J. ELECTROCARDIOLOGY, 8 (4) 343-349

Case Studies:

Refractory Paroxysmal Supraventricular Tachycardia Incited By Multiple Mechanisms* BY PAUL WALTER, M.D. AND LAURENCE LESSER, M.D.

SUMMARY

A patient with refractory paroxysmal supraventricular tachycardia post acute myocardial infarction is presented. His bundle recordings and atrial stimulation studies suggest atrioventricular nodal reentry precipitated by three different mechanisms. Therapy required permanent coronary vein pacing and drugs.

Recent studies in man suggest that atriov e n t r i c u l a r nodal r e e n t r y is a common mechanism for paroxysmal supraventricular t a c h y c a r d i a . 1-5 G o l d r e y e r and D a m a t o 2 d e m o n s t r a t e d t h a t atrioventricular nodal conduction delay was essential for inducing supraventricular tachycardia. This delay, triggering supraventricular tachycardia, has been initiated by atrial premature beats falling within a specific portion of the relative r e f r a c t o r y period of the a t r i o v e n t r i c u l a r node. 1'2'4'8 Conduction delay and supraventricular tachycardia have also been shown after a t r i o v e n t r i c u l a r nodal Wenckebach cycles.~a Similarly, supraventricular tachycardia has been initiated by sinus beats with prolonged atrioventricular nodal conduction due to retrograde concealed conduction.5 In this report we describe a patient in whom refractory paroxysmal supraventric-

*From the Division of Cardiology, Department of Medicine, Emory University School of Medicine, and the Atlanta Veterans Administration Hospital, Decatur, Georgia. Reprint requests to: Paul Walter, M.D., Cardiology Department, VA Hospital (Atlanta), 1670 Clairmont Road, Decatur, GA 30033. 343

u l a r t a c h y c a r d i a was i n i t i a t e d by t h r e e different events: p r e m a t u r e atrial beats, atrioventricular nodal Wenckebach cycles and premature ventricular beats. His bundle recordings and atrial stimulation studies suggest that the supraventricular tachycardia was sustained by atrioventricular nodal reentry. Permanent left atrial pacing from the coronary vein in conjunction with drug therapy was required to control the tachycardia. CASE REPORT A 53 year old man was admitted to the hospital following two hours of substernal chest pain. He had no history of palpitations or tachycardia, and was not t a k i n g cardiac medications. T h e physical examination revealed a blood pressure of 130/70 mm Hg. An atrial gallop was palpable and audible at the cardiac apex. The electrocardiogram (ECG) showed changes of an acute anterolateral myocardial infarction. The chest x-ray, serum electrolytes and BUN were within normal limits. On the third hospital day, still taking no cardiac drugs, the patient experienced his first episode of supraventriculartachycardia. Extension of the anterolateral myocardial infarction occurred on the ninth hospital day (Fig. 1). A single episode of v e n t r i c u l a r fibrillation was successfully treated with direct current countershock. Following extension of the infarction, left ventricular dysf u n c t i o n was m a n i f e s t e d by a t r i a l and v e n t r i c u l a r gallops and mild interstitial pulmonary edema on chest x-ray. During the patient's first seven weeks of hospitalization, supraventricular tachycardia was an almost daily occurrence. Fifty-five episodes of tachycardia were documented by ECG, and additional episodes were observed but not recorded. Supraventricular tachycardia was most commonly initiated by a

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were stopped. D i p h e n y l h y d a n t o i n (900 mg followed by 400 mg/day), a drug t h a t may enhance atrioventricular nodal conduction in man, ~~ was then given, but tachycardia was not abolished. Since the mechanism of the supraventricular tachycardia was difficult to determine from t h e s t a n d a r d E C G , His b u n d l e recordings with atrial stimulation studies were done on the 28th hospital day. A signed consent for this study was obtained from the patient. Diphenylhydantoin (100 rag) had been

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premature atrial beat (Fig. 2A). Occasionally, normal sinus rhythm, atrial tachycardia (Fig. 2B), or left atrial pacing produced an atypical atrioventricular nodal Wenckebach sequence and incited supraventricular tachycardia. On four occasions, two consecutive p r e m a t u r e ventricular beats followed by a sinus beat or a premature atrial beat initiated 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 (Fig. 2C). Single ventricular premature beats did not produce the tachycardia. A l t h o u g h the h e a r t r a t e d u r i n g supraventricular tachycardia was relatively slow (95-130 beats/min), prolonged runs of tachycardia were complicated by systemic arterial hypotension, ischemic chest pain, or, rarely, electrocardiographic changes of additional anterior epicardial injury. Tachycardia could usually be terminated by carotid sinus massage or by carotid sinus massage following elevation of the systolic blood pressure to 110-120 mm Hg. On one occasion, synchronous direct current cardioversion was needed to restore sinus rhythm. Attempts to prevent the p a r o x y s m s of s u p r a v e n t r i c u l a r tachycardia by abolishing the p r e m a t u r e a t r i a l beats with quinidine sulfate failed. When slowing of atrioventricular nodal conduction with digoxin and propranolol failed, all drugs

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Fig. 2. ECG rhythm strips with diagrams demonstrating postulated modes of onset of spontaneous supraventricular tachycardia. The P wave, preceding each onset of supraventricular tachycardia, is conducted with marked atrioventricular nodal delay. A. Premature atrial beat deforms the T wave. B. Atypical Wenckebach sequence showing greatest increment in the last beat of a run of atrial tachycardia. C. Concealed conduction into the atrioventricular node from two successive premature ventricular beats. The P wave that deforms the ST segment of the second ventricular beat is probably a premature atrial beat. It is not a retrograde P wave because the RP interval (0.15 sec) is shorter than the PR interval (0.18 sec),7 and the RP interval is too short for the occurrence of a ventricular echo.s MCL 1 -- modified CL s, MCL 6 -- modified CI~ s. J. ELECTROCARDIOLOGY. VOL. 8. NO. 4. 1975

MECHANISMS INCITING TACHYCARDIA

given 16 hours prior to study. Under local anesthesia, a tripolar catheter was introduced percutaneously into the right femoral vein and fluoroscopically positioned across the tricuspid valve. A bipolar pacing catheter was introduced by a right median basilic vein cutdown and positioned in the high right atrium. His bundle electrograms were obtained by the method of Scherlag et al, 11 and recorded on an Electronics for Medicine Recorder. Frequencies above 500 and below 40 Hz were filtered. Electrocardiographic leads I, II, and III, and the His bundle electrograms were recorded at a paper speed of 100 mm/sec. A battery-powered coupled pulse generator (Medtronics 5837) was used to couple premat u r e a t r i a l s t i m u l i to the p a t i e n t ' s spontaneous sinus beats and to introduce progressively more premature atrial beats. The stimulus pulse was 2 msec in duration and approximately twice diastolic threshold intensity. The A-H interval is the interval from the onset of low atrial depolarization to the onset of His bundle depolarization as recorded on the His bundle electrogram tracing. The H-V interval is the interval from the onset of the His bundle deflection to the onset of the QRS as recorded from the surface ECG. A1A2 is the interval between an atrial depolarization of sinus origin (A~) and a stimulated atrial premature beat (A2). HlI-h is the interval between the His bundle depolarization of the sinus and t h e atrial p r e m a t u r e beat. A2-I-h is the A-H interval of the stimulated atrial premature beat. As the A~-A2 interval was progressively shortened from 740 msec to 430 msec, the A2-I-h interval increased from 80 to 175 msec. At an A1-A2 interval of 395 msec, the A2-I-I2 interval increased markedly to 455 msec. Two episodes 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 , identical to those observed to arise spontaneously, were induced during p r e m a t u r e atrial stimulation (Fig. 3). These episodes of supraventricular tachycardia occurred when the A2-I-I2 intervals of the coupled b e a t s were 455 and 485 msec. Properly timed premature atrial impulses that did not terminate the t a c h y c a r d i a were conducted with a longer A-H interval and shortened the following R-R interval (Fig. 4A). Stimuli introduced in the atrial cycle abolished the tachycardia (Fig. 4B). Following the intracavitary studies, drug therapy was given a further trial. However, supraventricular tachycardia was not suppressed and drug toxicity occurred. Quinidine sulfate (2.4 gms/day) resulted in QRS complex widening which subsided when the dosage was reduced. The occurrence of sinoatrial Wenckebach suggested digitalis intoxication, substantiated by a plasma digoxin level of 4.3 J. ELECTROCARDIOLOGY, VOk. 8, NO. 4, 1975

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ng/m/. The only discernible effect of propranalol (160 mg/day) was a slower heart rate during supraventricular tachycardia. Since atrioventricular nodal Wenckebach sequences became a more frequent inciting mechanism of supraventricular tachycardia, it is possible that the digoxin and propranalol increased the episodes of tachycardia. Therefore, all drugs were discontinued for 1 week, but paroxysms of supraventricular tachycardia continued at least once a day. On the 48th hospital day, a bipolar transvenous pacing c a t h e t e r was placed in the coronary vein for left atrial pacing. A con-

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vein. LefL atrial pacing was obtained at a t h r e s h o l d of 3 ma. The c a t h e t e r was c o n nected to a power unit firing asynchronously at a rate of 81/min (Medtronic 5910). Propranalol (40 mg/day) and digoxin (0.125 rag/ day) were continued after hospital discharge. During the subsequent eight months, the patient has not experienced episodes of dizziness, weakness, or prolonged ischemic chest pain. Standard ECGs and a 24 hour Holter m o n i t o r tape have d o c u m e n t e d n u m e r o u s brief runs of supraventricular tachycardia, but the tachycardia has always been terminated within 30 sec by the pacemaker (Fig. 5B).

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tinuous pacing stimulus of 3 ma was delivered at a rate of 80/min using a Medtronic 5880A external pulse generator. Asynchronous pacing was selected because the patient was not always aware of his tachycardia until ischemic chest pain or generalized weakness occurred. Propranolol (40 mg/day) was given to slow the sinus node firing rate and thereby decrease competition between the sinus node and the atrial pacemaker. During the trial period of seven days, paroxysms of supraventricular tachycardia continued, but random pacemaker firing terminated the tachycardia within one minute of onset (Fig. 5A). Therefore, under local anesthesia a permanent bipolar pacing catheter (Medtronic 5810) was inserted into the coronary

DISCUSSION Studies in man 2 and in the isolated rabbit atrioventricular node preparation 12-14 show that supraventricular tachycardia can result from atrial reentry via the atrioventricular node. This mechanism appears to be responsible for supraventricular tachycardia in our patient. The tachycardia could be induced and terminated by premature atrial s t i m u l a t i o n } '2'~5'16 The p r e m a t u r e atrial beats that initiated tachycardia reached the a t r i o v e n t r i c u l a r node d u r i n g its r e l a t i v e refractory period and were conducted with marked delay, reflected in long A-H times. During supraventricular tachycardia atrial beats introduced late in the atrial cycle produced a variable amount of prematurity of the subsequent cycle length but did not terminate the tachycardia. A somewhat earlier atrial beat abolished the tachycardia, presumably b e c a u s e it e n c o u n t e r e d p a r t i a l l y or completely refractory tissue in the a n t e g r a d e pathway. 1~5 Although spontaneous supraventricular tachycardia did not occur during the time of intracavitary studies, episodes of tachycardia induced by atrial stimulation were identical to t h o s e o c c u r r i n g s p o n t a n e o u s l y . It is reasonable to assume that the same mechanism was responsible for the spontaneous arrhythmia. Stimulated atrial premature beats or atrial pacing at rates sufficient to produce atriov e n t r i c u l a r nodal Wenckebach cycles m a y initiate tachycardia in patients with paroxysmal supraventricular tachycardia. ~ 7 Multiple inciting mechanisms occurring spontaneously in a single patient have, to our knowledge, not been described. In our patient, supraventricular tachycardia was initiated by atrial premature beats, atrioventricular nodal Wenckebach cycles, and two successive premature ventricular beats. In all instances J. E L E C T R O C A R D I O L O G Y .

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MECHANISMS INCITING TACHYCARDIA

a m i n i m u m interval of 0.50 sec separated the premature atrial beats, the last P wave of a Wenckebach cycle, or the P wave following two v e n t r i c u l a r beats, from the onset of tachycardia. This is in accord with the finding of Goldreyer and Damato ~ t h a t the required prolongation of atrioventricular nodal conduction was nearly identical whether suprav e n t r i c u l a r t a c h y c a r d i a was produced by premature atrial beats or an atrioventricular nodal Wenckebach cycle. The initiation of supraventricular tachycardia in our patient by two successive p r e m a t u r e v e n t r i c u l a r beats is probably due to concealed retrograde conduction into the a t r i o v e n t r i c u l a r node. Therefore the following atrial beat would encounter sufficient atrioventricular nodal conduction delay to permit reentry.

347

It is known t h a t p r e m a t u r e v e n t r i c u l a r beats m a y prolong a t r i o v e n t r i c u l a r nodal conduction of the following sinus beat if the premature ventricular beats are interpolated or if there are two successive v e n t r i c u l a r beats. ~s Single premature ventricular beats do not lead to this prolongation. ~s What is common to all the inciting mechanism found in this p a t i e n t is the production of atrioventricular nodal conductive delay, providing the conditions necessary for supraventricular tachycardia. Microelectrode studies in the isolated rabbit h e a r t demonstrate t h a t the upper part of the atrioventricular node can be functionally dissociated into two pathways. ~=~a The presence of dual atrioventricular nodal pathways in m a n has been suggested by the finding of

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Fig. 5A. Temporary coronary vein pacemaker firing asynchronously at 81 beats/min. The third pacing stimulus (S) captures the atrium and terminates the tachycardia. B. Permanent coronary vein pacemaker with asynchronously discharge at 83 beats/min. Pacemaker artifacts are not well seen in the reproduction and are therefore each indicated by S. Negative P waves are produced by pacemaker capture. The second pacemaker stimulus (S) is conducted with marked atrioventricular nodal delay and induces tachycardia for two subsequent beats. The fourth pacemaker stimulus abolishes the tachycardia. J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975

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