Accelerated atrioventricular conduction during acute myocardial infarction S. Gavrilescu, M.D. Maria Gavrilescu, M.D. C. Luca, M.D. ~misoara, Romania
Accelerated atrioventricular (A-V) conduction manifesting as Wolff-Parkinson-White syndrome or as a short PR interval with normal QRS complex has been occasionally reported in association with acute myocardial infarction. 1-5 Three patients showing this association h a v e been observed and studied in order to explain the mechanism by which this phenomenon may occur. Case reports Case 1. An 82-year-old woman with a ten year history of angina pectoris was hospitalized with acute pulmonary edema. An electrocardiogram taken three months before showed nonspecific S T - T changes {Fig. 1A); on admission it revealed an inferior wall myocardial infarction {Fig. 1B), the PR interval measured 180 msec., and QRS duration was 60 msec. Serum glutamic oxalacetic transaminase was 125 units, blood glucose was 175 mg. per cent, other laboratory data were nonrelevant. On the second hospital day a delta wave was visible in Leads I and II; the P R interval was 100 msec., and QRS duration measured 90 msec. (Fig. 1C). The patient's status improved under treat m e nt with bed rest, digitalis, and diuretics. Ten days after the admission an His bundle electrogram was recorded with a tripolar electrode catheter i n t r o d u c e d via the right femoral vein. A second bipolar pacing electrode was introduced through the right mediobasilic vein into the right atrium. A specially constructed
From the Department of Internal Medicine and Cardiology, Institutul de Medicina, Timisoara, Romania. Received for publication March 10, 1976. Accepted for publication June 4, 1976. Reprint requests: Prof. S. Gavrilescu, Clinica I-a Medicala, Spital Judetean, Bul. St. Plavat Nr. 156, Timisoara 1900, Romania.
July, 1977, Vol. 94, No. 1, pp. 21-27
battery-powered impulse generator was used for pacing the heart. All recordings were obtained with a six-channel direct writing electrocardiograph (N E K 6-Zw6nitz, East Germany) at a paper speed of 50 or 100 mm./second. T he H-V intervals were measured from the spike of H deflection to the earliest ventricular recording in any surface lead (at least two leads in which the delta wave was most evident). This procedure was also used in the others studied cases. On the His bundle recording an A-H interval of 50 msec. and an H-V interval of 35 msec. were measured during sinus rhythm. Scanning of the cardiac cycle with an atrial stimulus, approximately twice diasto]ic threshold, during sinus r h y t h m was then performed. Stimuli falling at 240 to 280 msec. from the beginning of atrial depolarization were conducted to the ventricular with a stimulus to R interval of 280 to 300 msec. and a narrow QRS complex (Fig. 2B and C), while those falling at 300 msec. or more were conducted with the preexcitation pattern {Fig. 2A). T he beats with a narrow QRS complex had a frontal axis shifted upward and to the left. Such beats were conducted to the ventricle with A-H and H-V intervals of 160 and 80 msec., respectively, the latter value suggesting latent conduction disturbance in the HisPurkinje system (Fig. 2C). The patient recovered and was discharged after three weeks of hospital stay. She complained of shortness of breath and angina pectoris. Her electrocardiogram remained unchanged showing the WPW pattern. After four months she developed suddenly crushing chest pain followed by acute pulmonary edema. She was admitted in a state of profound shock and died on the following day. On autopsy a recent infarction involving the anterolateral wall of the left ventricle and the
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Gavrilescu, Gavrilescu, and Luca
Fig. 1. Case 1. A, Electrocardiogramtaken three months before. B, Electrocardiogram on admission showing inferior wall infarction. C, Electrocardiogramon the second hospital day showing preexcitation pattern.
Fig. 2. Case 1. Upper panels (A and B) show electrocardiogram taken during the scanning of the cardiac cycle with atrial electrostimuliduring sinus rhythm. A stimulus falling at 420 msec. from the beginning of the P wave is conducted to the ventricles with the preexcitation pattern (A) while a stimulus fallingat 280 msec. is conducted with a narrow Q R S complex and a leftward axis deviation (B). Lower panel (C) shows His bundle electrogram (HBE) recorded simultaneously with Leads I and If. A, H, and V are atrial, His bundle, and ventricularactivity.
22
interventricular septum was found. There was also an old infarction of the inferior wall and of the apex with aneurysmal dilatation and parietal thrombosis. Extensive atherosclerosis of the aorta and coronary arteries was present. The A-V conduction system was studied according to Davies6; the right and left A-V rings were also included in the histologic study, the sections being made perpendicularly to the A-V ring. A well-marked atrioventricular tract was found on the posterior wall of the right atrium. It passed superficially to the A-V node and ended at the level of the insertion of the posterior tricuspidal leaflet {Fig. 3A). At this level fibers of the accessory tract entered into the upper interventricular septum (Fig. 3B). No other abnormal A-V connections could be found. In the A-V conduction system there was a moderate degree of fibrosis, scattered foci of necrosis in the compact node area {Fig. 4), and leucocytic infiltrates within the bundle of His and its branches. The atrial and ventricular myocardium showed pronounced hypertrophy of cardiac muscle fibers, there were hemorrhages and vascular stasis around the corpus fibrosus. To summarize, this patient developed during an acute myocardial infarction a W P W pattern suggesting right posterior preexcitation. 7 On autopsy an accessory bundle was found on the posterior edge of the right A-V ring. The A-V
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Accelerated A V conduction during acute M I
Fig. 3. Case 1. A, Accessory atrioventricular tract (arrow) making the connection between the right atrial wall (RA) and the insertion of the posterior leaflet of the tricuspid valve (TR). B, The arrow points the connection between the fascicle shown in A and the interventricular septum (IV). C, Muscular fibers passing from the outer to the inner aspect of the insertion of the posterior leaflet of the tricuspid valve. (Hematoxylin and eosin. Original magnification; A • 12, B x 160, C • 300.)
Fig. 4. Case 1.4, The compact node area (N). B and C, Arrows showing loci of necrosis. (Hematoxylin and eosin. Original magnification: A, • 200, B, • 300, C, • 360.) conducting s y s t e m showed nonspecific degenerative changes due p r o b a b l y to ischemia a n d old age. No a t t a c k s 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 were n o t e d during the presence of the W P W pattern. Case 2. A 47-year-old m a n was a d m i t t e d to the hospital with a c u t e precordial pain. His p a s t h i s t o r y was n o n c o n t r i b u t o r y . On admission t h e e l e c t r o c a r d i o g r a m showed an a n t e r i o r wall m y o cardial infarction. T h e P R interval was 180 msec., Q R S d u r a t i o n was 80 msec. a n d h e a r t r a t e was 125 beats per m i n u t e {Fig. 5A). S e r u m g l u t a m i c oxalacetic t r a n s a m i n a s e was 200 units. T h e n e x t d a y a s h o r t e n i n g of the P R interval to 100 msec. (Fig. 5B) and f r e q u e n t atrial p r e m a t u r e b e a t s with atrial echoes were n o t e d (Fig. 6A). A His
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bundle recording p e r f o r m e d a t this t i m e (Fig. 6B) showed a s h o r t A - H i n t e r v a l (30 msec.) a n d a n o r m a l H - V i n t e r v a l (50 msec.). W i t h atrial pacing up to a r a t e of 130 per m i n u t e the A - H i n t e r v a l l e n g t h e n e d to 90 msec. (Fig. 6C). T h i s p r o c e d u r e was done to v a l i d a t e the H deflection. On the third hospital d a y a p a r o x y s m of t a c h y cardia with a r a t e of 187 per m i n u t e o c c u r r e d (Fig. 7A). A second His bundle recording during t h e a t t a c k of rapid h e a r t action showed t h a t e a c h v e n t r i c u l a r complex was preceded b y an atrial depolarization a n d a n H deflection (Fig. 7B). D u r i n g the a r r h y t h m i a the A - H i n t e r v a l was 150 msec. while the H - V i n t e r v a l r e m a i n e d unchanged (50 msec.). No r e t r o g r a d e H ' deflection could be observed. D u r i n g t h e ectopic r h y t h m t h e
23
Gavrilescu, Gavrilescu, and Luca
Fig. 7. Case 2. Electrocardiogram (A) and His bundle electrogram (B) recorded during tachycardia. H R A = high right atrial electrogram. Fig, 5l Case 2. A, Electrocardiogram on admission. B, Electrocardiogram on the second hospital day showing short P-R interval.
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Fig. 6. Case 2. A, Electrocardiogram showing atrial premature beats (P1) and echo beats (P2). The arrows point to retrograde P' wave which precedes the QRS complexes of the echo beats. B, His Bundle electrogram (HBE) showing short A-H interval. C, Atrial pacing at a rate of 130 per minute resulted in a lengthening of the A-H interval from 30 to 90 msec. p a t i e n t developed severe precordial pain a n d hypotension. DC shock stopped t h e a t t a c k b u t it recurred a f t e r two h o u r s and was successfully
24
controlled with digoxin. T h e s u b s e q u e n t course was uneventful. T h e electrocardiographic configu r a t i o n with s h o r t P R i n t e r v a l r e m a i n e d unchanged during a follow-up period of 20 m o n t h s a n d the p a t i e n t h a d no a t t a c k s of t a c h y c a r d i a ever since. C a s e 3. A 74-year-old m a n with diabetes mellitus a n d a five y e a r history of a n g i n a pectoris was a d m i t t e d with an a c u t e i n f e r o p o s t e r o l a t e r a l m y o c a r d i a l infarction. H e showed signs a n d s y m p t o m s of congestive failure a n d an apical systolic m u r m u r suggesting p a p i l l a r y m u s c l e dysfunction. D u r i n g t h e first two weeks the P R i n t e r v a l was 160 msec. (Fig. 8A). T h e p a t i e n t i m p r o v e d m a r k e d l y u n d e r t r e a t m e n t with digitalis a n d diuretics. However, in the t h i r d h o s p i t a l week his s t a t u s Worsened. H e p r e s e n t e d f r e q u e n t anginal episodes w i t h o u t a n y obvious reason. D u r i n g this period which lasted several days, a s h o r t P R interval and f r e q u e n t v e n t r i c u l a r ectopic b e a t s with r e t r o g r a d e c o n d u c t e d P ' w a v e s were n o t e d {Fig. 8C). A His b u n d l e recording showed an A - H i n t e r v a l of 30 msec. a n d an H - V interval of 40 msec. {Fig. 9A). W i t h a t r i a l pacing up to a r a t e of 120 per m i n u t e , the A - H i n t e r v a l l e n g t h e n e d to 80 msec. S h o r t b o u t s of s u p r a v e n tricular t a c h y c a r d i a which s t o p p e d s p o n t a n e o u s ly were also observed. T h e p a t i e n t was discharged a f t e r six weeks of h o s p i t a l stay. After four m o n t h s the e l e c t r o c a r d i o g r a m showed a n o r m a l P R interval (150 msec.), while on the His b u n d l e recording the following intervals were m e a s u r e d : P - A 60
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Accelerated A V conduction during acute M I
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msec., A-H 50 msec., and H-V 40 msec. T h e patient remained in congestive failure b u t h a d no a r r h y t h m i c episodes. Discussion
T h e reported cases are examples of the socalled acquired variety of the preexcitation syndrome. I t is now accepted t h a t the W P W s y n d r o m e is due to a b n o r m a l a t r i o v e n t r i c u l a r connections. 6-9 A n a t o m i c studies 16, 11 were able to d e m o n s t r a t e accessory m u s c u l a r bridges between the atria and ventricles in a p p a r e n t l y n o r m a l hearts. It is possible that u n d e r p a r t i c u l a r influences such accessory bundles m a y become functional and c o n d u c t the cardiac impulse. Levine and Burge 1 reported a p a t i e n t with an acute m y o c a r d i a l infarction and a high degree A-V block in whom occasionally c o n d u c t e d beats showed the W P W pattern. Goel and H a n 5 described two cases of the W P W s y n d r o m e appearing after the d e v e l o p m e n t of an acute m y o c a r d i a l infarction. T h e electrocardiographic configuration of the m y o c a r d i a l infarction disappeared completely with the occurrence of preexcitation. 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 occurred in both patients. T h e W P W p a t t e r n disappeared with the recovery from the acute phase. I t was assumed t h a t under the influence of increased a u t o n o m i c nervous activity associated with a c u t e
American Heart J o u r n a l
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Fig. 9. Case 3. A, His bundle electrogram showing an A-H interval of 30 msec. corresponding to the electrocardiogram shown in Fig. 8C. B, During atrial pacing at a rate of 120 per minute the A-H interval lengthened to 80 msec. This procedure was used to validate the H deflection. 25
Gavrilescu, Gavrilescu, and Luca
ischemia an aberrant A-V bundle became functional2 This hypothesis is supported by the observation t h a t the preexcitation pattern could be elicited in a patient with intermittent WPW syndrome by concomitant isoprenaline infusion and carotid sinus massage. 12 In Case 1 the WPW pattern appeared during the first myocardial infarction and persisted for four months until the death due to a second infarction. Nonspecific degenerative changes were present in the A-V conduction system, especially in the compact nodal area. It is possible t h a t theSe changes favored A-V conduction through the accessory bundle. No attacks of supraventricular tachycardia occurred, nor could be initiated during the scanning of the cardiac cycle with electric stimuli suggesting t h a t no reentry circuit could be initiated. This may be due to the pathologic changes within the A-V conducting system. However, stimuli falling at 240 to 280 msec. from the beginning of atrial depolarization were conducted through the normal A-V conduction system, with a prolonged H-V interval and ventricular aberrancy. There was a slight increase in the QRS duration from 60 to 90 msec. associated with the appearance of the WPW configuration suggesting that A-V conduction occurred over both normal pathways and also through the abnormal connection. Although the preexcitation syndrome in this patient appears as "acquired" it could not to be excluded that during its life this pattern was present in other occasions. The anatomic study showed a correspondence between the electrocardiographic configuration suggesting right posterior preexcitation 7 and the localization of the accessory bundle. The hypothesis of mismatch impedance, 1:~ which assumes an adequate relation between cable capacity of the conducting structure and the muscle mass which is to be activated, may explain the preferential utilization of the pathway by which the cardiac impulse is conducted. Autonomic nervous influences,~"~ as well as pathologic changes in the A-V conducting system can dissipate the mismatch impedance enhancing conduction over the accessory bundle. The appearance of the short PR interval associated with normal duration of the QRS complexes 14 during the course of acute myocardial infarction is more difficult to explain. Although this phenomenon is said to be a rare event, 4. 1~ it was noted with variable frequency when large series of patients with myocardial infarction were 2(}
studied.16. 17 The short PR intervals were noted especially on the first days of the illness, subsequently the tracings revealed normal PR intervals, except in a few instances in which it remained unchanged for months. 16 No mention is made about the associations with supraventricular tachycardia. In our Cases 2 and 3, both developed attacks of rapid heart action shortly after the appearance of the preexcitation pattern. This phenomenon was associated with atrial premature beats and atrial echoes in Case 2, and ventricular extrasystoles with retrograde activation of the atria in Case 3. Anginal pain was also a feature of the clinical picture. No arrhythmic episodes were encountered in both patients nor in the past history and the follow-up period. In the absence of anatomic studies the mechanism of the shortening of the P R interval remains speculative. It was suggested 7' 18 t h a t shortening of the PR interval may be due to abnormal connections of the atriofascicular bypas s type, ~ or to a particular pacemaker location and pattern of atrial activation. 18 The demonstration of shortened refractory periods of the A-V conducting system in patients with short PR intervals and normal QRS complexes was considered compatible with a partial A-V nodal bypass or dual A-V conduction but could not differentiate between these two possibilities. 19 In Case 2 an A-H interval of 30 msec. was measured on the His bundle recording during sinus rhythm, while during supraventricular tachycardia it was 150 msec. This phenomenon can be explained by prolongation of the A-H time with increased atrial rate or by the fact t h a t during ectopic r h y t h m an accessory pathway was active. ~~ During supraventricular tachycardia no retrograde H' deflections were recorded; however, this does not exclude the possibility t h a t ventriculoatrial conduction occurred via the abnormal Connection {Fig, 7). The H-V interval was unchanged in sinus a n d ectopic rhythm. There is no firm evidence that accelerated A-V conduction can be acquired during acute myocardial infarction. However, latent accessory A-V connections may become functional under the complex changes due to acute myocardial ischemia and show various electrocardiographic patterns of preexcitation syndrome.
Summary Three cases are described in which accelerated atrioventricular conduction occurred during an acute myocardial infarction. The first patient, an July, 1977, Vol. 94, No. 1
Accelerated A V conduction during acute M I
82-year-old woman, developed a W P W s y n d r o m e suggesting posterior right ventricular preexcitat i o n , a P a t t e r n w h i c h p e r s i s t e d for f o u r m o n t h s u n t i l her death. A n accessory b u n d l e was f o u n d on autopsy. Fibrotic changes, associated with acute lesions (hemorrhage, p o l y m o r p h o n u c l e a r ~infiltrates) were p r e s e n t i n t h e a t r i o v e n t r i c u l a r node and His-Purkinje system. T w o m e n , of 47 a n d 74 years, d e v e l o p e d a s h o r t PR interval associated with supraventricular t a c h y c a r d i a d u r i n g t h e c o u r s e of a n a c u t e m y o c a r d i a l i n f a r c t i o n . T h e P R i n t e r v a l r e t u r n e d to its i n i t i a l v a l u e i n o n e case a n d r e m a i n e d u n c h a n g e d for t h r e e m o n t h s i n t h e o t h e r . Accessory a t r i o v e n t r i c u l a r c o n n e c t i o n s which became functional during myocardial ischemia may explain the various electrocardiographic p a t t e r n s of p r e e x c i t a t i o n .
8. 9.
10.
11. 12. 13. 14.
REFERENCES
1. Levine, H. D., and Burge, J. C.: Septal infarction with complete heart block and intermittent anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome). Histologic demonstration of right lateral bundle, AM. HEARTJ. 36:431, 1948. 2. Scherf, D., and Cohen, J.: The atrioventricular node and selected cardiac arrhythmias, New-York, London, 1964, Grune & Stratton, Inc., p. 388. 3. Verani, M. S., Baron, H., and Maia, I. G.: Myocardial infarction associated with Wolff-Parkinson-White syndrome, AM. HEARTJ. 83:684, 1972. 4. Mathew, G., and Raftery, E. B.: Accelerated atrioventricular conduction after myocardial infarction. A study using His bundle electrogram, Br. Heart J. 35:985, 1973. 5. Goel, B. G., and Han, J.: Manifestation of the WPW syndrome after myocardial infarction, AM. HEART J. 87:633, 1974. 6. Davies, M. J.: Pathology of conducting tissue of the heart, London, 197!, Butterworth & Co., Ltd., p. 26. 7. Boineau, J. P., Moore, N. E., Spear, J. F., and Seaty, W. C.: Basis of clinical-ECG variations in right and left
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15.
16. 17. 18. 19.
20.
ventricular preexcitation: a unitary concept of WPW, in Cardiac Arrhythmias, Dreifus and Likoff, editors, New York, 1973, Grune & Stratton, Inc., p. 421. Durrer, D., and Wellens, H. J. J.: The Wolff-ParkinsonWhite syndrome, anno 1973, Eur. J. Cardiol. 1:347, 1974. Anderson, R. H., Becker, A. E., Brechenmacher, C., Davies, M. J., and Rossi, L.: Ventricular preexcitation. A proposed nomenclature of its substrates, Eur J. Cardiol. 3:27, 1975. Glomset, D. J., and Glomset, A. T. A.: A morphoiogic study of the cardiac conduction system in ungulates, dog 9and man. I. The sinoatrial node, AM. HEARTJ. 20:389, 1940. Anderson, R. H., and Taylor, M. I.: Development of atrioventricular specialized tissue in human heart, Br. Heart J. 34:1205, 1972. Gavrilescu, S.: Manifestation of the WPW syndrome during isoprenaline infusion and carotid sinus massage (In preparation, 1976}. Mendez, G., Mueller, W. J., and Uruiaga, X.: Propagation of impulse across the Purkinje fiber-muscle junctions in the dogs, Circ. Res. 26:135, 1970. Lown, B., Ganong, W. F., and Levine, S. A.: The syndrome of short PR interval, normal QRS complex and paroxysmal rapid heart action, Circulation 5:693, 1952. Kr~kler,D. M.: The Wolff-Parkinson-White and related syndromes, in Cardiac Arrhythmias, Krikler and Goodwin, editors, London, Philadelphia, Toronto, 1975, W. B. Saunders Company, p. 144. SoederstrSm, N.: Myocardial infarction and mural thrombosis in the atria of the heart, Acta Med. Scand. Suppl. 217:1948. Nazzi, V., Meda, A., and Paciello, D.: Le alterazioni dell' atriogramma e del tempo di conduzione atrio-ventricolare nell-infarto miocardico, Folio Cardiol. 15:53, 1956. Shed, L., and James, N. T.: A new electrocardiographic concept: Synchronized sinoventricular conductibn, Dis. Chest 55:127, 1969. Bisset, J. K., Soyza, N., Kane, J. J., and Murphy, M. L.: -Altered refractory periods in patients with short PR intervals and normal QRS complexes, Am. J. Cardiol. 35:487, 1975. Spurrel, R. A. J., Krikler, D. M., and Sowton, E.: Problems concerning assessment of anatomical site of accessory pathway in Wolff-Parkinson-Whitesyndrome, Br. Heart J. 37:127, 1975.
27
Accelerated atrioventricular (A-V) conduction manifesting as Wolff-Parkinson-White syndrome or as a short PR interval with normal QRS complex has been occasionally reported in association with acute myocardial infarction. 1-5 Three patients showing this association h a v e been observed and studied in order to explain the mechanism by which this phenomenon may occur. Case reports Case 1. An 82-year-old woman with a ten year history of angina pectoris was hospitalized with acute pulmonary edema. An electrocardiogram taken three months before showed nonspecific S T - T changes {Fig. 1A); on admission it revealed an inferior wall myocardial infarction {Fig. 1B), the PR interval measured 180 msec., and QRS duration was 60 msec. Serum glutamic oxalacetic transaminase was 125 units, blood glucose was 175 mg. per cent, other laboratory data were nonrelevant. On the second hospital day a delta wave was visible in Leads I and II; the P R interval was 100 msec., and QRS duration measured 90 msec. (Fig. 1C). The patient's status improved under treat m e nt with bed rest, digitalis, and diuretics. Ten days after the admission an His bundle electrogram was recorded with a tripolar electrode catheter i n t r o d u c e d via the right femoral vein. A second bipolar pacing electrode was introduced through the right mediobasilic vein into the right atrium. A specially constructed
From the Department of Internal Medicine and Cardiology, Institutul de Medicina, Timisoara, Romania. Received for publication March 10, 1976. Accepted for publication June 4, 1976. Reprint requests: Prof. S. Gavrilescu, Clinica I-a Medicala, Spital Judetean, Bul. St. Plavat Nr. 156, Timisoara 1900, Romania.
July, 1977, Vol. 94, No. 1, pp. 21-27
battery-powered impulse generator was used for pacing the heart. All recordings were obtained with a six-channel direct writing electrocardiograph (N E K 6-Zw6nitz, East Germany) at a paper speed of 50 or 100 mm./second. T he H-V intervals were measured from the spike of H deflection to the earliest ventricular recording in any surface lead (at least two leads in which the delta wave was most evident). This procedure was also used in the others studied cases. On the His bundle recording an A-H interval of 50 msec. and an H-V interval of 35 msec. were measured during sinus rhythm. Scanning of the cardiac cycle with an atrial stimulus, approximately twice diasto]ic threshold, during sinus r h y t h m was then performed. Stimuli falling at 240 to 280 msec. from the beginning of atrial depolarization were conducted to the ventricular with a stimulus to R interval of 280 to 300 msec. and a narrow QRS complex (Fig. 2B and C), while those falling at 300 msec. or more were conducted with the preexcitation pattern {Fig. 2A). T he beats with a narrow QRS complex had a frontal axis shifted upward and to the left. Such beats were conducted to the ventricle with A-H and H-V intervals of 160 and 80 msec., respectively, the latter value suggesting latent conduction disturbance in the HisPurkinje system (Fig. 2C). The patient recovered and was discharged after three weeks of hospital stay. She complained of shortness of breath and angina pectoris. Her electrocardiogram remained unchanged showing the WPW pattern. After four months she developed suddenly crushing chest pain followed by acute pulmonary edema. She was admitted in a state of profound shock and died on the following day. On autopsy a recent infarction involving the anterolateral wall of the left ventricle and the
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21
Gavrilescu, Gavrilescu, and Luca
Fig. 1. Case 1. A, Electrocardiogramtaken three months before. B, Electrocardiogram on admission showing inferior wall infarction. C, Electrocardiogramon the second hospital day showing preexcitation pattern.
Fig. 2. Case 1. Upper panels (A and B) show electrocardiogram taken during the scanning of the cardiac cycle with atrial electrostimuliduring sinus rhythm. A stimulus falling at 420 msec. from the beginning of the P wave is conducted to the ventricles with the preexcitation pattern (A) while a stimulus fallingat 280 msec. is conducted with a narrow Q R S complex and a leftward axis deviation (B). Lower panel (C) shows His bundle electrogram (HBE) recorded simultaneously with Leads I and If. A, H, and V are atrial, His bundle, and ventricularactivity.
22
interventricular septum was found. There was also an old infarction of the inferior wall and of the apex with aneurysmal dilatation and parietal thrombosis. Extensive atherosclerosis of the aorta and coronary arteries was present. The A-V conduction system was studied according to Davies6; the right and left A-V rings were also included in the histologic study, the sections being made perpendicularly to the A-V ring. A well-marked atrioventricular tract was found on the posterior wall of the right atrium. It passed superficially to the A-V node and ended at the level of the insertion of the posterior tricuspidal leaflet {Fig. 3A). At this level fibers of the accessory tract entered into the upper interventricular septum (Fig. 3B). No other abnormal A-V connections could be found. In the A-V conduction system there was a moderate degree of fibrosis, scattered foci of necrosis in the compact node area {Fig. 4), and leucocytic infiltrates within the bundle of His and its branches. The atrial and ventricular myocardium showed pronounced hypertrophy of cardiac muscle fibers, there were hemorrhages and vascular stasis around the corpus fibrosus. To summarize, this patient developed during an acute myocardial infarction a W P W pattern suggesting right posterior preexcitation. 7 On autopsy an accessory bundle was found on the posterior edge of the right A-V ring. The A-V
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Accelerated A V conduction during acute M I
Fig. 3. Case 1. A, Accessory atrioventricular tract (arrow) making the connection between the right atrial wall (RA) and the insertion of the posterior leaflet of the tricuspid valve (TR). B, The arrow points the connection between the fascicle shown in A and the interventricular septum (IV). C, Muscular fibers passing from the outer to the inner aspect of the insertion of the posterior leaflet of the tricuspid valve. (Hematoxylin and eosin. Original magnification; A • 12, B x 160, C • 300.)
Fig. 4. Case 1.4, The compact node area (N). B and C, Arrows showing loci of necrosis. (Hematoxylin and eosin. Original magnification: A, • 200, B, • 300, C, • 360.) conducting s y s t e m showed nonspecific degenerative changes due p r o b a b l y to ischemia a n d old age. No a t t a c k s 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 were n o t e d during the presence of the W P W pattern. Case 2. A 47-year-old m a n was a d m i t t e d to the hospital with a c u t e precordial pain. His p a s t h i s t o r y was n o n c o n t r i b u t o r y . On admission t h e e l e c t r o c a r d i o g r a m showed an a n t e r i o r wall m y o cardial infarction. T h e P R interval was 180 msec., Q R S d u r a t i o n was 80 msec. a n d h e a r t r a t e was 125 beats per m i n u t e {Fig. 5A). S e r u m g l u t a m i c oxalacetic t r a n s a m i n a s e was 200 units. T h e n e x t d a y a s h o r t e n i n g of the P R interval to 100 msec. (Fig. 5B) and f r e q u e n t atrial p r e m a t u r e b e a t s with atrial echoes were n o t e d (Fig. 6A). A His
American Heart Journal
bundle recording p e r f o r m e d a t this t i m e (Fig. 6B) showed a s h o r t A - H i n t e r v a l (30 msec.) a n d a n o r m a l H - V i n t e r v a l (50 msec.). W i t h atrial pacing up to a r a t e of 130 per m i n u t e the A - H i n t e r v a l l e n g t h e n e d to 90 msec. (Fig. 6C). T h i s p r o c e d u r e was done to v a l i d a t e the H deflection. On the third hospital d a y a p a r o x y s m of t a c h y cardia with a r a t e of 187 per m i n u t e o c c u r r e d (Fig. 7A). A second His bundle recording during t h e a t t a c k of rapid h e a r t action showed t h a t e a c h v e n t r i c u l a r complex was preceded b y an atrial depolarization a n d a n H deflection (Fig. 7B). D u r i n g the a r r h y t h m i a the A - H i n t e r v a l was 150 msec. while the H - V i n t e r v a l r e m a i n e d unchanged (50 msec.). No r e t r o g r a d e H ' deflection could be observed. D u r i n g t h e ectopic r h y t h m t h e
23
Gavrilescu, Gavrilescu, and Luca
Fig. 7. Case 2. Electrocardiogram (A) and His bundle electrogram (B) recorded during tachycardia. H R A = high right atrial electrogram. Fig, 5l Case 2. A, Electrocardiogram on admission. B, Electrocardiogram on the second hospital day showing short P-R interval.
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Fig. 6. Case 2. A, Electrocardiogram showing atrial premature beats (P1) and echo beats (P2). The arrows point to retrograde P' wave which precedes the QRS complexes of the echo beats. B, His Bundle electrogram (HBE) showing short A-H interval. C, Atrial pacing at a rate of 130 per minute resulted in a lengthening of the A-H interval from 30 to 90 msec. p a t i e n t developed severe precordial pain a n d hypotension. DC shock stopped t h e a t t a c k b u t it recurred a f t e r two h o u r s and was successfully
24
controlled with digoxin. T h e s u b s e q u e n t course was uneventful. T h e electrocardiographic configu r a t i o n with s h o r t P R i n t e r v a l r e m a i n e d unchanged during a follow-up period of 20 m o n t h s a n d the p a t i e n t h a d no a t t a c k s of t a c h y c a r d i a ever since. C a s e 3. A 74-year-old m a n with diabetes mellitus a n d a five y e a r history of a n g i n a pectoris was a d m i t t e d with an a c u t e i n f e r o p o s t e r o l a t e r a l m y o c a r d i a l infarction. H e showed signs a n d s y m p t o m s of congestive failure a n d an apical systolic m u r m u r suggesting p a p i l l a r y m u s c l e dysfunction. D u r i n g t h e first two weeks the P R i n t e r v a l was 160 msec. (Fig. 8A). T h e p a t i e n t i m p r o v e d m a r k e d l y u n d e r t r e a t m e n t with digitalis a n d diuretics. However, in the t h i r d h o s p i t a l week his s t a t u s Worsened. H e p r e s e n t e d f r e q u e n t anginal episodes w i t h o u t a n y obvious reason. D u r i n g this period which lasted several days, a s h o r t P R interval and f r e q u e n t v e n t r i c u l a r ectopic b e a t s with r e t r o g r a d e c o n d u c t e d P ' w a v e s were n o t e d {Fig. 8C). A His b u n d l e recording showed an A - H i n t e r v a l of 30 msec. a n d an H - V interval of 40 msec. {Fig. 9A). W i t h a t r i a l pacing up to a r a t e of 120 per m i n u t e , the A - H i n t e r v a l l e n g t h e n e d to 80 msec. S h o r t b o u t s of s u p r a v e n tricular t a c h y c a r d i a which s t o p p e d s p o n t a n e o u s ly were also observed. T h e p a t i e n t was discharged a f t e r six weeks of h o s p i t a l stay. After four m o n t h s the e l e c t r o c a r d i o g r a m showed a n o r m a l P R interval (150 msec.), while on the His b u n d l e recording the following intervals were m e a s u r e d : P - A 60
July, 1977, Vol. 94, No. 1
Accelerated A V conduction during acute M I
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msec., A-H 50 msec., and H-V 40 msec. T h e patient remained in congestive failure b u t h a d no a r r h y t h m i c episodes. Discussion
T h e reported cases are examples of the socalled acquired variety of the preexcitation syndrome. I t is now accepted t h a t the W P W s y n d r o m e is due to a b n o r m a l a t r i o v e n t r i c u l a r connections. 6-9 A n a t o m i c studies 16, 11 were able to d e m o n s t r a t e accessory m u s c u l a r bridges between the atria and ventricles in a p p a r e n t l y n o r m a l hearts. It is possible that u n d e r p a r t i c u l a r influences such accessory bundles m a y become functional and c o n d u c t the cardiac impulse. Levine and Burge 1 reported a p a t i e n t with an acute m y o c a r d i a l infarction and a high degree A-V block in whom occasionally c o n d u c t e d beats showed the W P W pattern. Goel and H a n 5 described two cases of the W P W s y n d r o m e appearing after the d e v e l o p m e n t of an acute m y o c a r d i a l infarction. T h e electrocardiographic configuration of the m y o c a r d i a l infarction disappeared completely with the occurrence of preexcitation. 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 occurred in both patients. T h e W P W p a t t e r n disappeared with the recovery from the acute phase. I t was assumed t h a t under the influence of increased a u t o n o m i c nervous activity associated with a c u t e
American Heart J o u r n a l
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Fig. 9. Case 3. A, His bundle electrogram showing an A-H interval of 30 msec. corresponding to the electrocardiogram shown in Fig. 8C. B, During atrial pacing at a rate of 120 per minute the A-H interval lengthened to 80 msec. This procedure was used to validate the H deflection. 25
Gavrilescu, Gavrilescu, and Luca
ischemia an aberrant A-V bundle became functional2 This hypothesis is supported by the observation t h a t the preexcitation pattern could be elicited in a patient with intermittent WPW syndrome by concomitant isoprenaline infusion and carotid sinus massage. 12 In Case 1 the WPW pattern appeared during the first myocardial infarction and persisted for four months until the death due to a second infarction. Nonspecific degenerative changes were present in the A-V conduction system, especially in the compact nodal area. It is possible t h a t theSe changes favored A-V conduction through the accessory bundle. No attacks of supraventricular tachycardia occurred, nor could be initiated during the scanning of the cardiac cycle with electric stimuli suggesting t h a t no reentry circuit could be initiated. This may be due to the pathologic changes within the A-V conducting system. However, stimuli falling at 240 to 280 msec. from the beginning of atrial depolarization were conducted through the normal A-V conduction system, with a prolonged H-V interval and ventricular aberrancy. There was a slight increase in the QRS duration from 60 to 90 msec. associated with the appearance of the WPW configuration suggesting that A-V conduction occurred over both normal pathways and also through the abnormal connection. Although the preexcitation syndrome in this patient appears as "acquired" it could not to be excluded that during its life this pattern was present in other occasions. The anatomic study showed a correspondence between the electrocardiographic configuration suggesting right posterior preexcitation 7 and the localization of the accessory bundle. The hypothesis of mismatch impedance, 1:~ which assumes an adequate relation between cable capacity of the conducting structure and the muscle mass which is to be activated, may explain the preferential utilization of the pathway by which the cardiac impulse is conducted. Autonomic nervous influences,~"~ as well as pathologic changes in the A-V conducting system can dissipate the mismatch impedance enhancing conduction over the accessory bundle. The appearance of the short PR interval associated with normal duration of the QRS complexes 14 during the course of acute myocardial infarction is more difficult to explain. Although this phenomenon is said to be a rare event, 4. 1~ it was noted with variable frequency when large series of patients with myocardial infarction were 2(}
studied.16. 17 The short PR intervals were noted especially on the first days of the illness, subsequently the tracings revealed normal PR intervals, except in a few instances in which it remained unchanged for months. 16 No mention is made about the associations with supraventricular tachycardia. In our Cases 2 and 3, both developed attacks of rapid heart action shortly after the appearance of the preexcitation pattern. This phenomenon was associated with atrial premature beats and atrial echoes in Case 2, and ventricular extrasystoles with retrograde activation of the atria in Case 3. Anginal pain was also a feature of the clinical picture. No arrhythmic episodes were encountered in both patients nor in the past history and the follow-up period. In the absence of anatomic studies the mechanism of the shortening of the P R interval remains speculative. It was suggested 7' 18 t h a t shortening of the PR interval may be due to abnormal connections of the atriofascicular bypas s type, ~ or to a particular pacemaker location and pattern of atrial activation. 18 The demonstration of shortened refractory periods of the A-V conducting system in patients with short PR intervals and normal QRS complexes was considered compatible with a partial A-V nodal bypass or dual A-V conduction but could not differentiate between these two possibilities. 19 In Case 2 an A-H interval of 30 msec. was measured on the His bundle recording during sinus rhythm, while during supraventricular tachycardia it was 150 msec. This phenomenon can be explained by prolongation of the A-H time with increased atrial rate or by the fact t h a t during ectopic r h y t h m an accessory pathway was active. ~~ During supraventricular tachycardia no retrograde H' deflections were recorded; however, this does not exclude the possibility t h a t ventriculoatrial conduction occurred via the abnormal Connection {Fig, 7). The H-V interval was unchanged in sinus a n d ectopic rhythm. There is no firm evidence that accelerated A-V conduction can be acquired during acute myocardial infarction. However, latent accessory A-V connections may become functional under the complex changes due to acute myocardial ischemia and show various electrocardiographic patterns of preexcitation syndrome.
Summary Three cases are described in which accelerated atrioventricular conduction occurred during an acute myocardial infarction. The first patient, an July, 1977, Vol. 94, No. 1
Accelerated A V conduction during acute M I
82-year-old woman, developed a W P W s y n d r o m e suggesting posterior right ventricular preexcitat i o n , a P a t t e r n w h i c h p e r s i s t e d for f o u r m o n t h s u n t i l her death. A n accessory b u n d l e was f o u n d on autopsy. Fibrotic changes, associated with acute lesions (hemorrhage, p o l y m o r p h o n u c l e a r ~infiltrates) were p r e s e n t i n t h e a t r i o v e n t r i c u l a r node and His-Purkinje system. T w o m e n , of 47 a n d 74 years, d e v e l o p e d a s h o r t PR interval associated with supraventricular t a c h y c a r d i a d u r i n g t h e c o u r s e of a n a c u t e m y o c a r d i a l i n f a r c t i o n . T h e P R i n t e r v a l r e t u r n e d to its i n i t i a l v a l u e i n o n e case a n d r e m a i n e d u n c h a n g e d for t h r e e m o n t h s i n t h e o t h e r . Accessory a t r i o v e n t r i c u l a r c o n n e c t i o n s which became functional during myocardial ischemia may explain the various electrocardiographic p a t t e r n s of p r e e x c i t a t i o n .
8. 9.
10.
11. 12. 13. 14.
REFERENCES
1. Levine, H. D., and Burge, J. C.: Septal infarction with complete heart block and intermittent anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome). Histologic demonstration of right lateral bundle, AM. HEARTJ. 36:431, 1948. 2. Scherf, D., and Cohen, J.: The atrioventricular node and selected cardiac arrhythmias, New-York, London, 1964, Grune & Stratton, Inc., p. 388. 3. Verani, M. S., Baron, H., and Maia, I. G.: Myocardial infarction associated with Wolff-Parkinson-White syndrome, AM. HEARTJ. 83:684, 1972. 4. Mathew, G., and Raftery, E. B.: Accelerated atrioventricular conduction after myocardial infarction. A study using His bundle electrogram, Br. Heart J. 35:985, 1973. 5. Goel, B. G., and Han, J.: Manifestation of the WPW syndrome after myocardial infarction, AM. HEART J. 87:633, 1974. 6. Davies, M. J.: Pathology of conducting tissue of the heart, London, 197!, Butterworth & Co., Ltd., p. 26. 7. Boineau, J. P., Moore, N. E., Spear, J. F., and Seaty, W. C.: Basis of clinical-ECG variations in right and left
American H e a r t J o u r n a l
15.
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20.
ventricular preexcitation: a unitary concept of WPW, in Cardiac Arrhythmias, Dreifus and Likoff, editors, New York, 1973, Grune & Stratton, Inc., p. 421. Durrer, D., and Wellens, H. J. J.: The Wolff-ParkinsonWhite syndrome, anno 1973, Eur. J. Cardiol. 1:347, 1974. Anderson, R. H., Becker, A. E., Brechenmacher, C., Davies, M. J., and Rossi, L.: Ventricular preexcitation. A proposed nomenclature of its substrates, Eur J. Cardiol. 3:27, 1975. Glomset, D. J., and Glomset, A. T. A.: A morphoiogic study of the cardiac conduction system in ungulates, dog 9and man. I. The sinoatrial node, AM. HEARTJ. 20:389, 1940. Anderson, R. H., and Taylor, M. I.: Development of atrioventricular specialized tissue in human heart, Br. Heart J. 34:1205, 1972. Gavrilescu, S.: Manifestation of the WPW syndrome during isoprenaline infusion and carotid sinus massage (In preparation, 1976}. Mendez, G., Mueller, W. J., and Uruiaga, X.: Propagation of impulse across the Purkinje fiber-muscle junctions in the dogs, Circ. Res. 26:135, 1970. Lown, B., Ganong, W. F., and Levine, S. A.: The syndrome of short PR interval, normal QRS complex and paroxysmal rapid heart action, Circulation 5:693, 1952. Kr~kler,D. M.: The Wolff-Parkinson-White and related syndromes, in Cardiac Arrhythmias, Krikler and Goodwin, editors, London, Philadelphia, Toronto, 1975, W. B. Saunders Company, p. 144. SoederstrSm, N.: Myocardial infarction and mural thrombosis in the atria of the heart, Acta Med. Scand. Suppl. 217:1948. Nazzi, V., Meda, A., and Paciello, D.: Le alterazioni dell' atriogramma e del tempo di conduzione atrio-ventricolare nell-infarto miocardico, Folio Cardiol. 15:53, 1956. Shed, L., and James, N. T.: A new electrocardiographic concept: Synchronized sinoventricular conductibn, Dis. Chest 55:127, 1969. Bisset, J. K., Soyza, N., Kane, J. J., and Murphy, M. L.: -Altered refractory periods in patients with short PR intervals and normal QRS complexes, Am. J. Cardiol. 35:487, 1975. Spurrel, R. A. J., Krikler, D. M., and Sowton, E.: Problems concerning assessment of anatomical site of accessory pathway in Wolff-Parkinson-Whitesyndrome, Br. Heart J. 37:127, 1975.
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