Fundamentals of clinical cardiology Clinical uses of His bundle electrocardiography. Part III Masood Akhtar, M.D. Anthony N. Damato, M,D. Sun H. Lau, M.D. Andres R. Ticzon, M.D. Staten Island, N. Y.
Wolff-Parkinson-White (WPW) syndrome Both His bundle 1-~ and epicardial mapping techniques 3-~ have significantly helped in clarifying some aspects of the WPW syndrome. In addition, these studies have given further testimony to the myriad complexities involved in this syndrome. Pre-excitation of the ventricles resulting in a delta wave and short P-R interval (p-todelta) constitute the basic electrocardiographic (ECG) abnormality and the hallmark for recognition of this syndrome,s During sinus rhythm, ventricular pre-excitation may always be present or may alternate for varying periods of time with normal ventricular activation. The frequent occurrence of supraventricular tachycardias (mostly re-entrant in nature) in patients with pre-excitation make this syndrome an important clinical entity. There exists considerable anatomic and electrophysiologic evidence indicating that the delta wave represents early activation of the ventricles by an atrial impulse which is antegradely conducted to the ventricles via a bypass or anomalous tract (bundle of Kent). Since atrial impulses are simultaneously conducted to the ventricles through the normal A-V pathway, the QRS complex in a majority of cases represents fusion activation, i.e., the delta wave represents ventricular pre-excitation through the bypass tract and the rest of the QRS complex is due to activation of the ventricles through the From the Cardiopulmonary Laboratory, United States Public Health Service Hospital. Staten Island. New York. This work was supported in part by the Bureau of Medical Services, USPHS Project Py 75-1, and National Heart and Lung Institute Projects HE 12536-04. Received for publication May 29, 1975. Reprint requests: Masood Akhtar, M.D., Cardiopulmonary Laboratory, United States Public Health Service Hospital. Staten Island, N. Y. 10304.
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normal A-V nodal HPS. Thus, most patients with the WPW syndrome will demonstrate a normal A-H interval and a foreshortened H-V interval (Fig. 1, panel A). If an atrial impulse is significantly delayed or blocked within the A-V nodalHis Purkinje System (HPS), the ventricles will be totally activated via the bypass tract. Conversely, if A-V nodal conduction is enhanced, a greater amount of ventricular excitation will occur through the normal A-V conducting system and the QRS complex will tend toward normalization. Total pre-excitation o f the ventricles can be achieved either by incremental atrial pacing or by premature depolarization of the atrium during the refractory period of the A-V node. Incremental atrial pacing causes progressive delay or block within the A-V node while the P-to-delta interval usually remains constant. As a result of the increasing A-H intervals, the bundle of His deflection merges into and is obscured by the ventricular electrogram (Fig. 1, panel A). Fig. 1 shows the effect of premature atrial depolarizations. The P-to-delta interval remains constant but there is progressive A-V nodal delay. The premature atrial beat in panel B reaches the bundle of His after the ventricles have been totally pre-excited by the anomalous pathway. If A-V nodal delay is significant and the ventricular muscle has recovered, double excitation of the ventricles by a single atrial impulse will occur (panel C). Pre-excitation can mimic the ECG pattern of myocardial infarction. 7, s The distinction can be made by "normalizing" the QRS complex, which can almost always be achieved by introducing a premature atrial depolarization during the effective refractory period of the accessory pathway. When the ventricles are activated entirely by the
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Fig. 1. Effect of atrial premature stimulation in ventricular pre-excitation. The first beat in panel A is a sinus beat. The A-H interval measures 115 msec. and the H-V interval (H-delta} is nonexistent. The orientation of delta on the surface ECG is suggestive of type A ventricular pre-excitation. A premature atrial beat (As)results in delay in A-V nodal conduction time such that H2 merges into and is obscured by the ventricular electrogram. The P-to-delta interval remains constant and the QRS shows more pre-excitation compared to the preceding sinus beat. In panel B an earlier premature beat results in further increase in A.~H2interval and H, now emerges from the ventricular electrogram. Ventricular activation occurred exclusively via the bypass tract since no contribution to ventricular activation can be expected from the premature impulse traveling along the normal pathway. Panel C demonstrates double ventricular activation from a single premature atrial beat, resulting first from exclusive conduction over the bypass tract and second by conduction along the normal pathway. A-V nodal H i s - P u r k i n j e system, t h e r e s u l t a n t Q R S p a t t e r n can be e x a m i n e d for t h e presence or absence of changes consistent with i n f a r c t i o n or ischemia (Fig. 2). T h e incidence of s u p r a v e n t r i c u l a r t a c h y c a r d i a s (SVT) in p a t i e n t s with the W P W s y n d r o m e h a s been e s t i m a t e d to be as high as 70 per cent a n d an overwhelming n u m b e r of these are r e - e n t r a n t in n a t u r e 2 -11 However, p a t i e n t s with this s y n d r o m e m a y also develop ectopic atrial t a c h y c a r d i a s or atrial fibrillation. D u r i n g atrial fibrillation a n t e grade conduction m a y occur along t h e A-V n o d e H P S or accessory p a t h w a y (Fig. 3). T h e l a t t e r m a y mimic or induce v e n t r i c u l a r t a c h y c a r d i a a n d fibrillation. R e - e n t r a n t t a c h y c a r d i a s are m o s t often initiated by p r e m a t u r e atrial b e a t s (Fig. 2, panels D and E) and less c o m m o n l y b y v e n t r i c u l a r e x t r a systoles. Since the m a j o r i t y of r e - e n t r a n t t a c h y cardias are associated with n o r m a l Q R S complexes, it is generally accepted t h a t the reciprocating impulse is a n t e g r a d e l y c o n d u c t e d to t h e ventricles b y the A-V n o d a l H P S a n d retrogradely b a c k to the a t r i u m b y t h e accessory p a t h w a y . This r o u t e of r e - e n t r y r e q u i r e s t h a t some portion of the ventricle be a c t i v a t e d prior to retrograde c o n d u c t i o n to the atria. However, in some cases t h e S V T m a y result entirely f r o m ree n t r y within t h e A-V node which is suggested b y the following: (1) initiation of a S V T (with lowto-high atrial sequence of a c t i v a t i o n ) following a
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p r e m a t u r e atrial b e a t which a n t e g r a d e l y blocks within the H P S , i.e., no v e n t r i c u l a r depolarizationl~; A-V nodal r e - e n t r y is also suggested w h e n a functional A-V block within the H P S occurs during a sustained t a c h y c a r d i a (Fig. 5 of P a r t II); (2) if, during a SVT, r e t r o g r a d e a c t i v a t i o n of the atria (Ae) precedes v e n t r i c u l a r d e p o l a r i z a t i o n (i.e,, H - A e < H - V interval), it is unlikely t h a t retrograde conduction via a K e n t b u n d l e is required to sustain the t a c h y c a r d i a (Fig. 3 of P a r t II); (3) initiation of a S V T (with low-to-high sequence o f atrial a c t i v a t i o n ) during an A-V nodal W e n c k e b a c h cycle in which criterion No. 2 is satisfied, i.e., atrial a c t i v a t i o n of echo b e a t s precedes ventricular depolarization; (4) w h e n i n c r e m e n t a l v e n t r i c u l a r pacing reveals exclusive retrograde conduction via the n o r m a l A-V conduction system. 13 Utilization of the accessory p a t h w a y for retrograde conduction to the a t r i a during a S V T with n o r m a l Q R S complexes is suggested b y the following. (1) A short c o n s t a n t V-A i n t e r v a l over a full range of i n c r e m e n t a l l y paced v e n t r i c u l a r rates: T h e suggestion t h a t r e t r o g r a d e c o n d u c t i o n is occurring via an accessory p a t h w a y is m o r e firmly established when, during p r e m a t u r e ventricular stimulation, it can be d e m o n s t r a t e d t h a t the V-A i n t e r v a l r e m a i n s c o n s t a n t a n d short, a n d retrograde atrial a c t i v a t i o n (A2) precedes a delayed retrograde His b u n d l e a c t i v a t i o n (H2)~ (2) If during a S V T a single v e n t r i c u l a r b e a t oc-
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Fig. 2. Effects of atl4al premature stimulation in WPW syndrome. Panel A shows sinus rhythm. The A-H and H-V intervals measure 90 and 30 msec., respectively. The superior orientation of the delta wave mimics a diaphragmatic myocardial infarction (Q waves in Leads II and III). Panels B to D show the effects of progressive premature atrial beats on ventricular excitation. The premature beat in panel B results in more pre-excitation (the H deflection is obscured by ventricular electrogram). In panel C, at an atrial coupling interval of 370 msec. the accessory pathway if refractory and conduction occurs over the normal pathway, resulting in a "normalized" QRS complex {slightly aberrant). In panel D an earlier premature beat conducts exclusively over the normal pathway and returns to the atria (Ae) via the accessory pathway which initiates a sustained SVT {panel E). The narrow QRS complexes and H-V interval in panel E suggest that ventricular activation during the SVT occurred over the normal pathway. Note also the absence of Q waves in Leads II and III during the tachycardia. c u r r i n g s i m u l t a n e o u s l y w i t h or f o l l o w i n g s h o r t l y a f t e r t h e a n t e g r a d e His b u n d l e d e p o l a r i z a t i o n r e s u l t s i n a s h o r t e r a t r i a l cycle l e n g t h w i t h s i m i l a r a t r i a l a c t i v a t i o n s e q u e n c e as d u r i n g t h e s p o n t a n e o u s S V T . 14 (3) I f t h e r a t e of S V T d u r i n g t h e
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d e v e l o p m e n t of a f u n c t i o n a l b u n d l e b r a n c h b l o c k is less t h a n d u r i n g n o r m a l v e n t r i c u l a r a c t i v a tion15, 1~: T h i s o b s e r v a t i o n n o t 0 n l y s u g g e s t s r e t r o g r a d e c o n d u c t i o n Via a n a c c e s s o r y p a t h w a y b u t also i n d i c a t e s w h e t h e r t h e site of i n s e r t i o n of
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Fig. 3. Atrial fibrillation in the WPW syndrome. The cop panel shows t h a t during atrial fibrillation ventricular activation initially occurs exclusively over the normal pathway as indicated by the absence of delta, narrow QRS complexes, and H-V intervals of 50 msec. (first four beats}, Subsequently ventricular activation occurred over the accessory pathway (wide QRS complexes), which mimics a ventricular tachycardia. The bottom panel shows spontaneous termination of atrial fibrillation. Note ventricular pre-excitation during sinus beats.
Fig. 4. The tracing shows a SVT (cycle length 365 msec.) with a low-to-high sequence of atrial activation (Ae) in a patient without evidence of WPW syndrome. A premature ventricular beat (S) introduced during the SVT conducts to the atria (Ar) and results in a similar atrial activation sequence. The atrial cycle length is shortened to 300 msec. and the SVT is terminated, The constant H-H intervals prior to termination of the tachycardia suggest that the last H deflection results from antegrade depolarization and was unaffected by the premature ventricular beat. Thus retrograde activation of the atria by the premature ventricular beat in all probability occurred via anomalous pathway, which was not operative antegradely. 808
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t h e b y p a s s t r a c t is i n t o t h e left or r i g h t v e n t r i c l e . T h i s is especially t r u e i f a c o n t r a l a t e r a l b u n d l e b r a n c h b l o c k h a s n o i n f l u e n c e o n t h e r a t e of SVT. I f a p a t i e n t w i t h a left v e n t r i c u l a r b y p a s s connection develops L B B B during a r e - e n t r a n t S V T , d e l a y e d left v e n t r i c u l a r a c t i v a t i o n will r e s u l t i n d e l a y e d a c t i v a t i o n of t h e a t r i a via t h e left-sided b y p a s s . I f s u c h a p a t i e n t d e v e l o p s a f u n c t i o n a l r i g h t b u n d l e b r a n c h block, t h e a t r i a l r a t e d u r i n g t h e S V T will b e u n a f f e c t e d . R e e n t r a n t circuits l o c a t e d e n t i r e l y i,n t h e A - V n o d e are i n d e p e n d e n t of c o n d u c t i o n d e l a y or b l o c k within the HPS. Therefore, atrial rates in A-V n o d a l r e - e n t r a n t S V T do n o t c h a n g e w i t h t h e o n s e t of f u n c t i o n a l b l o c k i n t h e H P S . I t m u s t b e emphasized that ventricular rates in A-V nodal r e - e n t r a n t S V T m a y v a r y if f u n c t i o n a l b l o c k i n t h e H P S is a s s o c i a t e d w i t h v a r i a b l e H - V p r o l o n g a t i o n or c o m p l e t e f a i l u r e of c o n d u c t i o n i n t h e H P S (Fig. 5, of P a r t II). W i t h t h e use of s o m e of t h e a b o v e c r i t e r i a it is possible to a c c u m u l a t e e v i d e n c e t h a t i n s o m e p a t i e n t s w i t h o u t e v i d e n c e of a n t e g r a d e v e n t r i c u l a r p r e - e x c i t a t i o n o n t h e s t a n d a r d E C G , reentrant supraventricular tachycardias utilize a r e t r o g r a d e b y p a s s t r a c t (Fig. 4). I t s h o u l d be n o t e d t h a t a n a t o m i c l o c a l i z a t i o n of r e - e n t r a n t c i r c u i t s i n p a t i e n t s w i t h W P W s y n d r o m e is of m o r e t h a n a c a d e m i c i n t e r e s t s i n c e surgical t r e a t m e n t is b e i n g u s e d i n c r e a s i n g l y i n those p a t i e n t s w i t h d i s a b l i n g r e - e n t r a n t t a c h y c a r dias which are r e f r a c t o r y t o m e d i c a l t h e r a py.17.18 REFERENCES
L Castellanos, A., Chapunoff, E.. Castillo, C., Maytin, O., and Lemburg, L.: His bundle electrograms in two cases of Wolff-Parkinson-White (we-excitation syndrome), Circulation 41:399, 1970. 2. Castillo. C.. and Castellanos, A.: His bundle recordings in patients with reciprocating tachycardias and WolffParkinson-White syndrome, Circulation 42:271, 1970. 3. Svenson, R. H., Gallagher, J. J., Sealy, W. C., and Wallace, A. G.: An electrophysiologic approach to the surgical treatment of the Wolff-Parkinson-White syndrome. Report of two cases utilizing catheter recording and epicardial mapping techniques, Circulation 49:799, 1974.
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4. Durrer, D., and Roos, J. P.: Epicardial excitation of the ventricles in a patient with Wolff-Parkinson-White syndrome (Type B), Circulation 35:15, 1967. 5. Sealy, W. C., Boineau, J. P., and Wallace, A. G.: The identification and division of the bundle of Kent for premature excitation and supraventricular tachycardia, Surgery 68:1009, 1970. 6. Wolff,L., Parkinson, J., and White, P. D.: Bundle branch block with short P-R interval in healthy young people prone to paroxysmal tachycardla, AM. HEART J. 5:685, 1930. 7. Wolff, L.: Electrocardiography: Fundamentals and clinical application, Philadelphia, 1950,~W. B. Saunders Company, p. 178. 8. Wolff,L., and Richman, J. L.: The diagnosis of myocardial infarction in patients with anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome), AM. HEART J. 45:545, 1953. 9. Durrer, D., Schoo, L., Schuilenburg, R. M., and Wellens, H. J. J.: The role of premature beats in the initiation and termination of supraventricular tachycardias in the Wolff-Parkinson-White syndrome, Circulation 36:644, 1967. 10. Wellens, H. J. J., Schuilenberg, R. M., and Durrer, D.: Electrical stimulation of the heart in patients with Wolff-Parkinson-White syndrome (Type A), Circulation 43:99, 1971. 11. Lister, J. W., Worthington, F. X., Gentsch, T. 0. Swenson, J. A., Nathan, D. A., and Grosselin, A. J.: Preexcitation and tachycardias in the Wolff-Parkinson-White syndrome, Type B, Circulation 45:1081, 1972: 12. Lau, S. H., Caracta, A. R., Josephson, M. E., Batsford, W. P., Akhtar, M., and Damato, A. N.: Mechanisms of paroxysmal atrial tachycardia in the WPW syndrome (abst.), Circulation 47, 48(Suppl. IV): 1973. 13. Wellens, H. J. J., and Durrer, D.: Pathways of tachycardia in WPW syndrome (abst.), Circulation 49, 50(Suppl. III): 1974. 14. Zipes, D. P., DeJoseph, R. L., and Rothbaum, D.: Unusual properties of accessory pathways, Circulation 49:1200, 1974. 15. Coumel, P., and Attuel, P.: Reciprocating tachycardia in overt and latent pre-excitation influence of functional bundle branch block on the rate of tachycardia, Eur. J. Cardiol. 1:423, 1974. 16. Coumel, P., and Attuel, P.: Localization of the circus movement during reciprocating tachycardia in WolffParkinson-White syndrome, in His bundle electrocardiography and clinical electrophysiology, Narula, O. S., ed., Philadelphia, 1975, F. A. Davis Company, Chap. 16, p. 343. 17. Cobb, F. R., Blumenschein, S. D., Sealy, W. C., Boineau, J. P., Wagner, G. S., and Wallace, A. G.: Successful surgical interruption of the bundle of Kent in a patient with Wolff-Parkinson-White syndrome, Circulation 38:1018, 1968. 18. lwa, T., Kazui, T., Sagii, S., and Wada, J.: Surgical treatment of the Wolff-Parkinson-Whitesyndrome, Jap. J. Thorac. Surg. 23:513, 1970.
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Wolff-Parkinson-White (WPW) syndrome Both His bundle 1-~ and epicardial mapping techniques 3-~ have significantly helped in clarifying some aspects of the WPW syndrome. In addition, these studies have given further testimony to the myriad complexities involved in this syndrome. Pre-excitation of the ventricles resulting in a delta wave and short P-R interval (p-todelta) constitute the basic electrocardiographic (ECG) abnormality and the hallmark for recognition of this syndrome,s During sinus rhythm, ventricular pre-excitation may always be present or may alternate for varying periods of time with normal ventricular activation. The frequent occurrence of supraventricular tachycardias (mostly re-entrant in nature) in patients with pre-excitation make this syndrome an important clinical entity. There exists considerable anatomic and electrophysiologic evidence indicating that the delta wave represents early activation of the ventricles by an atrial impulse which is antegradely conducted to the ventricles via a bypass or anomalous tract (bundle of Kent). Since atrial impulses are simultaneously conducted to the ventricles through the normal A-V pathway, the QRS complex in a majority of cases represents fusion activation, i.e., the delta wave represents ventricular pre-excitation through the bypass tract and the rest of the QRS complex is due to activation of the ventricles through the From the Cardiopulmonary Laboratory, United States Public Health Service Hospital. Staten Island. New York. This work was supported in part by the Bureau of Medical Services, USPHS Project Py 75-1, and National Heart and Lung Institute Projects HE 12536-04. Received for publication May 29, 1975. Reprint requests: Masood Akhtar, M.D., Cardiopulmonary Laboratory, United States Public Health Service Hospital. Staten Island, N. Y. 10304.
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normal A-V nodal HPS. Thus, most patients with the WPW syndrome will demonstrate a normal A-H interval and a foreshortened H-V interval (Fig. 1, panel A). If an atrial impulse is significantly delayed or blocked within the A-V nodalHis Purkinje System (HPS), the ventricles will be totally activated via the bypass tract. Conversely, if A-V nodal conduction is enhanced, a greater amount of ventricular excitation will occur through the normal A-V conducting system and the QRS complex will tend toward normalization. Total pre-excitation o f the ventricles can be achieved either by incremental atrial pacing or by premature depolarization of the atrium during the refractory period of the A-V node. Incremental atrial pacing causes progressive delay or block within the A-V node while the P-to-delta interval usually remains constant. As a result of the increasing A-H intervals, the bundle of His deflection merges into and is obscured by the ventricular electrogram (Fig. 1, panel A). Fig. 1 shows the effect of premature atrial depolarizations. The P-to-delta interval remains constant but there is progressive A-V nodal delay. The premature atrial beat in panel B reaches the bundle of His after the ventricles have been totally pre-excited by the anomalous pathway. If A-V nodal delay is significant and the ventricular muscle has recovered, double excitation of the ventricles by a single atrial impulse will occur (panel C). Pre-excitation can mimic the ECG pattern of myocardial infarction. 7, s The distinction can be made by "normalizing" the QRS complex, which can almost always be achieved by introducing a premature atrial depolarization during the effective refractory period of the accessory pathway. When the ventricles are activated entirely by the
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Fig. 1. Effect of atrial premature stimulation in ventricular pre-excitation. The first beat in panel A is a sinus beat. The A-H interval measures 115 msec. and the H-V interval (H-delta} is nonexistent. The orientation of delta on the surface ECG is suggestive of type A ventricular pre-excitation. A premature atrial beat (As)results in delay in A-V nodal conduction time such that H2 merges into and is obscured by the ventricular electrogram. The P-to-delta interval remains constant and the QRS shows more pre-excitation compared to the preceding sinus beat. In panel B an earlier premature beat results in further increase in A.~H2interval and H, now emerges from the ventricular electrogram. Ventricular activation occurred exclusively via the bypass tract since no contribution to ventricular activation can be expected from the premature impulse traveling along the normal pathway. Panel C demonstrates double ventricular activation from a single premature atrial beat, resulting first from exclusive conduction over the bypass tract and second by conduction along the normal pathway. A-V nodal H i s - P u r k i n j e system, t h e r e s u l t a n t Q R S p a t t e r n can be e x a m i n e d for t h e presence or absence of changes consistent with i n f a r c t i o n or ischemia (Fig. 2). T h e incidence of s u p r a v e n t r i c u l a r t a c h y c a r d i a s (SVT) in p a t i e n t s with the W P W s y n d r o m e h a s been e s t i m a t e d to be as high as 70 per cent a n d an overwhelming n u m b e r of these are r e - e n t r a n t in n a t u r e 2 -11 However, p a t i e n t s with this s y n d r o m e m a y also develop ectopic atrial t a c h y c a r d i a s or atrial fibrillation. D u r i n g atrial fibrillation a n t e grade conduction m a y occur along t h e A-V n o d e H P S or accessory p a t h w a y (Fig. 3). T h e l a t t e r m a y mimic or induce v e n t r i c u l a r t a c h y c a r d i a a n d fibrillation. R e - e n t r a n t t a c h y c a r d i a s are m o s t often initiated by p r e m a t u r e atrial b e a t s (Fig. 2, panels D and E) and less c o m m o n l y b y v e n t r i c u l a r e x t r a systoles. Since the m a j o r i t y of r e - e n t r a n t t a c h y cardias are associated with n o r m a l Q R S complexes, it is generally accepted t h a t the reciprocating impulse is a n t e g r a d e l y c o n d u c t e d to t h e ventricles b y the A-V n o d a l H P S a n d retrogradely b a c k to the a t r i u m b y t h e accessory p a t h w a y . This r o u t e of r e - e n t r y r e q u i r e s t h a t some portion of the ventricle be a c t i v a t e d prior to retrograde c o n d u c t i o n to the atria. However, in some cases t h e S V T m a y result entirely f r o m ree n t r y within t h e A-V node which is suggested b y the following: (1) initiation of a S V T (with lowto-high atrial sequence of a c t i v a t i o n ) following a
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p r e m a t u r e atrial b e a t which a n t e g r a d e l y blocks within the H P S , i.e., no v e n t r i c u l a r depolarizationl~; A-V nodal r e - e n t r y is also suggested w h e n a functional A-V block within the H P S occurs during a sustained t a c h y c a r d i a (Fig. 5 of P a r t II); (2) if, during a SVT, r e t r o g r a d e a c t i v a t i o n of the atria (Ae) precedes v e n t r i c u l a r d e p o l a r i z a t i o n (i.e,, H - A e < H - V interval), it is unlikely t h a t retrograde conduction via a K e n t b u n d l e is required to sustain the t a c h y c a r d i a (Fig. 3 of P a r t II); (3) initiation of a S V T (with low-to-high sequence o f atrial a c t i v a t i o n ) during an A-V nodal W e n c k e b a c h cycle in which criterion No. 2 is satisfied, i.e., atrial a c t i v a t i o n of echo b e a t s precedes ventricular depolarization; (4) w h e n i n c r e m e n t a l v e n t r i c u l a r pacing reveals exclusive retrograde conduction via the n o r m a l A-V conduction system. 13 Utilization of the accessory p a t h w a y for retrograde conduction to the a t r i a during a S V T with n o r m a l Q R S complexes is suggested b y the following. (1) A short c o n s t a n t V-A i n t e r v a l over a full range of i n c r e m e n t a l l y paced v e n t r i c u l a r rates: T h e suggestion t h a t r e t r o g r a d e c o n d u c t i o n is occurring via an accessory p a t h w a y is m o r e firmly established when, during p r e m a t u r e ventricular stimulation, it can be d e m o n s t r a t e d t h a t the V-A i n t e r v a l r e m a i n s c o n s t a n t a n d short, a n d retrograde atrial a c t i v a t i o n (A2) precedes a delayed retrograde His b u n d l e a c t i v a t i o n (H2)~ (2) If during a S V T a single v e n t r i c u l a r b e a t oc-
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Fig. 2. Effects of atl4al premature stimulation in WPW syndrome. Panel A shows sinus rhythm. The A-H and H-V intervals measure 90 and 30 msec., respectively. The superior orientation of the delta wave mimics a diaphragmatic myocardial infarction (Q waves in Leads II and III). Panels B to D show the effects of progressive premature atrial beats on ventricular excitation. The premature beat in panel B results in more pre-excitation (the H deflection is obscured by ventricular electrogram). In panel C, at an atrial coupling interval of 370 msec. the accessory pathway if refractory and conduction occurs over the normal pathway, resulting in a "normalized" QRS complex {slightly aberrant). In panel D an earlier premature beat conducts exclusively over the normal pathway and returns to the atria (Ae) via the accessory pathway which initiates a sustained SVT {panel E). The narrow QRS complexes and H-V interval in panel E suggest that ventricular activation during the SVT occurred over the normal pathway. Note also the absence of Q waves in Leads II and III during the tachycardia. c u r r i n g s i m u l t a n e o u s l y w i t h or f o l l o w i n g s h o r t l y a f t e r t h e a n t e g r a d e His b u n d l e d e p o l a r i z a t i o n r e s u l t s i n a s h o r t e r a t r i a l cycle l e n g t h w i t h s i m i l a r a t r i a l a c t i v a t i o n s e q u e n c e as d u r i n g t h e s p o n t a n e o u s S V T . 14 (3) I f t h e r a t e of S V T d u r i n g t h e
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d e v e l o p m e n t of a f u n c t i o n a l b u n d l e b r a n c h b l o c k is less t h a n d u r i n g n o r m a l v e n t r i c u l a r a c t i v a tion15, 1~: T h i s o b s e r v a t i o n n o t 0 n l y s u g g e s t s r e t r o g r a d e c o n d u c t i o n Via a n a c c e s s o r y p a t h w a y b u t also i n d i c a t e s w h e t h e r t h e site of i n s e r t i o n of
807
A k h t a r et al.
Fig. 3. Atrial fibrillation in the WPW syndrome. The cop panel shows t h a t during atrial fibrillation ventricular activation initially occurs exclusively over the normal pathway as indicated by the absence of delta, narrow QRS complexes, and H-V intervals of 50 msec. (first four beats}, Subsequently ventricular activation occurred over the accessory pathway (wide QRS complexes), which mimics a ventricular tachycardia. The bottom panel shows spontaneous termination of atrial fibrillation. Note ventricular pre-excitation during sinus beats.
Fig. 4. The tracing shows a SVT (cycle length 365 msec.) with a low-to-high sequence of atrial activation (Ae) in a patient without evidence of WPW syndrome. A premature ventricular beat (S) introduced during the SVT conducts to the atria (Ar) and results in a similar atrial activation sequence. The atrial cycle length is shortened to 300 msec. and the SVT is terminated, The constant H-H intervals prior to termination of the tachycardia suggest that the last H deflection results from antegrade depolarization and was unaffected by the premature ventricular beat. Thus retrograde activation of the atria by the premature ventricular beat in all probability occurred via anomalous pathway, which was not operative antegradely. 808
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Clinical uses of His bundle electrocardiography. I I I
t h e b y p a s s t r a c t is i n t o t h e left or r i g h t v e n t r i c l e . T h i s is especially t r u e i f a c o n t r a l a t e r a l b u n d l e b r a n c h b l o c k h a s n o i n f l u e n c e o n t h e r a t e of SVT. I f a p a t i e n t w i t h a left v e n t r i c u l a r b y p a s s connection develops L B B B during a r e - e n t r a n t S V T , d e l a y e d left v e n t r i c u l a r a c t i v a t i o n will r e s u l t i n d e l a y e d a c t i v a t i o n of t h e a t r i a via t h e left-sided b y p a s s . I f s u c h a p a t i e n t d e v e l o p s a f u n c t i o n a l r i g h t b u n d l e b r a n c h block, t h e a t r i a l r a t e d u r i n g t h e S V T will b e u n a f f e c t e d . R e e n t r a n t circuits l o c a t e d e n t i r e l y i,n t h e A - V n o d e are i n d e p e n d e n t of c o n d u c t i o n d e l a y or b l o c k within the HPS. Therefore, atrial rates in A-V n o d a l r e - e n t r a n t S V T do n o t c h a n g e w i t h t h e o n s e t of f u n c t i o n a l b l o c k i n t h e H P S . I t m u s t b e emphasized that ventricular rates in A-V nodal r e - e n t r a n t S V T m a y v a r y if f u n c t i o n a l b l o c k i n t h e H P S is a s s o c i a t e d w i t h v a r i a b l e H - V p r o l o n g a t i o n or c o m p l e t e f a i l u r e of c o n d u c t i o n i n t h e H P S (Fig. 5, of P a r t II). W i t h t h e use of s o m e of t h e a b o v e c r i t e r i a it is possible to a c c u m u l a t e e v i d e n c e t h a t i n s o m e p a t i e n t s w i t h o u t e v i d e n c e of a n t e g r a d e v e n t r i c u l a r p r e - e x c i t a t i o n o n t h e s t a n d a r d E C G , reentrant supraventricular tachycardias utilize a r e t r o g r a d e b y p a s s t r a c t (Fig. 4). I t s h o u l d be n o t e d t h a t a n a t o m i c l o c a l i z a t i o n of r e - e n t r a n t c i r c u i t s i n p a t i e n t s w i t h W P W s y n d r o m e is of m o r e t h a n a c a d e m i c i n t e r e s t s i n c e surgical t r e a t m e n t is b e i n g u s e d i n c r e a s i n g l y i n those p a t i e n t s w i t h d i s a b l i n g r e - e n t r a n t t a c h y c a r dias which are r e f r a c t o r y t o m e d i c a l t h e r a py.17.18 REFERENCES
L Castellanos, A., Chapunoff, E.. Castillo, C., Maytin, O., and Lemburg, L.: His bundle electrograms in two cases of Wolff-Parkinson-White (we-excitation syndrome), Circulation 41:399, 1970. 2. Castillo. C.. and Castellanos, A.: His bundle recordings in patients with reciprocating tachycardias and WolffParkinson-White syndrome, Circulation 42:271, 1970. 3. Svenson, R. H., Gallagher, J. J., Sealy, W. C., and Wallace, A. G.: An electrophysiologic approach to the surgical treatment of the Wolff-Parkinson-White syndrome. Report of two cases utilizing catheter recording and epicardial mapping techniques, Circulation 49:799, 1974.
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4. Durrer, D., and Roos, J. P.: Epicardial excitation of the ventricles in a patient with Wolff-Parkinson-White syndrome (Type B), Circulation 35:15, 1967. 5. Sealy, W. C., Boineau, J. P., and Wallace, A. G.: The identification and division of the bundle of Kent for premature excitation and supraventricular tachycardia, Surgery 68:1009, 1970. 6. Wolff,L., Parkinson, J., and White, P. D.: Bundle branch block with short P-R interval in healthy young people prone to paroxysmal tachycardla, AM. HEART J. 5:685, 1930. 7. Wolff, L.: Electrocardiography: Fundamentals and clinical application, Philadelphia, 1950,~W. B. Saunders Company, p. 178. 8. Wolff,L., and Richman, J. L.: The diagnosis of myocardial infarction in patients with anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome), AM. HEART J. 45:545, 1953. 9. Durrer, D., Schoo, L., Schuilenburg, R. M., and Wellens, H. J. J.: The role of premature beats in the initiation and termination of supraventricular tachycardias in the Wolff-Parkinson-White syndrome, Circulation 36:644, 1967. 10. Wellens, H. J. J., Schuilenberg, R. M., and Durrer, D.: Electrical stimulation of the heart in patients with Wolff-Parkinson-White syndrome (Type A), Circulation 43:99, 1971. 11. Lister, J. W., Worthington, F. X., Gentsch, T. 0. Swenson, J. A., Nathan, D. A., and Grosselin, A. J.: Preexcitation and tachycardias in the Wolff-Parkinson-White syndrome, Type B, Circulation 45:1081, 1972: 12. Lau, S. H., Caracta, A. R., Josephson, M. E., Batsford, W. P., Akhtar, M., and Damato, A. N.: Mechanisms of paroxysmal atrial tachycardia in the WPW syndrome (abst.), Circulation 47, 48(Suppl. IV): 1973. 13. Wellens, H. J. J., and Durrer, D.: Pathways of tachycardia in WPW syndrome (abst.), Circulation 49, 50(Suppl. III): 1974. 14. Zipes, D. P., DeJoseph, R. L., and Rothbaum, D.: Unusual properties of accessory pathways, Circulation 49:1200, 1974. 15. Coumel, P., and Attuel, P.: Reciprocating tachycardia in overt and latent pre-excitation influence of functional bundle branch block on the rate of tachycardia, Eur. J. Cardiol. 1:423, 1974. 16. Coumel, P., and Attuel, P.: Localization of the circus movement during reciprocating tachycardia in WolffParkinson-White syndrome, in His bundle electrocardiography and clinical electrophysiology, Narula, O. S., ed., Philadelphia, 1975, F. A. Davis Company, Chap. 16, p. 343. 17. Cobb, F. R., Blumenschein, S. D., Sealy, W. C., Boineau, J. P., Wagner, G. S., and Wallace, A. G.: Successful surgical interruption of the bundle of Kent in a patient with Wolff-Parkinson-White syndrome, Circulation 38:1018, 1968. 18. lwa, T., Kazui, T., Sagii, S., and Wada, J.: Surgical treatment of the Wolff-Parkinson-Whitesyndrome, Jap. J. Thorac. Surg. 23:513, 1970.
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