.
From the Bronx VA Hospital and Mount Sinai School of Medicine, New York, N.Y. Dr. Gomes is now at United States Public Health Service Hospital, Staten Island. N.Y. Reprint requests to: J . I . Haft, M . D . . Cardiology Department. St. Michael’s Medical Center. 306 High St.. Newark. New Jersey 07102
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Fig. 1. Surface E.C.G.: Normal sinus rhythm with a PR interval of 0.08 sec.QRS of 0.12 sec, and positive delta waves in leads I, II, AVL, V5, V6.
THEORETICAL CONSIDERATIONS
Over the years numerous theories have been developed to explain both the abnormal electrocardiographic pattern of WPW and the supraventricular tachycardias associated with the syndrome. The most prevalent has been the presence of an abnormal AV conduction pathway that bypasses the AV node and results in premature depolarization of a portion of one of the ventricles (8). The WPW QRS has been felt to be a fusion beat (9) formed by the algebraic sum of the electrical forces generated by the portion of the ventricle prematurely depolarized via the abnormal pathway and the forces generated by depolarization of the remaining parts of the ventricles that are activated in the normal sequence via conduction through the normal pathways, i.e. the AV node, the bundle of HIS, and the bundle branches. It has been postulated that if the abnormal bypass of the AV node caused premature depolarization of a portion of the left ventricle, the delta wave on the ECG would have an anterior vector with a slurred positive deflection in leads V1 and V2 (Type A). If a portion of the RV were prematurely activated, the vector of the delta wave would be posterior and leftward with a negative slurred deflection in V1 and positive tall slurred Rs in the left-sided leads (Type B). Although these patterns have been found to have some value in predicting the site of the by pass,
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there have been instances when they have been found to be misleading when mapping has been performed at surgery and when surgical severence of tracts has been attempted. The electrocardiographic diagnosis of the site of bypass has been disappointing, first because pure Type A or pure Type B is rarely seen and second because bypass tracts in the septum can cause either pattern. Normally, as the impulse from the atrium is conducted through the AV node there is a significant delay that accounts for much of the PR interval. This delay is accentuated if the atrial rate is inappropriately accelerated by the occurrence of PAT, atrial flutter, or artificially pacing the atrium. As the atrial rate increases. the PR interval increases and with further rise in rate, Wenckebach-type block, or 2 or 3 to 1 block at the AV node occurs (10). It is this property of the AV node, to retard conduction as the atrial rate increases inappropriately, that protects the ventricles from inordinately high rates that might occur. e.g. if I to I AV conduction were to take place during atrial flutter. Premature atrial beats, either due to spontaneous APCs or produced by atrial pacing, are affected similarly, with slowed conduction through the AV node causing a prolonged PR interval in the APC if it is premature enough. The presence of a functioning abnormal pathway that bypasses the AV node results in the loss of the normal AV nodal delay and is manifested on the ECG by a shortened PR interval. With atrial pacing the PR interval does not increase. Anatomically, two types of AV nodal bypass pathways have been demonstrated (Fig. 2). In the early 1900s Kent ( 1 1) found muscular bridges across the fibrous tissue of the AV groove and postulated that these were the normal pathways for conduction from the atria t o the ventricles. Subsequently it was shown that these Kent bundles do not function in the normal heart even when present, but AV conduction procedes via the AV node. These bundles are frequently found in patients with WPW, however, and in these cases, they have been postulated to be functional (8). Recent studies using ventricular mapping and the successful normalization of the WPW QRS by surgically interrupting these pathways, have
POSTERIOR INTERNODAL TRACTS OF JAMES
"
BRANCHES
Fig. 2. Potential accessory AV conduction pathways that bypass the normal routes of atrioventricular conduction (schematic representation).
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confirmed that in many patients with WPW, such Kent bundles are operant. The presence of a functioning Kent bundle can produce all of the features of WPW: the shortened PR interval, the preexcitation of a part of the ventricle resulting in a delta wave, and prolongation of the QRS. The second anatomical pathway that has been found that can lead to bypass of the AV node is the posterior internodal tract described by James (12). Normally the impulse to initiate the heart beat originates at the sinoatrial node. Conduction from the SA node to the AV node occurs through the atrium via preferential pathways, the three internodal tracts of James. These structures have been defined both anatomically and functionally (13-15). In some instances the posterior internodal tract does not terminate on the atrial part of the AV node but instead bypasses most of the AV node to enter the node at its distal portion or bypasses the node entirely to enter the proximal bundle of HIS directly (12, 16). Such a functioning tract would explain the short PR interval seen in patients with WPW but not the presence of the delta wave. In the 1930s, Mahaim and Benatt (17) found Purkinje fibers that went from the distal AV node or the proximal bundle of HIS directly to the ventricular myocardium, bypassing the normal bundle branch system. Function of these pathways would lead to preexcitation of a portion of the ventricles and would result in the occurrence of a delta wave on the ECG. The fortuitous combination of a functioning James tract and a functioning Mahaim fiber would result in the ECG pattern of WPW. Studies utilizing the HIS bundle electrogram have suggested that either a functioning Kent bundle (3) or the combination of James and Mahaim fibers occur in patients with WPW and can be used to explain the abnormalities seen with the syndrome (18, 19). The supraventricular tachycardias that occur in WPW are also due to the presence of an abnormal pathway that bypasses the AV node (4). During sinus rhythm in the WPW patient, AV conduction proceeds simultaneously through both the accessory and the normal conduction routes, so that both pathways are depolarized and become refractory* at the same time. If one of the two pathways does not conduct antegrade, as after an atrial premature contraction, that pathway will not be refractory when the ventricles are depolarized and may conduct the impulse retrograde to the atrium, setting up the circumstances for a reentrant tachycardia. For example, if an APC occurs early in the cardiac cycle, the bypass pathway (either a Kent bundle or a James tract) may be totally refractory. The A V node may * In this paper. the term "refractory" will refer to the readiness of conduction tissue to conduct an impulse from the atrium to the ventricle (antegrade) or from the ventricle to the atrium (retrograde). "Absolute refractory period" will refer to the interval of time following conduction of an impulse over the conduction pathway during which further conduction will not occur at any rate. "Relative refractory period" will refer to that period immediately following the absolute refractory period during which conduction will occur. but at a rate slower than normal. In studying atrioventricular conduction. refractory periods are determined by stiumulating the atrium prematurely by atrial pacing ("deliverying APCs"). The interval between the normal P wave (or the P wave resulting from the basic pacing rate) and the premature atrial stimulus is gradually narrowed. The longest interval that does not result in any conduction defines the absolute refractory period. As the time from the normal P to the test impulse is again increased, the interval following the absolute refractory period during which conduction occurs but is delayed, until conduction occurs at the normal rate, is the relative refractory period. Conduction tissue that is absolutely refractory will not conduct; conduction tissue that is relatively refractory will conduct at a slower than normal rate.
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be only relatively refractory and will allow conduction, with a delay, to the ventricle. As the ventricles depolarize in a normal sequence, the accessory pathway will have sufficient time to recover. When the area of the ventricle on the ventricular side of the bypass is depolarized, the accessory route is no longer refractory and may conduct back to (reenter) the atrium, depolarizing it. By the time the impulse is conducted through the atrium from the area on the atrial side of the bypass tract to the AV node, the AV node has recovered, and conduction through it can proceed to the ventricles. The route of the reentrant tachycardia would be atrium-AV nodeventricle (antegrade)-accessory pathway-atrium (retrograde)-AV node, and so on. Breaking the tachycardia can be accomplished by making a part of the reentry route refractory to the oncoming impulse, thereby interrupting the circuit. Vagal maneuvers (i.e. carotid massage, gagging, raising the blood pressure with vasopressors) or vagally active drugs (digitalis, T e n d o n ) will break the circuit at the AV node; quinidine or Pronestyl will break the circuit at the ventricular part of the circuit or in the bypass tract; premature atrial stimulation by atrial pacing, at the atrial part of the circuit; and premature ventricular stimulation, at the ventricular part of the circuit. THE HIS BUNDLE ELECTROGRAM
The development of the bundle of HIS electrogram by Damato’s group in the late 1960s has provided a tool for the investigation of AV conduction in intact man (20). By placing an electrode catheter in close proximity to the bundle of HIS, depolarization of the HIS can be recorded and its timing with relation to depolarization of the atrium and the ventricles can be measured. The depolarization of the bundle of HIS separates AV conduction into two parts, the period required for conduction from the onset of atrial depolarization through the atrium and through the AV node to the HIS bundle, and the period for conduction from the bundle of HIS through the bundle branch system to the ventricles. Normally the duration of the AH interval is from 55 to 130 rnsec, and the HV interval is from 35 to 55 msec (21). Delay at the AV node will prolong the AH interval, and delay in the distal bundle of His or in the bundle branch system will prolong the HV interval. Acceleration of the atrial rate by atrial pacing will prolong the AH interval as conduction through the AV node is slowed but in most instances will have little effect on the HV interval (Fig. 3). In patients with WPW, findings on the HIS bundle electrogram are characteristic and can be used to confirm the diagnosis (Fig. 4). In patients with a Kent bundle type of accessory pathway, the AH interval will be normal during NSR. However. the HV interval will be either markedly shortened or the HIS deflection will occur simultaneously with the onset of the QRS on the peripheral leads, i.e. the delta wave. The abnormal position of the HIS deflection with respect to the onset of the QRS is due to the fact that the onset of depolarization of the ventricles, i.e. the delta wave, does not occur via the normal bundle branch route, but depolarization is initiated prematurely via the Kent bundle pathway. Hence the normal interval necessary for conduction from the HIS bundle through the bundle branches to the ventricular myocardium is not seen, and the onset of depolarization of the ventricles (QRS) occurs almost simultaneously with the HIS bundle depolarization. The effects of atrial pacing on the HIS bundle electrogram are diagnostic. In the presence of WPW, artificially accelerating the rate does not result in the normal
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Fig. 3. Normal HIS bundle electrogram and normal response to atrial pacing. P=atrial depolarization on the HIS bundle electrogram. H=HIS bundledeflection on the HIS bundle electrogram. S1-atrialstimulation artifact. P-H interval is measuredfrom the initial deflection of the atrial depolarlzationto the initial deflection of the HIS potential on the HIS bundle electrogram. H-V interval is measured from the initial HIS bundle deflection to the initial rapid ventricular depolarizatlon spike on the HBE. S1-H interval is measured from the atrial pacing stimulus artifact to the initial HIS bundle deflection of the HBE. As the heart rate is increasedfrom 85/min to 150lmin there is gradual prolongation of the S1-H interval whereas the H-V interval stays constant. At a heart rate of 1621min there is 4:3 Wenckebach block.
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NSR PH 75 MSEC PO-7SMSEC Fig. 4. HIS bundle electrogram during NSR in WPW (Kent bundle). The P-H interval measures 75Msec. The P-Q internal, measured from the P wave to the initial portion of the delta wave, measures 75 Msec. The onset of the QRS and the HIS spike occur simultaneously.
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prolongation of the PR interval seen in patients without WPW (Fig. 5). Because the AV node is the area in the AV conduction system that is effected by rate change and because the AV node is bypassed by the accessory pathway, the PR interval. as seen on the standard electrocardiogram. remains constant, and any slowing of conduction through the AV node is not manifest on the peripheral ECG. Although masked on the ECG by the presence of the accessory pathway and the occurrence of the delta wave. conduction across the AV node is normally affected by rate in these patients, but this effect can be seen easily only on the HBE. As the rate is increased the AH interval prolongs normally. Because it is conduction via the accessory pathway rather than via the bundle of HIS and the bundle branches that initiates the QRS, the interval from the onset of the P wave to the onset of the QRS remains constant and the HIS deflection appears to move into the QRS, occurring later and later after the onset of the QRS until it is lost in the deflections that are due to ventricular depolarization. Simultaneously, the delta wave and the QRS become wider as depolarization of the ventricle via the normal pathways becomes more and more delayed. and, by default, more ventricular tissue is depolarized via the accessory pathway. The combination of (1) a fixed PR interval. (2) a gradually prolonging AH interval with the H deflection moving into the QRS. and (3) prolongation of the delta wave and the QRS as the atrial pacing rate is increased signify the presence of WPW and suggest that the mechanism is a functioning Kent bundle (4, 18). Patients with WPW that is due to combination of a James tract and a Mahaim fiber have similar findings on the HIS bundle electrogram during sinus rhythm but respond to atrial pacing differently (5.7,19,22,23). During sinus rhythm these patients also have a moderately shortened (though occasionally normal) AH interval because of the James tract and a markedly shortened HV interval with the HIS
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Fig. 5. HIS bundleeiectrograms and atrial pacing in a patient with WPW (Kent bundle). During NSR the HIS potential occurs simultaneously with the initial deflection of the delta wave (0 ). As the atrium is paced at increasing rates, 91 to lZO/min, the S H Interval measured from the pacing stimulus to the initialdeflectionof the HIS splke increasesfrom 120 Msec to l65 Ysec. However, the SQ interval remains relativelyconstant. The HIS spike Is seen tocome progressively later and later in relation to the Q wave until it is lost in the rapid ventricular depolarizationspikes.
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deflection occurring simultaneously with or shortly before the onset of the peripheral QRS because of the Mahaim fiber. Because the AV node is bypassed by the James tract, accelerating the rate by atrial pacing results in little change in the PR interval as seen on the peripheral ECG (Fig. 6). On the HIS bundle electrogram. however. findings are somewhat different. Because the James tract terminates in the distal node or the proximal bundle of HIS, the AV node is bypassed above the site of recording of the HBE. With atrial pacing the AH remains relatively constant, increasing only slightly, if at all. Because the AH interval does not increase with pacing, the HIS deflection does not move into the QRS, and the relationship of the HIS to the QRS remains constant. The combination of a markedly short HV interval during sinus rhythm, a relatively constant AH interval, and a constant HV interval during atrial pacing is suggestive of WPW due to the combination of a functioning James tract and a functioning Mahaim fiber. The response to premature atrial stimulation with respect to the PR. AH. and HV intervals is similar to that seen with atrial pacing and carries the same connotations with regard to the diagnosis of WPW and the mechanism for its occurrence. Of eight patients with WPW recently studied in our laboratory, six showed evidence of Kent conduction and two of conduction via a combination of a James tract and a Mahaim fiber (18). THE HBE DURING TACHYCARDIAS
The mechanism for the supraventricular tachycardias seen in WPW has also been elucidated using the HIS bundle electrogram. With the presence of two conduction pathways from the ventricles to the atria, the normal AV node-HIS pathway and the accessory pathway. the possibility for a
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Fig. 6. HIS bundle electrograms during sinus rhythm and atrial pacing in a patient with James and Mahaim fiber conduction. During sinus rhythm the HIS spike occurs before the onset of the Q wave with a short Minterval. On atrial pacing the S-H interval, which is 90 Msec at a heart rate of 100/min, does not show any increase at a heart rate of 162/min. The relationship of the HIS deflection and the Q wave on the surface ECG stays constant at all pacing rates.
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reentrant tachycardia exists. If the ventricles are depolarized antegrade via one of the pathways, it is possible for the impulse to be conducted retrograde back to the atrium via the second pathway. During tachycardia in most patients with WPW, the QRS is of normal duration and configuration, suggesting that antegrade conduction from the atria to the ventricles has occurred via the normal pathway (Fig. 7). This has been confirmed with HIS bundle electrograms taken during tachycardia that have documented that a HIS bundle depolarization occurs before each QRS with a normal HV interval (6). Although not recorded on the HBE, it can be postulated that retrograde conduction then occurs via the acessory pathway. Confirmation for this sequence of events in seen when the mechanism of onset of the tachycardia is analyzed using the HBE. During sinus rhythm, conduction to the ventricles in patients with WPW occurs via both the normal and the accessory pathway simultaneously, causing both pathways to be depolarized simultaneously and both pathways to be refractory simultaneously, so that reentry via one of the two pathways does not occur. The length of time that the two pathways are refractory is not the same, however; the refractory period of the accessory pathway is usually longer than that of the normal node-HIS pathway (7,24). If a premature atrial beat occurs and is early enough in the cardiac cycle to arrive at the accessory pathway when it is still refractory but arrives at the AV node when the node is no longer refractory, the impulse will be conducted to the ventricles solely over the normal pathway and will depolarize the ventricles in the normal sequence with no delta wave and a normal HV interval. By the time the area of the ventricle on the ventricular side of the accessory pathway is depolarized, however, the accessory pathway may have recovered, be no longer refractory, and will conduct retrograde to the atria leading to a reentrant tachycardia. The route of the reentry tachycardia is atrium to A V node-HIS to ventricles (antegrade) to accessory pathway to atrium (retrograde) to node to ventricles and so on. Evidence for the disparity between the refractory periods of the normal and the accessory pathways has come from the work of Durrer's group in Holland (24). In five of six patients with WPW, who were studied using the HBE and the extrastimulus technique, the absolute refractory period of the AV node pathway was
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'I. Fig. 7. Supraventricular tachycardia induced by a premature atrial beat. After the second QRS complex a premature atrial beat delivered at a short coupling interval(280 Msec), is conducted to the HIS bundle with a prolonged P-H interval. Conduction through the anomalous pathway falls, as evidenced by the normal QRS configuration with absence of the delta wave. The subsequent p waves represent retrograde depolarization of the atria via the anomalous pathway and are followed by a HIS bundlespike and a QRS with a normal K V interval. There is no delta wave on the QRSs during tachycardia. Right bundle branch block is present during tachycardia.
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found to be shorter than that of the accessory pathway. Of interest was the finding by this group that digitals tended to shorten the refractory period of the accessory pathway and lengthen the R F of the normal pathway. This equalization of the two refractory periods leads to a decrease in the opportunity for reentrant tachycardias and may explain the clinical finding that in some patients with WPW, digitalization will inhibit the occurrence of tachycardia. During atrial fibrillation in patients with WPW, the AV conduction pathway varies between purely AV nodal conduction with a normal QRS (because the accessory pathway is refractory), purely accessory pathway conduction with widely aberrant QRSs (because the node is refractory), and combination beats of varying form with varying lengths of the delta wave (depending on the relative refractoriness of each of the pathways). Because of its effect on the refractory period of the accessory pathway, digitalis may be dangerous in patients with WPW who have bouts of atrial fibrillation, because the decrease in the period of refractoriness of the accessory pathway may result in a more rapid ventricular response rate. The mechanism of termination of the tachycardia by pacing the right atrium has also been demonstrated using the HBE (6, 25). Depolarization of the atria or ventricles prematurely by electrical pacing, if produced at a time in the cycle that results in causing the chamber to be refractory to the reentering impulse, will interrupt the reentry circuit and terminate the tachycardia. One of the newer modes of thereapy for the tachycardias associated with WPW, the implantation of a permanent demand pacemaker in the right ventricle (26), utilizes this mechanism. The demand rate is set low so that the pacemaker does not fire when the patient is in sinus rhythm. If a tachycardia occurs, the demand circuit is turned off externally by placing a magnet over the pacemaker generator, and the pacer is allowed to fire regularly. The impulses fall at varying times in the cardiac cycle during the tachycardia because the rate of the tachycardia and of the pacer are different. If the pacer impulse depolarizes the ventricle at an appropriate time, the reentry pathway will be broken and normal sinus rhythm will occur. In recent years, a number of reports, primarily from the group at Duke, have documented the success of surgically treating WPW by cutting the bypass tract (27). Surgery of this type is a serious undertaking, and there have been a number of reports of failure of the procedure (28); this mode of therapy should be considered only in those patients with recurrent arrhythmias that are refractory to medical therapy. Prior to the procedure it is wise to document the presence of a Kent bundle by HBE and atrial pacing; as yet there are no reported cases with the combination of James and Mahaim fibers that have been successfully operated upon. The operative procedure consists of thoracotomy and mapping of the sequence of depolarization in the ventricles to find the area of the ventricles that is depolarized earliest and causes the delta wave. This area is usually in the region of the right atrial-right ventricular groove in patients with Type B WPW (27) and is found in the area of the basal endocardium of the left ventricle in Type A (29). On the right side, the AV groove is cut, separating the atrium from the ventricle in the area of earliest ventricular depolarization. On the left side, success is best achieved if the LA is opened and the AV groove incised on the endothelial surface. Occasionally, the
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peripheral ECG is inaccurate in predicting the site of the bypass tract. The procedure is, as yet. experimental and much work must be done yet to document its long-term success before patients with less than intractable life-threatening arrhythmia are subjected to it. REFERENCES I . Wolff L. Parkinson J and White, PD: Bundle branch block with short P-R interval in healthy young people prone to paroxysmal atrial tachycardia. Am. Heart:; 5 5 8 5 , 1930. 2. Wilson, FN: A case in which the Vagus influences the form of the ventricular complex of the electrocardiogram. Arch. Int. Med. 16:1008, 1951. 3 . Rosenbaum FF, Hecht HH. Wilson FN and Johnston FD: The potential variations of the thorax and the oesophagus in anomalous A-V excitation (WPW syndrome). Am. Heart J. 29:281, 1945. 4. Castellanos A Jr, Chapunoff E. Castillo CA, Maytin 0 and Lemberg L: His-bundle electrograms in two cases of Wolff-Parkinson-White (pre-excitation). Circulation 41:399. 1970. 5 . Narula 0s: Wolff-Parkinson-White syndrome - A review. Circulation 47:872, 1973. 6. Durrer D, Schoo L, Schuilenburg RM and Wellens HJJ: The role of premature beats in the initiation of supraventricular tachycardia in the WPW syndrome. Circulation 36544, 1967. 7. Lau SH, Josephson ME, Gallagher JJ, Caracta AR, Varghese PJ and Damato AN: Refractoriness of the accessory pathway and mechanisms of reentry in the Wolff-Parkinson-White phenomenon (abstract). Am. J. Cardiol. 29:275, 1972. 8. Lev M: The pre-excitation syndrome: Anatomic considerations of anomalous AV pathways. I n (Dreifus LS and Likoff WS, eds): Mechanisms and Therapy of Cardiac Arrhythmias. New York: Grune and Stratton, 1966. p. 665. 9. Butterworth JS and Pointdexter CA: Fusion beats and their relation to the syndrome of short P-R interval associated with a prolonged QRS complex. Am. Heart J. 2 8 149, 1944. 10. Lister JW. Stein E, Kosowsky BD, Lau SH and Damato AN: Atrioventricular conduction in man. Effects of rate, exercise, isoproterenol and atropine on the P-R interval. Am. J. Cardiol. 16516, 1965. 1 1 . Kent AFS: The Right lateral auriculo-ventricular junction of the heart. J. Physiol. 48:22, 1914. 12. James TN: Morphology of the human A-V node with remarks pertinent to its electrophysiology. Am. Heart J. 62:756, 1%1. 13. Sano T and Yamagishi S: Spread of excitation from the sinus node. Circ. Res. 16:423, 1%5. 14. Vasalle M and Hoffman BF: The spread of sinus activation during potassium administration. Circ. Res. 17:285, 1965. 15. Hogan PM and Davis LD: Evidence for specialized fibers in the canine right atrium. Circ. Res. 23:387, 1968. 16. Ferrer MI: New concepts relating to the pre-excitation syndrome. JAMA 201:163, 1967. 17. Mahaim I and Benatt A: Nouvelles recherches sur les connexions superieures de la branche gauche du faisceau de His-Tawara avec la cloison interventriculairie. Cardiologia 1:61, 1937. 18. Gomes JA and Haft JI: His bundle electrograms and atrial pacing studies in eight cases of W.P.W. (abstract). Clin. Res. 22:277A, 1974. 19. Caracta AR, Damato AN, Gallagher JJ, Josephson ME, Varghese PJ, Lau SH and Westura EE: Electrophysiologic studies in the syndrome of short P-R interval and normal QRS complex. Am. J. Cardiol. 31:245, 1973. 20. Scherlag JB, Lau SH. Helfant RH, Berkowitz MD, Stein E and Damato AN: Catheter technique for recording His bundle activity in man. Circulation 39:13, 1969. 21. Hecht HH, Kossman CE, Childers RW, Langedorf R, Lev M, Rosen KM, Pruitt RD, Truex RC, Uhley HN and Watt TB: Atrioventricular and intraventricular conduction. Revised nomenclature and concepts. Am. J. Cardiol. 31:232-244, 1973. 22. Coumel P, Waynberger M, Fabiato A Slama R, Aigueperse J and Bouvrain J: Wolf€-ParkinsonWhite syndrome: Problem in evaluation of multiple accessory pathway and surgical therapy. Circulation 45:1212, 1972.
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23. Castillo CA, Castellanos A Jr, Agha AS and Myerburg RJ: Significance of His-bundle recordings with short H-V intervals. Chest 60:142. 1972. 24. Wellens HJ and Durrer D: Effects of digitalis on A-V conduction and circus movement tachycardias in patients with W.P.W. Circulation 47:1229. 1973. 25. Haft JI: Treatment ofarrhythmias by intracardiac stimulation. Prog. Cardiovasc. Dis. 16339. 1974. 26. Ryan GF, Easley RM. Zaroff LI and Goldstein S: Paradoxical use of a demand pacemaker in treatment of supraventricular tachycardia due to the W.P. W. syndrome. Circulation 38: 1037, 1968. 27. Cobb FR. Blumenschien SD. Sealy WC. Boineau JP. Wagner GS and Wallace AC: Successful surgical interruption of the bundle of Kent in a patient with Wolff-Parkinson-White syndrome. Circulation 38: 1018. 1968. 28. Burchell HB. Frye RL. Anderson MW and McGoon DC: Atrioventricular and ventriculo-atrial excitation in W.P. W. syndrome (Type B). Temporary ablationat surgery. Circulation 36:663,1%7. 29. Neutze JM, Kerr AR and Whitlock RML: Epicardial mapping in a variant of Type A. W.P.W. syndrome. Circulation 48: 662. 1973.
Comprehensive Review THE WOLFF-PARKINSON-WHITE SYNDROME: The Value of the HIS Bundle Electrogram Jacob I. Haft, M.D., and Joseph Anthony C. Gomes, M.D. The HIS bundle electrogram has led to the aquisition of additional information on the physiology of the WPW syndrome and has become a useful technique for its dlagnosis. The findings on the HBE and their interpretation in WPW are reviewed. Key words: HIS bundle electrogram, Wolff-Parkinson-White syndrome, supraventricular tachycardia, atrioventricular conduction, atrial pacing.
In 1930, Wolff, Parkinson, and White ( 1 ) described a group of patients who had recurrent paroxysmal tachycardias, the absence of abnormal cardiac physical findings when not in tachycardia, and a peculiar ECG pattern with a short PR interval and a slurred, prolonged QRS that could occasionally be reverted to normal by exercise or by the administration of atropine (Fig. I ) . Wilson had published a similar case in 1915 (2), but the importance of his findings was not realized until the work of Wolff et al (I). Since the original description of the WPW syndrome there have been numerous investigations performed and theories suggested to explain the mechanism of the syndrome and to establish criteriafor its diagnosis. Until recently the diagnosis of WPW has depended almost solely on the recognition of the characteristic ECG or VCG pattern (3). With the advent of the HIS bundle electrogram, electrophysiological studies on AV conduction in man have been made possible, and more objective criteria for the diagnosis of WPW are now available. HIS bundle studies in conjunction with atrial pacing have lead to further elucidation of the mechanism of the syndrome and its associated tachycardias. Results of these studies have supported much of the previous theoretical work and have allowed the delineation of the electrophysiological properties of the abnormal conduction pathways (4-7). It is the purpose of this communication to review the information on the physiology of WPW derived from the HBE, to demonstrate HIS bundle electrographic findings in patients with WPW and to discuss the value of HIS bundle electrogram in confirming the diagnosis of the syndrome.
From the Bronx VA Hospital and Mount Sinai School of Medicine, New York, N.Y. Dr. Gomes is now at United States Public Health Service Hospital, Staten Island. N.Y. Reprint requests to: J . I . Haft, M . D . . Cardiology Department. St. Michael’s Medical Center. 306 High St.. Newark. New Jersey 07102
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Fig. 1. Surface E.C.G.: Normal sinus rhythm with a PR interval of 0.08 sec.QRS of 0.12 sec, and positive delta waves in leads I, II, AVL, V5, V6.
THEORETICAL CONSIDERATIONS
Over the years numerous theories have been developed to explain both the abnormal electrocardiographic pattern of WPW and the supraventricular tachycardias associated with the syndrome. The most prevalent has been the presence of an abnormal AV conduction pathway that bypasses the AV node and results in premature depolarization of a portion of one of the ventricles (8). The WPW QRS has been felt to be a fusion beat (9) formed by the algebraic sum of the electrical forces generated by the portion of the ventricle prematurely depolarized via the abnormal pathway and the forces generated by depolarization of the remaining parts of the ventricles that are activated in the normal sequence via conduction through the normal pathways, i.e. the AV node, the bundle of HIS, and the bundle branches. It has been postulated that if the abnormal bypass of the AV node caused premature depolarization of a portion of the left ventricle, the delta wave on the ECG would have an anterior vector with a slurred positive deflection in leads V1 and V2 (Type A). If a portion of the RV were prematurely activated, the vector of the delta wave would be posterior and leftward with a negative slurred deflection in V1 and positive tall slurred Rs in the left-sided leads (Type B). Although these patterns have been found to have some value in predicting the site of the by pass,
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there have been instances when they have been found to be misleading when mapping has been performed at surgery and when surgical severence of tracts has been attempted. The electrocardiographic diagnosis of the site of bypass has been disappointing, first because pure Type A or pure Type B is rarely seen and second because bypass tracts in the septum can cause either pattern. Normally, as the impulse from the atrium is conducted through the AV node there is a significant delay that accounts for much of the PR interval. This delay is accentuated if the atrial rate is inappropriately accelerated by the occurrence of PAT, atrial flutter, or artificially pacing the atrium. As the atrial rate increases. the PR interval increases and with further rise in rate, Wenckebach-type block, or 2 or 3 to 1 block at the AV node occurs (10). It is this property of the AV node, to retard conduction as the atrial rate increases inappropriately, that protects the ventricles from inordinately high rates that might occur. e.g. if I to I AV conduction were to take place during atrial flutter. Premature atrial beats, either due to spontaneous APCs or produced by atrial pacing, are affected similarly, with slowed conduction through the AV node causing a prolonged PR interval in the APC if it is premature enough. The presence of a functioning abnormal pathway that bypasses the AV node results in the loss of the normal AV nodal delay and is manifested on the ECG by a shortened PR interval. With atrial pacing the PR interval does not increase. Anatomically, two types of AV nodal bypass pathways have been demonstrated (Fig. 2). In the early 1900s Kent ( 1 1) found muscular bridges across the fibrous tissue of the AV groove and postulated that these were the normal pathways for conduction from the atria t o the ventricles. Subsequently it was shown that these Kent bundles do not function in the normal heart even when present, but AV conduction procedes via the AV node. These bundles are frequently found in patients with WPW, however, and in these cases, they have been postulated to be functional (8). Recent studies using ventricular mapping and the successful normalization of the WPW QRS by surgically interrupting these pathways, have
POSTERIOR INTERNODAL TRACTS OF JAMES
"
BRANCHES
Fig. 2. Potential accessory AV conduction pathways that bypass the normal routes of atrioventricular conduction (schematic representation).
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confirmed that in many patients with WPW, such Kent bundles are operant. The presence of a functioning Kent bundle can produce all of the features of WPW: the shortened PR interval, the preexcitation of a part of the ventricle resulting in a delta wave, and prolongation of the QRS. The second anatomical pathway that has been found that can lead to bypass of the AV node is the posterior internodal tract described by James (12). Normally the impulse to initiate the heart beat originates at the sinoatrial node. Conduction from the SA node to the AV node occurs through the atrium via preferential pathways, the three internodal tracts of James. These structures have been defined both anatomically and functionally (13-15). In some instances the posterior internodal tract does not terminate on the atrial part of the AV node but instead bypasses most of the AV node to enter the node at its distal portion or bypasses the node entirely to enter the proximal bundle of HIS directly (12, 16). Such a functioning tract would explain the short PR interval seen in patients with WPW but not the presence of the delta wave. In the 1930s, Mahaim and Benatt (17) found Purkinje fibers that went from the distal AV node or the proximal bundle of HIS directly to the ventricular myocardium, bypassing the normal bundle branch system. Function of these pathways would lead to preexcitation of a portion of the ventricles and would result in the occurrence of a delta wave on the ECG. The fortuitous combination of a functioning James tract and a functioning Mahaim fiber would result in the ECG pattern of WPW. Studies utilizing the HIS bundle electrogram have suggested that either a functioning Kent bundle (3) or the combination of James and Mahaim fibers occur in patients with WPW and can be used to explain the abnormalities seen with the syndrome (18, 19). The supraventricular tachycardias that occur in WPW are also due to the presence of an abnormal pathway that bypasses the AV node (4). During sinus rhythm in the WPW patient, AV conduction proceeds simultaneously through both the accessory and the normal conduction routes, so that both pathways are depolarized and become refractory* at the same time. If one of the two pathways does not conduct antegrade, as after an atrial premature contraction, that pathway will not be refractory when the ventricles are depolarized and may conduct the impulse retrograde to the atrium, setting up the circumstances for a reentrant tachycardia. For example, if an APC occurs early in the cardiac cycle, the bypass pathway (either a Kent bundle or a James tract) may be totally refractory. The A V node may * In this paper. the term "refractory" will refer to the readiness of conduction tissue to conduct an impulse from the atrium to the ventricle (antegrade) or from the ventricle to the atrium (retrograde). "Absolute refractory period" will refer to the interval of time following conduction of an impulse over the conduction pathway during which further conduction will not occur at any rate. "Relative refractory period" will refer to that period immediately following the absolute refractory period during which conduction will occur. but at a rate slower than normal. In studying atrioventricular conduction. refractory periods are determined by stiumulating the atrium prematurely by atrial pacing ("deliverying APCs"). The interval between the normal P wave (or the P wave resulting from the basic pacing rate) and the premature atrial stimulus is gradually narrowed. The longest interval that does not result in any conduction defines the absolute refractory period. As the time from the normal P to the test impulse is again increased, the interval following the absolute refractory period during which conduction occurs but is delayed, until conduction occurs at the normal rate, is the relative refractory period. Conduction tissue that is absolutely refractory will not conduct; conduction tissue that is relatively refractory will conduct at a slower than normal rate.
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be only relatively refractory and will allow conduction, with a delay, to the ventricle. As the ventricles depolarize in a normal sequence, the accessory pathway will have sufficient time to recover. When the area of the ventricle on the ventricular side of the bypass is depolarized, the accessory route is no longer refractory and may conduct back to (reenter) the atrium, depolarizing it. By the time the impulse is conducted through the atrium from the area on the atrial side of the bypass tract to the AV node, the AV node has recovered, and conduction through it can proceed to the ventricles. The route of the reentrant tachycardia would be atrium-AV nodeventricle (antegrade)-accessory pathway-atrium (retrograde)-AV node, and so on. Breaking the tachycardia can be accomplished by making a part of the reentry route refractory to the oncoming impulse, thereby interrupting the circuit. Vagal maneuvers (i.e. carotid massage, gagging, raising the blood pressure with vasopressors) or vagally active drugs (digitalis, T e n d o n ) will break the circuit at the AV node; quinidine or Pronestyl will break the circuit at the ventricular part of the circuit or in the bypass tract; premature atrial stimulation by atrial pacing, at the atrial part of the circuit; and premature ventricular stimulation, at the ventricular part of the circuit. THE HIS BUNDLE ELECTROGRAM
The development of the bundle of HIS electrogram by Damato’s group in the late 1960s has provided a tool for the investigation of AV conduction in intact man (20). By placing an electrode catheter in close proximity to the bundle of HIS, depolarization of the HIS can be recorded and its timing with relation to depolarization of the atrium and the ventricles can be measured. The depolarization of the bundle of HIS separates AV conduction into two parts, the period required for conduction from the onset of atrial depolarization through the atrium and through the AV node to the HIS bundle, and the period for conduction from the bundle of HIS through the bundle branch system to the ventricles. Normally the duration of the AH interval is from 55 to 130 rnsec, and the HV interval is from 35 to 55 msec (21). Delay at the AV node will prolong the AH interval, and delay in the distal bundle of His or in the bundle branch system will prolong the HV interval. Acceleration of the atrial rate by atrial pacing will prolong the AH interval as conduction through the AV node is slowed but in most instances will have little effect on the HV interval (Fig. 3). In patients with WPW, findings on the HIS bundle electrogram are characteristic and can be used to confirm the diagnosis (Fig. 4). In patients with a Kent bundle type of accessory pathway, the AH interval will be normal during NSR. However. the HV interval will be either markedly shortened or the HIS deflection will occur simultaneously with the onset of the QRS on the peripheral leads, i.e. the delta wave. The abnormal position of the HIS deflection with respect to the onset of the QRS is due to the fact that the onset of depolarization of the ventricles, i.e. the delta wave, does not occur via the normal bundle branch route, but depolarization is initiated prematurely via the Kent bundle pathway. Hence the normal interval necessary for conduction from the HIS bundle through the bundle branches to the ventricular myocardium is not seen, and the onset of depolarization of the ventricles (QRS) occurs almost simultaneously with the HIS bundle depolarization. The effects of atrial pacing on the HIS bundle electrogram are diagnostic. In the presence of WPW, artificially accelerating the rate does not result in the normal
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Fig. 3. Normal HIS bundle electrogram and normal response to atrial pacing. P=atrial depolarization on the HIS bundle electrogram. H=HIS bundledeflection on the HIS bundle electrogram. S1-atrialstimulation artifact. P-H interval is measuredfrom the initial deflection of the atrial depolarlzationto the initial deflection of the HIS potential on the HIS bundle electrogram. H-V interval is measured from the initial HIS bundle deflection to the initial rapid ventricular depolarizatlon spike on the HBE. S1-H interval is measured from the atrial pacing stimulus artifact to the initial HIS bundle deflection of the HBE. As the heart rate is increasedfrom 85/min to 150lmin there is gradual prolongation of the S1-H interval whereas the H-V interval stays constant. At a heart rate of 1621min there is 4:3 Wenckebach block.
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NSR PH 75 MSEC PO-7SMSEC Fig. 4. HIS bundle electrogram during NSR in WPW (Kent bundle). The P-H interval measures 75Msec. The P-Q internal, measured from the P wave to the initial portion of the delta wave, measures 75 Msec. The onset of the QRS and the HIS spike occur simultaneously.
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prolongation of the PR interval seen in patients without WPW (Fig. 5). Because the AV node is the area in the AV conduction system that is effected by rate change and because the AV node is bypassed by the accessory pathway, the PR interval. as seen on the standard electrocardiogram. remains constant, and any slowing of conduction through the AV node is not manifest on the peripheral ECG. Although masked on the ECG by the presence of the accessory pathway and the occurrence of the delta wave. conduction across the AV node is normally affected by rate in these patients, but this effect can be seen easily only on the HBE. As the rate is increased the AH interval prolongs normally. Because it is conduction via the accessory pathway rather than via the bundle of HIS and the bundle branches that initiates the QRS, the interval from the onset of the P wave to the onset of the QRS remains constant and the HIS deflection appears to move into the QRS, occurring later and later after the onset of the QRS until it is lost in the deflections that are due to ventricular depolarization. Simultaneously, the delta wave and the QRS become wider as depolarization of the ventricle via the normal pathways becomes more and more delayed. and, by default, more ventricular tissue is depolarized via the accessory pathway. The combination of (1) a fixed PR interval. (2) a gradually prolonging AH interval with the H deflection moving into the QRS. and (3) prolongation of the delta wave and the QRS as the atrial pacing rate is increased signify the presence of WPW and suggest that the mechanism is a functioning Kent bundle (4, 18). Patients with WPW that is due to combination of a James tract and a Mahaim fiber have similar findings on the HIS bundle electrogram during sinus rhythm but respond to atrial pacing differently (5.7,19,22,23). During sinus rhythm these patients also have a moderately shortened (though occasionally normal) AH interval because of the James tract and a markedly shortened HV interval with the HIS
-
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Fig. 5. HIS bundleeiectrograms and atrial pacing in a patient with WPW (Kent bundle). During NSR the HIS potential occurs simultaneously with the initial deflection of the delta wave (0 ). As the atrium is paced at increasing rates, 91 to lZO/min, the S H Interval measured from the pacing stimulus to the initialdeflectionof the HIS splke increasesfrom 120 Msec to l65 Ysec. However, the SQ interval remains relativelyconstant. The HIS spike Is seen tocome progressively later and later in relation to the Q wave until it is lost in the rapid ventricular depolarizationspikes.
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deflection occurring simultaneously with or shortly before the onset of the peripheral QRS because of the Mahaim fiber. Because the AV node is bypassed by the James tract, accelerating the rate by atrial pacing results in little change in the PR interval as seen on the peripheral ECG (Fig. 6). On the HIS bundle electrogram. however. findings are somewhat different. Because the James tract terminates in the distal node or the proximal bundle of HIS, the AV node is bypassed above the site of recording of the HBE. With atrial pacing the AH remains relatively constant, increasing only slightly, if at all. Because the AH interval does not increase with pacing, the HIS deflection does not move into the QRS, and the relationship of the HIS to the QRS remains constant. The combination of a markedly short HV interval during sinus rhythm, a relatively constant AH interval, and a constant HV interval during atrial pacing is suggestive of WPW due to the combination of a functioning James tract and a functioning Mahaim fiber. The response to premature atrial stimulation with respect to the PR. AH. and HV intervals is similar to that seen with atrial pacing and carries the same connotations with regard to the diagnosis of WPW and the mechanism for its occurrence. Of eight patients with WPW recently studied in our laboratory, six showed evidence of Kent conduction and two of conduction via a combination of a James tract and a Mahaim fiber (18). THE HBE DURING TACHYCARDIAS
The mechanism for the supraventricular tachycardias seen in WPW has also been elucidated using the HIS bundle electrogram. With the presence of two conduction pathways from the ventricles to the atria, the normal AV node-HIS pathway and the accessory pathway. the possibility for a
..
1
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HR lOO/MlN SH-SO YSEC SO-110 YSEC
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Fig. 6. HIS bundle electrograms during sinus rhythm and atrial pacing in a patient with James and Mahaim fiber conduction. During sinus rhythm the HIS spike occurs before the onset of the Q wave with a short Minterval. On atrial pacing the S-H interval, which is 90 Msec at a heart rate of 100/min, does not show any increase at a heart rate of 162/min. The relationship of the HIS deflection and the Q wave on the surface ECG stays constant at all pacing rates.
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reentrant tachycardia exists. If the ventricles are depolarized antegrade via one of the pathways, it is possible for the impulse to be conducted retrograde back to the atrium via the second pathway. During tachycardia in most patients with WPW, the QRS is of normal duration and configuration, suggesting that antegrade conduction from the atria to the ventricles has occurred via the normal pathway (Fig. 7). This has been confirmed with HIS bundle electrograms taken during tachycardia that have documented that a HIS bundle depolarization occurs before each QRS with a normal HV interval (6). Although not recorded on the HBE, it can be postulated that retrograde conduction then occurs via the acessory pathway. Confirmation for this sequence of events in seen when the mechanism of onset of the tachycardia is analyzed using the HBE. During sinus rhythm, conduction to the ventricles in patients with WPW occurs via both the normal and the accessory pathway simultaneously, causing both pathways to be depolarized simultaneously and both pathways to be refractory simultaneously, so that reentry via one of the two pathways does not occur. The length of time that the two pathways are refractory is not the same, however; the refractory period of the accessory pathway is usually longer than that of the normal node-HIS pathway (7,24). If a premature atrial beat occurs and is early enough in the cardiac cycle to arrive at the accessory pathway when it is still refractory but arrives at the AV node when the node is no longer refractory, the impulse will be conducted to the ventricles solely over the normal pathway and will depolarize the ventricles in the normal sequence with no delta wave and a normal HV interval. By the time the area of the ventricle on the ventricular side of the accessory pathway is depolarized, however, the accessory pathway may have recovered, be no longer refractory, and will conduct retrograde to the atria leading to a reentrant tachycardia. The route of the reentry tachycardia is atrium to A V node-HIS to ventricles (antegrade) to accessory pathway to atrium (retrograde) to node to ventricles and so on. Evidence for the disparity between the refractory periods of the normal and the accessory pathways has come from the work of Durrer's group in Holland (24). In five of six patients with WPW, who were studied using the HBE and the extrastimulus technique, the absolute refractory period of the AV node pathway was
one
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o n
'I. Fig. 7. Supraventricular tachycardia induced by a premature atrial beat. After the second QRS complex a premature atrial beat delivered at a short coupling interval(280 Msec), is conducted to the HIS bundle with a prolonged P-H interval. Conduction through the anomalous pathway falls, as evidenced by the normal QRS configuration with absence of the delta wave. The subsequent p waves represent retrograde depolarization of the atria via the anomalous pathway and are followed by a HIS bundlespike and a QRS with a normal K V interval. There is no delta wave on the QRSs during tachycardia. Right bundle branch block is present during tachycardia.
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found to be shorter than that of the accessory pathway. Of interest was the finding by this group that digitals tended to shorten the refractory period of the accessory pathway and lengthen the R F of the normal pathway. This equalization of the two refractory periods leads to a decrease in the opportunity for reentrant tachycardias and may explain the clinical finding that in some patients with WPW, digitalization will inhibit the occurrence of tachycardia. During atrial fibrillation in patients with WPW, the AV conduction pathway varies between purely AV nodal conduction with a normal QRS (because the accessory pathway is refractory), purely accessory pathway conduction with widely aberrant QRSs (because the node is refractory), and combination beats of varying form with varying lengths of the delta wave (depending on the relative refractoriness of each of the pathways). Because of its effect on the refractory period of the accessory pathway, digitalis may be dangerous in patients with WPW who have bouts of atrial fibrillation, because the decrease in the period of refractoriness of the accessory pathway may result in a more rapid ventricular response rate. The mechanism of termination of the tachycardia by pacing the right atrium has also been demonstrated using the HBE (6, 25). Depolarization of the atria or ventricles prematurely by electrical pacing, if produced at a time in the cycle that results in causing the chamber to be refractory to the reentering impulse, will interrupt the reentry circuit and terminate the tachycardia. One of the newer modes of thereapy for the tachycardias associated with WPW, the implantation of a permanent demand pacemaker in the right ventricle (26), utilizes this mechanism. The demand rate is set low so that the pacemaker does not fire when the patient is in sinus rhythm. If a tachycardia occurs, the demand circuit is turned off externally by placing a magnet over the pacemaker generator, and the pacer is allowed to fire regularly. The impulses fall at varying times in the cardiac cycle during the tachycardia because the rate of the tachycardia and of the pacer are different. If the pacer impulse depolarizes the ventricle at an appropriate time, the reentry pathway will be broken and normal sinus rhythm will occur. In recent years, a number of reports, primarily from the group at Duke, have documented the success of surgically treating WPW by cutting the bypass tract (27). Surgery of this type is a serious undertaking, and there have been a number of reports of failure of the procedure (28); this mode of therapy should be considered only in those patients with recurrent arrhythmias that are refractory to medical therapy. Prior to the procedure it is wise to document the presence of a Kent bundle by HBE and atrial pacing; as yet there are no reported cases with the combination of James and Mahaim fibers that have been successfully operated upon. The operative procedure consists of thoracotomy and mapping of the sequence of depolarization in the ventricles to find the area of the ventricles that is depolarized earliest and causes the delta wave. This area is usually in the region of the right atrial-right ventricular groove in patients with Type B WPW (27) and is found in the area of the basal endocardium of the left ventricle in Type A (29). On the right side, the AV groove is cut, separating the atrium from the ventricle in the area of earliest ventricular depolarization. On the left side, success is best achieved if the LA is opened and the AV groove incised on the endothelial surface. Occasionally, the
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peripheral ECG is inaccurate in predicting the site of the bypass tract. The procedure is, as yet. experimental and much work must be done yet to document its long-term success before patients with less than intractable life-threatening arrhythmia are subjected to it. REFERENCES I . Wolff L. Parkinson J and White, PD: Bundle branch block with short P-R interval in healthy young people prone to paroxysmal atrial tachycardia. Am. Heart:; 5 5 8 5 , 1930. 2. Wilson, FN: A case in which the Vagus influences the form of the ventricular complex of the electrocardiogram. Arch. Int. Med. 16:1008, 1951. 3 . Rosenbaum FF, Hecht HH. Wilson FN and Johnston FD: The potential variations of the thorax and the oesophagus in anomalous A-V excitation (WPW syndrome). Am. Heart J. 29:281, 1945. 4. Castellanos A Jr, Chapunoff E. Castillo CA, Maytin 0 and Lemberg L: His-bundle electrograms in two cases of Wolff-Parkinson-White (pre-excitation). Circulation 41:399. 1970. 5 . Narula 0s: Wolff-Parkinson-White syndrome - A review. Circulation 47:872, 1973. 6. Durrer D, Schoo L, Schuilenburg RM and Wellens HJJ: The role of premature beats in the initiation of supraventricular tachycardia in the WPW syndrome. Circulation 36544, 1967. 7. Lau SH, Josephson ME, Gallagher JJ, Caracta AR, Varghese PJ and Damato AN: Refractoriness of the accessory pathway and mechanisms of reentry in the Wolff-Parkinson-White phenomenon (abstract). Am. J. Cardiol. 29:275, 1972. 8. Lev M: The pre-excitation syndrome: Anatomic considerations of anomalous AV pathways. I n (Dreifus LS and Likoff WS, eds): Mechanisms and Therapy of Cardiac Arrhythmias. New York: Grune and Stratton, 1966. p. 665. 9. Butterworth JS and Pointdexter CA: Fusion beats and their relation to the syndrome of short P-R interval associated with a prolonged QRS complex. Am. Heart J. 2 8 149, 1944. 10. Lister JW. Stein E, Kosowsky BD, Lau SH and Damato AN: Atrioventricular conduction in man. Effects of rate, exercise, isoproterenol and atropine on the P-R interval. Am. J. Cardiol. 16516, 1965. 1 1 . Kent AFS: The Right lateral auriculo-ventricular junction of the heart. J. Physiol. 48:22, 1914. 12. James TN: Morphology of the human A-V node with remarks pertinent to its electrophysiology. Am. Heart J. 62:756, 1%1. 13. Sano T and Yamagishi S: Spread of excitation from the sinus node. Circ. Res. 16:423, 1%5. 14. Vasalle M and Hoffman BF: The spread of sinus activation during potassium administration. Circ. Res. 17:285, 1965. 15. Hogan PM and Davis LD: Evidence for specialized fibers in the canine right atrium. Circ. Res. 23:387, 1968. 16. Ferrer MI: New concepts relating to the pre-excitation syndrome. JAMA 201:163, 1967. 17. Mahaim I and Benatt A: Nouvelles recherches sur les connexions superieures de la branche gauche du faisceau de His-Tawara avec la cloison interventriculairie. Cardiologia 1:61, 1937. 18. Gomes JA and Haft JI: His bundle electrograms and atrial pacing studies in eight cases of W.P.W. (abstract). Clin. Res. 22:277A, 1974. 19. Caracta AR, Damato AN, Gallagher JJ, Josephson ME, Varghese PJ, Lau SH and Westura EE: Electrophysiologic studies in the syndrome of short P-R interval and normal QRS complex. Am. J. Cardiol. 31:245, 1973. 20. Scherlag JB, Lau SH. Helfant RH, Berkowitz MD, Stein E and Damato AN: Catheter technique for recording His bundle activity in man. Circulation 39:13, 1969. 21. Hecht HH, Kossman CE, Childers RW, Langedorf R, Lev M, Rosen KM, Pruitt RD, Truex RC, Uhley HN and Watt TB: Atrioventricular and intraventricular conduction. Revised nomenclature and concepts. Am. J. Cardiol. 31:232-244, 1973. 22. Coumel P, Waynberger M, Fabiato A Slama R, Aigueperse J and Bouvrain J: Wolf€-ParkinsonWhite syndrome: Problem in evaluation of multiple accessory pathway and surgical therapy. Circulation 45:1212, 1972.
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23. Castillo CA, Castellanos A Jr, Agha AS and Myerburg RJ: Significance of His-bundle recordings with short H-V intervals. Chest 60:142. 1972. 24. Wellens HJ and Durrer D: Effects of digitalis on A-V conduction and circus movement tachycardias in patients with W.P.W. Circulation 47:1229. 1973. 25. Haft JI: Treatment ofarrhythmias by intracardiac stimulation. Prog. Cardiovasc. Dis. 16339. 1974. 26. Ryan GF, Easley RM. Zaroff LI and Goldstein S: Paradoxical use of a demand pacemaker in treatment of supraventricular tachycardia due to the W.P. W. syndrome. Circulation 38: 1037, 1968. 27. Cobb FR. Blumenschien SD. Sealy WC. Boineau JP. Wagner GS and Wallace AC: Successful surgical interruption of the bundle of Kent in a patient with Wolff-Parkinson-White syndrome. Circulation 38: 1018. 1968. 28. Burchell HB. Frye RL. Anderson MW and McGoon DC: Atrioventricular and ventriculo-atrial excitation in W.P. W. syndrome (Type B). Temporary ablationat surgery. Circulation 36:663,1%7. 29. Neutze JM, Kerr AR and Whitlock RML: Epicardial mapping in a variant of Type A. W.P.W. syndrome. Circulation 48: 662. 1973.
