Wolff-Parkinson-White syndrome

j. ELECTROCARDIOLOGY; 4 (1) 77-79, 1971

Wolff-Parkinson-White Syndrome* BY DONALD E. LOEW, M.D.t

SUMMARY An unusual case of W-P-W syndrome with paroxysmal rapid atrial fibrillation in association with a Group B pattern is reported. The significance of this arrhythmia and etiology of the mechanism are discussed. INTRODUCTION I n a recent review of the W-P-W syndrome, no difference was found to exist in the incidence of atrial arrhythmias associated with Group A and Group B ventricular pre-excitation, but atrial flutter and fibrillation were seen only in Group A patients 1. The purpose of this report is to describe a patient with W-P-W syndrome Group B who had prolonged episodes of atrial fibrillation at a ventrlcular rate up to 300 beats/min. No previous report of the ~/2P-W syndrome Group B associated with atrial fibrillation has been encountered. CASE R E P O R T D. C., BCH:~2111485, a 31-year-old laborer arrived at the Accident Floor of the Boston City Hospital complaining of three days of recurrent precordial palpitations that were incapacitating him. H e noted associated dull chest pain of a pressing quality and also nausea, shortness of breath and diaphoresis. He related that since age 13 he had recurrent episodes of palpitations, and that at age 16 he was hospitalized for a syncopal episode and was told that he had a "short circuit in his heart." Since age 16, he had about six

*From the Thorndike Memorial Laboratory, Harvard Medical Unit, Boston City Hospital, and the Department of Medicine, Harvard Medical Schoo!, Boston, Massachusetts. "~Research Fellow, Deparment of Medicine, Harvard Medical School. This work was supported by Grants HE 5244 and HE 10539 from the National Heart Institute, National Institutes of Health, U. S. Public Health Service. Reprint requests: Donald E. Loew, M.D., Thorndike Memorial Laboratory, Boston City Hospital, 818 Harrison Avenue, Boston, Massachusetts 02118.

visits to hospital emergency rooms when the attacks became prolonged, but never had been told of having had a myocardial infarction. H e did not recall having intravenous medication or electrical cardioversion in t h e past admissions. Two years previously he had a testicular teratocarcinoma excised, and there was no evidence of recurrence. T h e r e was no family history of palpitation or heart disease. He had previously been confined at a state prison, and he had been treated at several hospitals and clinics for alcoholism. The physical examination at the time of admission revealed a thin, alert, anxious male complaining of dull chest discomfort with oral temperature 98.6~ b l o o d pressure 120/70, pulse 140-180/min. at the apex and slightly irregular. There was no distension of the veins at 30 ~, the thyroid was not enlarged. The chest was clear and the heart was not enlarged to percussion. No murmurs or thrills were present, and $1 was normal. The abdomen had a healed lower abdominal midline scar with no masses or organomegaly. T h e left testicle was absent and no masses or adenopathy were present. Neurological exam was normal. An electrocardiogram rhythm strip in the emergency room showed atrial fibrillation (ventricular rate 160/min.), with short runs lasting up to one second of ventrieular activity at 300/min. which resembled ventricular tachycardia (Fig. 1. A and B). Because of his clinical history, W-P-W syndrome was strongly suspected. He received no specific therapy. After about 20 minutes the diagnosis was confirmed when he spontaneously reverted to normal sinus rhythm at 76/rain. showing W-P-W syndrome (Fig. 1. C). Before he was to be discharged from the Accident Floor, the rapid atrial fibrillation recurred with chest discomfort,~=and the blood pressure gradually fell to 90/70. The patient was therefore admitted to the hospital, where sedation (Nembutal 100 mg p.o.) and quinidine sulfate (400 mg p.o.) were administered. After two hours of persistent rapid atrial fibrillation not. responding to the latter medications, procaine amide 100 mg I.V. was given with conversion to normal sinus rhythm in about 15 minutes. T h e blood pressure increased and repeated cardiac auscultation 77

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Fig. 1. A and B: Electrocardiogram, continuous lead 2 rhythm strip, showing paroxysmal atrial fibrillation with ventricular rate up to 300 beats/rain. Note "concertina effect" prormnent in beats marked with arrows--progressive lengthening of the R-R interval, decrease in height and duration of the delta wave, and narrowing of the QRS complex. C: Electrocardiogram lead 2 rhythm strip taken on Accident Floor showing W-P-W syndrome characteristics.

nature of this patient's recurring symptoms, his description of a "short circuit" in his heart, and his young age, made the initial clinical suspicion of the W-P-W syndrome relatively simple. This was subsequently confirmed when his rapid atrial fibrillation converted transiently to normal sinus rhythm revealing a Group B pattern (rS in V1-V2) with short DISCUSSION PR interval (0.11 sec) and delta wave In W-P-W syndrome Group A, the prema- ( Q R S ~ 0 . 1 4 sec) characteristic of anomalous ture activation probably occurs in the left atrioventricular excitation (Fig. 2). In the ventricle, causing the premature component absence of the above clinical findings, diag(delta wave) and remainder of the QRS nosis and treatment might have been more complex to be primarily upright in both right difficultlz,ls't4. One could have erroneously and left precordial leads (V1 shows R, RS, interpreted the slightly irregular rapid venRs, RSr, or Rsr patterns and Ve shows Rs or tricular rate (up to 300/min) as ventricular R patterns). In Group B, on the other hand, tachycardia6,7,s,g and thereby possibly exposed the right precordial leads show the premature the patient to greater hazard by aggressive component and remainder of the QRS com- emergency attempts at cardioversion by medplex to be primarily negative (V1--rS or QS), ical or electrical measures. Such an approach and the left precordial leads show delta waves perhaps would have been justified if one had excluded rapid atrial fibrillation in W-P-W and tall R waves. There is no theoretical reason why Group syndrome by the Group B pattern noted on B pattern could not be associated with the electrocardiogram, since this association paroxysmal atrial fibrillation. It has been pro- has never been reported. Although ventricposed that reentry of an atrial impulse from ular tachycardia with W-P-W syndrome has the ventricle through an accessory pathway been reported occasionally in the literaarriving at the relative refractory or vulner- ture6,r, s,9, WolfP ,1~ and Chung et al.1 have able period of atrial repolarization would considered the evidence equivocal and state cause the onset of atrial flutter or fibrilla- that the probable diagnosis was rapid atrial fibrillation or/'lt~ter with anomalous conduction3,4. The clinical history of the longstanding tion associated with Group A. Chung et al. ~

was unremarkable. He thereafter remained stable for 12 hours and was discharged against medical advice on quinidine sulfate 400 mg p.o. every six hours. When in the Outpatient Clinic four days later, he was asymptomatic.

J.

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WOL FF- PARK INSON - WHITE SYND ROME

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Fig. 2. Standard 12 lead electrocardiogram showing W-P-W characteristics and Group B pattern best seen in lead V v present evidence of such a b n o r m a l conduction in G r o u p A with aberration of Q R S complex in atrial fibrillation resembling ventricular tachycardia. M a r r i o t et al. 11, critically discuss the issues of ventricular tachycardia in W - P - W syndrome a n d present a rare example of probable ventricular tachycardia in a patient with W - P - W syndrome a n d a n acute myocardial infarction. I n the treatment of atrial fibrillation associated with W - P - W syndrome, the use of digitalis is probably contra-indicated due to the evidence that digitalis increases the excitability of the anomalous conduction pathway a n d consequently fails to slow the rapid ventricular rate in atrial fibrillation or ftutterlE H e j t m a n c i k a n d H e r r m a n n 2 had success with intravenous injections of procaine amide. Acknowledgement: The author is indebted to Dr. W. H. Abelmann and Dr. B. J. Polansky for their criticism, and to Mrs. D. Powell for her secretarial assistance. REFERENCES 1. Chung, K., Walsh, T. J., and Massie, E.: Wolff-Parkinson-White Syndrome. Am. Heart J. 69:116, 1965. 2. Hejtmancik, M. T., and Hermann, G. R.: The electrocardiographic syndrome of short P-R interval and broad QRS complexes: A clinical study of 80 cases: Am. Heart J: 54:708, 1957. 3. Hecht, H. H., Kennamer, R., Prinzmetal, M., Rosenbaum, F. F., Sodi-Pallares, D., Wolff, L., Brooks, C., Pick, A., Rijlant, P., and Robb, J. S.: Anomalous atrioventricular excitation, panel discussion, Ann. N. Y. Acad. Sci. 65:826, 1956. 4. Wolff, L.: Anomalous atrioventricular excitation (Wolff-Parkinson-White Syndrome) CircJ, E L E C T R O C A R D I O L O G Y , . V O L .

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ulation 19:14, 1959. 5. Langendorf, R., Lev, M., and Pick, A.: Auricular fibrillation with anomalous A-V excitation (WPW syndrome) initiating ventricular paroxysmal tachycardia. A case report with clinical and autopsy findings and critical review of the literature. Acta Cardiol. 7:241, 1952. 6. Levine, S. A., and Beeson, P. B.: The WolffParkinson-White syndrome with paroxysms of ventricular tachycardia. Am. Heart J. 22:401, 1941. 7. Missal, M. E., Wood, D. J., and Leo, S. D.: Paroxysmal ventricular tachycardia associated with short P-R intervals and prolonged QRS complexes. Ann. Int. Med. 24:911, 1946. 8. Klainer, M. J., and Jaffe, H. H.: A case of short P-R interval and prolonged QRS complexes with a paroxysm of ventricular tachycardia. Ann. Int. Med. 24:920, 1946. 9. Langendorf, R.: Auricular fibrillation with anomalous conduction (WPW syndrome) initiating ventricular paroxysmal tachycardia. Am. Heart J. 37:645, 1949. 10. Wolff, L.: Syndrome of short P-R interval with abnormal QRS complexes and paroxysmal tachycardia (WPW syndrome). Circulation 10:282, 1954. 11. Marriott, H. J., and Rodgers, H. M.: Mimics of ventricular tachycardia associated with the WPW syndrome. J. Electrocardiol. 2:77, 1969. 12. Eichert, H. : Wolff-Parkinson-White syndrome simulating myocardial infarction. Ann. Int. Med. 21:907, 1944. 13. Gazes, P. D. : False-positive exercise test in the presence of the Wolff-Parkinson-White syndrome. Am. Heart J. 78:13, 1969. 14. Lamb, L. E.: Multiple variations of WPW conduction in one subject: Intermittent normal conduction and a false positive exercise tolerance test. Am. J. Cardiol. 4:346, 1959. 15. Fox, T. T., Travell, J., and Molorsky, L.: Action of digitalis on conduction in the syndrome of short P-R interval and prolonged QRS complex. Arch. Int. Med. 71:206, 1943. 16. Kaplan, M. A., and Cohen, K. L. : Ventricular fibrillation in the Wolff-Parkinson-White syndrome. Am. J. Cardiol. 24:259, 1959.