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Two cases of the pre-excitation syndrome
J. ELECTROCARDIOLOGY, 2 (2),177-184,1969
Two Cases of the Pre-Excitation Syndrome* BY DAVID SCHERF, M.D. AND CARL BORNEMANN, M.D.
SUMMARY In this report 2 unusual examples of the preexcitation syndrome are described. In the first observation, the form of the ventricular complex changed as the P wave changed. Pre-excitation followed only 1 type of P, left bundle branch block with normal A-V conduction the other type. At other times transitional complexes with short P-R intervals were present. This case is explained best on the basis of a by-pass within the AV node region. In the second observation, attacks of paroxysmal supraventricular tachycardia in a patient with coarctation of the aorta and pre-excitation repeatedly exhibited a pattern of an acute inferior wall myocardial infarction. This may result from several causes although we favor preexisting infarction masked in the control electrocardiogram. INTRODUCTION The mechanism of pre-excitation remains disputed. More than 60 theories have been advanced, but many cannot stand criticism. Most authorities accept the explanation that an accessory bundle provides an anomalous pathway from atria to ventricles 8• The electrocardiogram of pre-excitation may, however, result from several mechanisms. Thus when pre-excitation is observed during cardiac catheterization or electrical stimulation of certain areas in the central nervous system, the mechanism seems to be a chance co-existance of a sinus and an ectopic ventricular rhythm having almost identical rates22 • The old theories do not readily explain the pre-excitation which only follows abnormal P waves while normal ventricular complexes follow regular sinus rhythm P waves after a normal P-R interval. This fact has been mentioned in 2 previously appearing publications21 ,23. Sherf and James23 explain this phenomenon by invoking the concept that an abnormal order of depolarization of the atria leads to an abnormal order of depolar-
* Department of Medicine, New York Medical College. Aided by the Hans Petschek Fund.
ization of the A-V node and common bundle so that the delaying mass of A-V node fibers is bypassed. "Distorted" excitation of A-V node fibers which circumvent the main portion of the A- V node would shorten the P-R interval. In addition, the abnormal QRS complexes couid be explained if we assumed, as Kaufmann and Rothberger first postulatedl 4, that individual muscular strands in the A-V node, common bundle and bundle branches separately activate specific portions of the ventricles. Borduas et al. suggested, but did not prove, a similar mechanism3• PERSONAL OBSERVATIONS Our first observation supports the validity of the theory advanced by Sherf and James. Mrs. R. R, a 54-year-old grey-haired mother of 5 children, had a 20-year history of an intermittent "terrible pressure pain" in the mid-anterior chest radiating to the throat, lower jaw and interscapular region, lasting 5 to 60 minutes or even several hours. Initiated by sudden movements, reaching, bending, mopping floors, walking uphill, especially "if real cold," the pain was always associated with the "heart going very fast ... all of a sudden my heart will flip around and then I get my heart racing and pain comes ... (once or twice a week or after a lapse of 1-2 months) ... pain may go but heart will keep on racing as long as one half a day." If she sits down at the onset of the attack, it passes sooner. If she takes a deep breath and holds it for a minute, the pain is said to ease off. Her blood pressure has varied between 180/100 and 200/100 mm. Hg. Fundoscopic examination showed early Grade II retinal sclerosis. Her mother and a brother, who both died of heart attacks at the age of 66, are said to have had similar attacks. Fig. 1 from R. B. shows leads aVR, aVF and 2 strips of lead II. Lead aVR shows an aiternation of pre-excitation and left bundle branch block, ventricular complexes with P-R intervals measuring respectively 0.11 second and 0.17 second. Of greater interest is the alternation in the form of the P waves; those preceding the wider QRS complexes being definitely deeper than the
177
178
SCHERF AND BORNEMANN
Fig. 1. Observation I.-Leads aVR, aVF and two strips of lead If. Description in text. others. In this strip the successive poP intervals measure: 0.73, 0.74, 0.72, 0.70, 0.70, 0.68, 0.70, 0.68, and 0.70 second. In lead aVF (second strip) the alternation is only visible in the beginning of the tracing where the form of the P waves alternates less conspicuously and the delta wave in the beats following a short P-R interval is separated from the QRS complexes. The successive pop intervals measure: 0.71, 0.68, 0.68, 0.66, 0.64, 0.66, 0.68, 0.68, and 0.71 second. In the third strip (lead II) where the alternation is very clearly demonstrated, the delta wave preceding every second ventricular complex appears about 0.08 second after the onset of the P wave. The QRS complexes following the longer P-R intervals have a width of 0.14 second. Here again the form of the P wave alternates, the P waves followed by the shorter P-R intervals being distinctly lower than the others. This difference cannot be the result of partial fusion with the "delta" wave since this wave is positive. The successive Pop intervals measure: 0.72, 0.76, 0.72, 0.80, 0.72, 0.74,0.74,0.75, and 0.71 second. Because the rate is irregular, the objection could be raised that the alternation in the form of the ventricular complexes relates to the different durations of diastole. The last tracing, however, showing an unbroken succession of anomalous conduction (lead II), also presents similar variations in diastole with pop intervals measuring 0.68,0.69, 0.70,0.68,0.68, 0.74, 0.74, 0.74, and 0.75 second. Variation in diastole, therefore, could not account for the alternation observed. The pre-excitation pattern of this patient was of Type A. Fig. 2 was obtained when the patient visited
the office again. It shows lead II, and the precordial leads. In all leads the P wave followed by a pre-excitation complex is different from that showing a normal A-V conduction. This is particularly clear in lead VI where the P waves with a normal A-V conduction are biphasic, whereas the P waves preceding pre-excitation complexes are positive. Fig. 3 shows the results of 2 applications of carotid sinus pressure. In the upper tracing (lead V5) the first 3 typical pre-excitation ventricular complexes are preceded by very low biphasic P waves. During carotid sinus pressure, indicated approximately by the horizontal black line, the P waves change form and are followed by 2 different types of ventricular complexes. The first type (2 beats) appears after a P-R interval of 0.10 second, and the second (2 beats) after an interval of 0.18 second. We believe that it is probable that the first 2 complexes following the clearly defined P waves represent mixed, combination beats between those at the beginning of the tracing and the following 2 which show typical bundle branch block complexes. A similar pattern was present 6 years earlier (Fig. 4B). When carotid sinus pressure was applied during the registration of lead II (Fig. 3B) the pattern changed into a different form of P wave and normal A-V conduction. In addition, the form of the bundle branch block complexes changed and a notch appeared in the descending portion of the R wave nearer the base line. After the end of the carotid sinus pressure alternation between normal A-V conduction and pre-excitation started again, and the btmdle branch block QRS complexes of the
THE PRE-EXCITATION SYNDROME
179
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Fig. 2. Observation I.-Leads II, and VI through V7, showing alternation of the form of the P waves, of the P-R intervals and of the form of the ventricular complexes.
Fig. 3. Observation I.-Leads V5 and II, showing the effect of carotid sinus pressure on form of the P waves and of the ventricular complexes. beats with a normal A-V conduction returned to their usual form. This tracing shows therefore the unusual phenomenon of a change of the configuration of the QRS complexes during carotid sinus pressure. Carotid sinus pressure abolished pre-excitation. When repeated 3 11l months later, the electrocardiogram was essentially normal (Fig. 4C) at rest and during carotid sinus pressure. Our second observation is recorded from a 54-year-old man with both coarctation of the
aorta and the pre-excitation syndrome. A hypertensive, with blood pressures between 180/90 and and 200/120 mm. Hg., he also manifested 3 to 5 attacks of paroxysmal tachycardia a year, lasting up to 12 hours. For 18 years this man's electrocardiogram disclosed usually a pre-excitation pattern as seen in Fig. SA. In lead I, a distinct delta wave follows a short P-R interval of 0.08 second. In leads II, III and aVF, inverted delta waves consistently simulated Q waves. Only rarely the pre-excitation
180
SCHERF AND BORNEMANN
disappeared and a normal sinus rhythm with a left ventricular hypertrophy pattern was recorded (Fig. 5B). The P-R intervals measured 0.16 second, ventricular extrasystoles were recorded showing reversed conduction to the atria (Fig. 5B). Three times the patient was observed during an attack of paroxysmal tachycardia with a rate of 200. Each time during the tachycardia an identical electrocardiogram was obtained. Twice he was hospitalized because the deep Q waves, plus elevation of the RS-T segments, suggested an acute inferior wall myocardial infarction (Fig. 6). No other clinical signs (blood pressure changes, enzyme levels, sedimentation rate, etc.) substantiated the diagnosis of an acute infarction and with cessation of the tachycardia, the RS-T segment deviations disappeared immediately. DISCUSSION Figs. 1 through 3 demonstrate clearly that P waves with different configurations precede different QRS complexes both spontaneously and
during carotid sinus pressure. Hunter et al. 9 first stressed the variations in the form of the P waves in the pre-excitation syndrome and Sherf and James 23 collected a large number of similar observations and offered the best explanation of this phenomenon. Impulses conducted over the posterior inter-nodal tract of James can arrive at the lower end of the A-V node before the impulses conducted via the other tracts (anterior and middle inter-nodal tracts) can traverse the other portions of the node ll ,l2. According to this opinion, a part of the ventricle may be activated early provided given tracts within the A-V node, common bundle and bundle branches connect with specific parts of the ventricles. That a given region of the A-V node sends its impulses to a given area of the ventricles is anatomically conceivable because of the many connective tissue septa found in the A-V node and common bundle. These septa facilitate also the longitudinal dissociation which makes return extrasystoJes possible 22 • The discovery of abnormal A-V connections (Kent bundles) elsewhere in the heart, for
181
THEPR~ExcrrATIONSYNDROME
instance on the right lateral wall, in persons who had shown pre-excitation, does not refute this theory since several mechanisms may lead to the same electrocardiographic pattern (see above). The observation that a point at the base of the right ventricle was activated 0.08 second after the appearance of the P wave in a patient with the pre-excitation syndrome 6 is most reasonably explained by an anomalous connection between the right atrium and ventricle. The finding that normal and abnormal A-V conduction frequently follow each other without change in the form of the P wave does not
militate against the explanation of Sherf and James for obvious reasons. On the other hand, the observation of a prolonged P-R interval in the same individual with normal as well as the anomalous conduction13 ,19,21 ,23 is understandable only if we assume that delaying parts of the A-V system are used in both instances. In two recent reports the change of the form of the QRS complex with a change of the form of the P wave is illustrated. In one patient with a congenital heart lesion, this change occurred during ocular pressure 17 • In another patient, also with congenital heart disease, 4 different types of
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Fig. 6. Observation 2. Electrocardiogram during an attack of supraventricular tachycardia. "pacemakers" were observed, each with a distinct QRS complex of normal duration4• It has been postulated that even junctional escape beats by using "paraspecific" fibers 15 can circumvent the A-V node and have ventricular complexes different from those of the sinus beats in the same patient 10,18,24. Several authors 1 •2 ,D.7, have described the combination of pre-excitation and coarctation of the aorta which appears to be as frequent as the combination of other congenital lesions with preexcitation. In pre-excitation, deep wide Q waves in leads II, III and aVF may be observed in the absence of an inferior wall infarction, when the axis of the delta wave in the standard leads is less than - 30°. . Although these Q waves caused by inverted delta waves are not infrequent, the appearance of an acute myocardial infarction pattern with elevated RS-T segments during paroxysmal tachycardia is rare. One instance was reported in a 90-year-old woman with coronary sclerosis, and an old anterior wall infarction 2o , whose electrocardiogram during normal sinus rhythm without pre-excitation showed a deep Q wave in lead V3. During 4 bouts of a supraventricular tachycardia, deep wide Qwaves appeared in leads 11, III and a VF. Deep Q waves and elevated S-T segments were seen in all chest leads, suggesting an acute inferior as well as anterior wall myocardial infarction.
tion of sinus rhythm, the electrocardiogram returned to the control pattern. One ventricular extrasystole during sinus rhythm in lead V2 showed the same broad Q wave and elevated S-T segments as had been seen during the tachycardia. The authors considered two possible mechanisms to explain these changes. One was the ischemia which may occur during tachycardia. The other was an abnormal spread of the excitation wave during tachycardia leading to "secondary" elevation of SoT. In our opinion the second mechanism is favored by the appearance of the myocardial infarction pattern in the extrasystole during sinus rhythm. The unmasking of an old jnfarction not recognized during sinus rhythm in the electrocardiogram of a single ventricular extrasystole is a wellknown and common phenomenon. One should expect that it also occurs in every beat during a paroxysmal tachycardia. Even in a supraventricular tachycardia aberrant ventricular conduction may lead to the same phenomenon. We cannot, therefore, rule out the possibility that our patient once had a myocardial infarction which was not diagnosed and that the tachycardia only unmasked it. Ischemia, while common in tachycardia, involves chiefly the subendocardial layers of the myocardium and should result in elevation of the SoT segments only in lead aVR, whereas in our observation elevation occurred in leads III and aVF as well. Another factor which may be responsible for a pattern of myocardial infarction is dilatation of the heart. At first, a tachycardia reduces heart size; later it causes dilatation. Myers has observed QR and QS patterns as well as elevated and caved S-T segments in right ventricular hypertrophy and dilatation16 • Thus patterns imitating myocardial infarctions might be encountered during tachycardias inducing dilatation of the heart and especially of the right ventricle.
REFERENCES 1. Ask-Upmark, E.: Coal'ctatio aortae, Acta Med.
Scand. 112: 7, 1942. 2. Bodlander, ]. W.: The Wolff-Parkinson-White syndrome in association with congenital heart disease: Coarctation of the aorta, Report of a case. Am. Heart 1. 31: 785, 1946. 3. Borduas, ], L., Rakita, L., Kennamer, R., and Prinzmetal, M.: Studies on the mechanism of ventricular activity. Circulation 11: 69, 1955.
THE PRE-EXCITATION SYNDROME
4. Castellanos, A., Balais, M., Lemberg, L., Salhanick, L., and Castellanos, A. Jr.: Double ectopic left atrial rhythms. Dis. Chest. 52: 87, 1967. 5. Comberiati, L.: Due casi di sindrome di Wolff, Parkinson e White in cardiopatia congenita operata. Cuore e Circo!' 39: 169, 1955. 6. Durrer, D., and Ross, J. P.: Epicardial excitation oftbe ventricles in a patient with Wolff-ParkinsonWhite syndrome. Circulation 35: 15, 1967. 7. Grosse-Brockhoff, F., Loogen, F., and Scbaede, A.: Angeborene Herziund Gefaessmissbildungen. In Handbuch Inn. Med., Springer, 1960, 9, Third Part, p. 105. 8. Holzmann, M., and Scherf, D.: Ueber Elektrokardiogramme mit verkuerzter Vorhof-KammerDistanz und positiven P-Zacken. Ztschr. Klin. Med., 121: 404, 1932. 9. Hunter, A., Papp, c., and Parkinson, J.: The syndrome of short P-R interval, apparent bundle branch block, and associated paroxysmal tachycardia. Brit. Heart J. 2: 107, 1940. 10. Hwang, W., and Langendorf, R.: Auriculoventricular nodal escape in the presence of ventricular fibrillation. Circulation 1: 930, 1950. 11. James, T. N.: The connecting pathways between the sinus node and A-V node and between tbe right and left atrium of the human heart. Am. Heart J. 66: 498, 1963. 12. James, T. N.: Morphology of the human atrioventricular node, with remarks pertinent to its electrophysiology. Am. Heart J. 62: 756, 1961. 13. Katz, L. N., and Pick, A.: Clinical Electrocardiography, Part I. The Arrhytbmias. Philadelphia, Lea and Febiger, 1956. 14. Kaufmann, R., and Rothberger, C. J.: Beitraege zur Entstehungsweise extrasystolischer Allorhythmien, 2. Mitteilung, Ztschr. ges. expo Med. 7:
183
199, 1919. 15. Mahaim, 1.: Kent's fibers and the A-V paraspecific conduction through the upper connections of the bundle of His-Tawara. Am. Heart J. 33: 651, 1967. 16. Myers, G. B.: QRS-T patterns in multiple precordial leads that may be mistaken for myocardial infarction. II. Right ventricular hypertrophy and dilatation. Circulation 1: 860, 1950. 17. Mirowski, M., Neill, C. A., and Taussig, H. B. ~ Left atrial rhythm in mirror image dextrocardia and in normally placed malformed hearts. Circulation. 27: 864, 1963. 18. Pick, A.: Aberrant ventricular conduction of escaped beats. Preferential and accessory pathways in the A-V junction. Circulation 13: 702, 1958. 19. Rodstein, M.: A case of anomalous auriculoventricular conduction with auriculo-ventricular block and a history of rheumatic fever. New York State Med. J. 51: 789,1951. 20. Rubin, L L., Gross, H., and Arbeit, S. R.: Transitory abnormal Q waves during bouts of tachycardia. Am. 1. Cardio!. 11: 659, 1963. 21. Scherf, D.: Mechanisms of arrhythmias associated with the WPW syndrome. In Mechanisms and Therapy of Cardiac Arrhythmias. Ed. Dreifus and Likoff, New York, Grune and Stratton, 1966, pp. 671. 22. Scherf, D., and Cohen, J.: The Atrioventricular Node and Selected Cardiac Arrhythmias. New York, Gmne and Stratton, 1964. 23. Sherf, L., and James, T. N.: A new look at some old questions in clinical electrocardiography. Henry Ford Hasp. Med. Bull., 14: 265, 1966. 24. Walsh, T. J.: Ventricular aberration of A- V nodal escape beats: Comments concerning the mechanism of abenation. Am. J. Cardio!. 10: 217,1962.
Two Cases of the Pre-Excitation Syndrome* BY DAVID SCHERF, M.D. AND CARL BORNEMANN, M.D.
SUMMARY In this report 2 unusual examples of the preexcitation syndrome are described. In the first observation, the form of the ventricular complex changed as the P wave changed. Pre-excitation followed only 1 type of P, left bundle branch block with normal A-V conduction the other type. At other times transitional complexes with short P-R intervals were present. This case is explained best on the basis of a by-pass within the AV node region. In the second observation, attacks of paroxysmal supraventricular tachycardia in a patient with coarctation of the aorta and pre-excitation repeatedly exhibited a pattern of an acute inferior wall myocardial infarction. This may result from several causes although we favor preexisting infarction masked in the control electrocardiogram. INTRODUCTION The mechanism of pre-excitation remains disputed. More than 60 theories have been advanced, but many cannot stand criticism. Most authorities accept the explanation that an accessory bundle provides an anomalous pathway from atria to ventricles 8• The electrocardiogram of pre-excitation may, however, result from several mechanisms. Thus when pre-excitation is observed during cardiac catheterization or electrical stimulation of certain areas in the central nervous system, the mechanism seems to be a chance co-existance of a sinus and an ectopic ventricular rhythm having almost identical rates22 • The old theories do not readily explain the pre-excitation which only follows abnormal P waves while normal ventricular complexes follow regular sinus rhythm P waves after a normal P-R interval. This fact has been mentioned in 2 previously appearing publications21 ,23. Sherf and James23 explain this phenomenon by invoking the concept that an abnormal order of depolarization of the atria leads to an abnormal order of depolar-
* Department of Medicine, New York Medical College. Aided by the Hans Petschek Fund.
ization of the A-V node and common bundle so that the delaying mass of A-V node fibers is bypassed. "Distorted" excitation of A-V node fibers which circumvent the main portion of the A- V node would shorten the P-R interval. In addition, the abnormal QRS complexes couid be explained if we assumed, as Kaufmann and Rothberger first postulatedl 4, that individual muscular strands in the A-V node, common bundle and bundle branches separately activate specific portions of the ventricles. Borduas et al. suggested, but did not prove, a similar mechanism3• PERSONAL OBSERVATIONS Our first observation supports the validity of the theory advanced by Sherf and James. Mrs. R. R, a 54-year-old grey-haired mother of 5 children, had a 20-year history of an intermittent "terrible pressure pain" in the mid-anterior chest radiating to the throat, lower jaw and interscapular region, lasting 5 to 60 minutes or even several hours. Initiated by sudden movements, reaching, bending, mopping floors, walking uphill, especially "if real cold," the pain was always associated with the "heart going very fast ... all of a sudden my heart will flip around and then I get my heart racing and pain comes ... (once or twice a week or after a lapse of 1-2 months) ... pain may go but heart will keep on racing as long as one half a day." If she sits down at the onset of the attack, it passes sooner. If she takes a deep breath and holds it for a minute, the pain is said to ease off. Her blood pressure has varied between 180/100 and 200/100 mm. Hg. Fundoscopic examination showed early Grade II retinal sclerosis. Her mother and a brother, who both died of heart attacks at the age of 66, are said to have had similar attacks. Fig. 1 from R. B. shows leads aVR, aVF and 2 strips of lead II. Lead aVR shows an aiternation of pre-excitation and left bundle branch block, ventricular complexes with P-R intervals measuring respectively 0.11 second and 0.17 second. Of greater interest is the alternation in the form of the P waves; those preceding the wider QRS complexes being definitely deeper than the
177
178
SCHERF AND BORNEMANN
Fig. 1. Observation I.-Leads aVR, aVF and two strips of lead If. Description in text. others. In this strip the successive poP intervals measure: 0.73, 0.74, 0.72, 0.70, 0.70, 0.68, 0.70, 0.68, and 0.70 second. In lead aVF (second strip) the alternation is only visible in the beginning of the tracing where the form of the P waves alternates less conspicuously and the delta wave in the beats following a short P-R interval is separated from the QRS complexes. The successive pop intervals measure: 0.71, 0.68, 0.68, 0.66, 0.64, 0.66, 0.68, 0.68, and 0.71 second. In the third strip (lead II) where the alternation is very clearly demonstrated, the delta wave preceding every second ventricular complex appears about 0.08 second after the onset of the P wave. The QRS complexes following the longer P-R intervals have a width of 0.14 second. Here again the form of the P wave alternates, the P waves followed by the shorter P-R intervals being distinctly lower than the others. This difference cannot be the result of partial fusion with the "delta" wave since this wave is positive. The successive Pop intervals measure: 0.72, 0.76, 0.72, 0.80, 0.72, 0.74,0.74,0.75, and 0.71 second. Because the rate is irregular, the objection could be raised that the alternation in the form of the ventricular complexes relates to the different durations of diastole. The last tracing, however, showing an unbroken succession of anomalous conduction (lead II), also presents similar variations in diastole with pop intervals measuring 0.68,0.69, 0.70,0.68,0.68, 0.74, 0.74, 0.74, and 0.75 second. Variation in diastole, therefore, could not account for the alternation observed. The pre-excitation pattern of this patient was of Type A. Fig. 2 was obtained when the patient visited
the office again. It shows lead II, and the precordial leads. In all leads the P wave followed by a pre-excitation complex is different from that showing a normal A-V conduction. This is particularly clear in lead VI where the P waves with a normal A-V conduction are biphasic, whereas the P waves preceding pre-excitation complexes are positive. Fig. 3 shows the results of 2 applications of carotid sinus pressure. In the upper tracing (lead V5) the first 3 typical pre-excitation ventricular complexes are preceded by very low biphasic P waves. During carotid sinus pressure, indicated approximately by the horizontal black line, the P waves change form and are followed by 2 different types of ventricular complexes. The first type (2 beats) appears after a P-R interval of 0.10 second, and the second (2 beats) after an interval of 0.18 second. We believe that it is probable that the first 2 complexes following the clearly defined P waves represent mixed, combination beats between those at the beginning of the tracing and the following 2 which show typical bundle branch block complexes. A similar pattern was present 6 years earlier (Fig. 4B). When carotid sinus pressure was applied during the registration of lead II (Fig. 3B) the pattern changed into a different form of P wave and normal A-V conduction. In addition, the form of the bundle branch block complexes changed and a notch appeared in the descending portion of the R wave nearer the base line. After the end of the carotid sinus pressure alternation between normal A-V conduction and pre-excitation started again, and the btmdle branch block QRS complexes of the
THE PRE-EXCITATION SYNDROME
179
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Fig. 2. Observation I.-Leads II, and VI through V7, showing alternation of the form of the P waves, of the P-R intervals and of the form of the ventricular complexes.
Fig. 3. Observation I.-Leads V5 and II, showing the effect of carotid sinus pressure on form of the P waves and of the ventricular complexes. beats with a normal A-V conduction returned to their usual form. This tracing shows therefore the unusual phenomenon of a change of the configuration of the QRS complexes during carotid sinus pressure. Carotid sinus pressure abolished pre-excitation. When repeated 3 11l months later, the electrocardiogram was essentially normal (Fig. 4C) at rest and during carotid sinus pressure. Our second observation is recorded from a 54-year-old man with both coarctation of the
aorta and the pre-excitation syndrome. A hypertensive, with blood pressures between 180/90 and and 200/120 mm. Hg., he also manifested 3 to 5 attacks of paroxysmal tachycardia a year, lasting up to 12 hours. For 18 years this man's electrocardiogram disclosed usually a pre-excitation pattern as seen in Fig. SA. In lead I, a distinct delta wave follows a short P-R interval of 0.08 second. In leads II, III and aVF, inverted delta waves consistently simulated Q waves. Only rarely the pre-excitation
180
SCHERF AND BORNEMANN
disappeared and a normal sinus rhythm with a left ventricular hypertrophy pattern was recorded (Fig. 5B). The P-R intervals measured 0.16 second, ventricular extrasystoles were recorded showing reversed conduction to the atria (Fig. 5B). Three times the patient was observed during an attack of paroxysmal tachycardia with a rate of 200. Each time during the tachycardia an identical electrocardiogram was obtained. Twice he was hospitalized because the deep Q waves, plus elevation of the RS-T segments, suggested an acute inferior wall myocardial infarction (Fig. 6). No other clinical signs (blood pressure changes, enzyme levels, sedimentation rate, etc.) substantiated the diagnosis of an acute infarction and with cessation of the tachycardia, the RS-T segment deviations disappeared immediately. DISCUSSION Figs. 1 through 3 demonstrate clearly that P waves with different configurations precede different QRS complexes both spontaneously and
during carotid sinus pressure. Hunter et al. 9 first stressed the variations in the form of the P waves in the pre-excitation syndrome and Sherf and James 23 collected a large number of similar observations and offered the best explanation of this phenomenon. Impulses conducted over the posterior inter-nodal tract of James can arrive at the lower end of the A-V node before the impulses conducted via the other tracts (anterior and middle inter-nodal tracts) can traverse the other portions of the node ll ,l2. According to this opinion, a part of the ventricle may be activated early provided given tracts within the A-V node, common bundle and bundle branches connect with specific parts of the ventricles. That a given region of the A-V node sends its impulses to a given area of the ventricles is anatomically conceivable because of the many connective tissue septa found in the A-V node and common bundle. These septa facilitate also the longitudinal dissociation which makes return extrasystoJes possible 22 • The discovery of abnormal A-V connections (Kent bundles) elsewhere in the heart, for
181
THEPR~ExcrrATIONSYNDROME
instance on the right lateral wall, in persons who had shown pre-excitation, does not refute this theory since several mechanisms may lead to the same electrocardiographic pattern (see above). The observation that a point at the base of the right ventricle was activated 0.08 second after the appearance of the P wave in a patient with the pre-excitation syndrome 6 is most reasonably explained by an anomalous connection between the right atrium and ventricle. The finding that normal and abnormal A-V conduction frequently follow each other without change in the form of the P wave does not
militate against the explanation of Sherf and James for obvious reasons. On the other hand, the observation of a prolonged P-R interval in the same individual with normal as well as the anomalous conduction13 ,19,21 ,23 is understandable only if we assume that delaying parts of the A-V system are used in both instances. In two recent reports the change of the form of the QRS complex with a change of the form of the P wave is illustrated. In one patient with a congenital heart lesion, this change occurred during ocular pressure 17 • In another patient, also with congenital heart disease, 4 different types of
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Fig. 5. Observation 2. A: Leads I, IT, Ill, V2 and V5 exhibiting a pre-excitation pattern. B: Occasional normal electrocardiogram of the same patient.
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Fig. 6. Observation 2. Electrocardiogram during an attack of supraventricular tachycardia. "pacemakers" were observed, each with a distinct QRS complex of normal duration4• It has been postulated that even junctional escape beats by using "paraspecific" fibers 15 can circumvent the A-V node and have ventricular complexes different from those of the sinus beats in the same patient 10,18,24. Several authors 1 •2 ,D.7, have described the combination of pre-excitation and coarctation of the aorta which appears to be as frequent as the combination of other congenital lesions with preexcitation. In pre-excitation, deep wide Q waves in leads II, III and aVF may be observed in the absence of an inferior wall infarction, when the axis of the delta wave in the standard leads is less than - 30°. . Although these Q waves caused by inverted delta waves are not infrequent, the appearance of an acute myocardial infarction pattern with elevated RS-T segments during paroxysmal tachycardia is rare. One instance was reported in a 90-year-old woman with coronary sclerosis, and an old anterior wall infarction 2o , whose electrocardiogram during normal sinus rhythm without pre-excitation showed a deep Q wave in lead V3. During 4 bouts of a supraventricular tachycardia, deep wide Qwaves appeared in leads 11, III and a VF. Deep Q waves and elevated S-T segments were seen in all chest leads, suggesting an acute inferior as well as anterior wall myocardial infarction.
tion of sinus rhythm, the electrocardiogram returned to the control pattern. One ventricular extrasystole during sinus rhythm in lead V2 showed the same broad Q wave and elevated S-T segments as had been seen during the tachycardia. The authors considered two possible mechanisms to explain these changes. One was the ischemia which may occur during tachycardia. The other was an abnormal spread of the excitation wave during tachycardia leading to "secondary" elevation of SoT. In our opinion the second mechanism is favored by the appearance of the myocardial infarction pattern in the extrasystole during sinus rhythm. The unmasking of an old jnfarction not recognized during sinus rhythm in the electrocardiogram of a single ventricular extrasystole is a wellknown and common phenomenon. One should expect that it also occurs in every beat during a paroxysmal tachycardia. Even in a supraventricular tachycardia aberrant ventricular conduction may lead to the same phenomenon. We cannot, therefore, rule out the possibility that our patient once had a myocardial infarction which was not diagnosed and that the tachycardia only unmasked it. Ischemia, while common in tachycardia, involves chiefly the subendocardial layers of the myocardium and should result in elevation of the SoT segments only in lead aVR, whereas in our observation elevation occurred in leads III and aVF as well. Another factor which may be responsible for a pattern of myocardial infarction is dilatation of the heart. At first, a tachycardia reduces heart size; later it causes dilatation. Myers has observed QR and QS patterns as well as elevated and caved S-T segments in right ventricular hypertrophy and dilatation16 • Thus patterns imitating myocardial infarctions might be encountered during tachycardias inducing dilatation of the heart and especially of the right ventricle.
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THE PRE-EXCITATION SYNDROME
4. Castellanos, A., Balais, M., Lemberg, L., Salhanick, L., and Castellanos, A. Jr.: Double ectopic left atrial rhythms. Dis. Chest. 52: 87, 1967. 5. Comberiati, L.: Due casi di sindrome di Wolff, Parkinson e White in cardiopatia congenita operata. Cuore e Circo!' 39: 169, 1955. 6. Durrer, D., and Ross, J. P.: Epicardial excitation oftbe ventricles in a patient with Wolff-ParkinsonWhite syndrome. Circulation 35: 15, 1967. 7. Grosse-Brockhoff, F., Loogen, F., and Scbaede, A.: Angeborene Herziund Gefaessmissbildungen. In Handbuch Inn. Med., Springer, 1960, 9, Third Part, p. 105. 8. Holzmann, M., and Scherf, D.: Ueber Elektrokardiogramme mit verkuerzter Vorhof-KammerDistanz und positiven P-Zacken. Ztschr. Klin. Med., 121: 404, 1932. 9. Hunter, A., Papp, c., and Parkinson, J.: The syndrome of short P-R interval, apparent bundle branch block, and associated paroxysmal tachycardia. Brit. Heart J. 2: 107, 1940. 10. Hwang, W., and Langendorf, R.: Auriculoventricular nodal escape in the presence of ventricular fibrillation. Circulation 1: 930, 1950. 11. James, T. N.: The connecting pathways between the sinus node and A-V node and between tbe right and left atrium of the human heart. Am. Heart J. 66: 498, 1963. 12. James, T. N.: Morphology of the human atrioventricular node, with remarks pertinent to its electrophysiology. Am. Heart J. 62: 756, 1961. 13. Katz, L. N., and Pick, A.: Clinical Electrocardiography, Part I. The Arrhytbmias. Philadelphia, Lea and Febiger, 1956. 14. Kaufmann, R., and Rothberger, C. J.: Beitraege zur Entstehungsweise extrasystolischer Allorhythmien, 2. Mitteilung, Ztschr. ges. expo Med. 7:
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