Paroxysmal Supraventricular Tachycardia: An Electrophysiologic Approach *







The techniques of intracardiac recording and programmed stimulation have greatly expanded understanding of the mechanisms of supraventricular tachycardia and have resulted in a reclassification of these arrhythmias based on their electrophysiologic mechanism. Although several mechanisms of supraventricular tachycardia exist, the incidence and clinical features of each have not previously been evaluated systematically. The paper by Wu et al.1 in this issue of the Journal is the first attempt to classify the electrophysiologic and clinical features of a large group of patients with paroxysmal supraventricular tachycardia without manifest anterograde preexcitation. As expected, reentry was the mechanism of supraventricular tachycardia in the vast majority of patients. Reentry could be localized to several sites including the sinus node, atrium, atrioventricular (A-V) node or a macroreentrant circuit involving the normal A-V conducting system in anterograde manner and a concealed A-V bypass tract in retrograde manner. As suggested in recent reviews,2*3 Wu et al.l noted that the most common mechanism (69 percent) of supraventricular tachycardia was A-V nodal reentry. Significantly, the second most common cause (15 percent) was A-V reentry utilizing a concealed A-V bypass tract. In one patient with a

From the Electrophyslology Laboratory, Hospital of the University of Pennsylvania, and the Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104. Manuscript received November 29, 1977, accepted January 4, 1978. Address for reprints: Mark E. Josephson, MD, 666 White Building, Hospital of the Univetslty of Pennsylvania, 3400 Spruce Street, Phlladelphia, Pennsylvania 19104.

concealed bypass tract, atria1 stimulation from the coronary sinus, near the atria1 insertion of the bypass tract, revealed that the bypass tract was able to function in an anterograde direction. Previous authors4f5 have also recognized that A-V bypass tracts may not be evident in the surface electrocardiogram because of delayed or inadequate input into the bypass tract. In a comparable group of 60 consecutive patients with supraventricular tachycardia and absence of anterograde preexcitation, we found a similar frequency of the cause of tachycardia: 66 percent had A-V nodal reentry and 20 percent had concealed A-V bypass tracts (unpublished observations). Two of the 12 patients with concealed bypass tracts manifested anterograde preexcitation during pacing from the coronary sinus. Thus, bypass tracts, clinically inapparent in the surface electrocardiogram, commonly form‘the retrograde limb of a reentrant circuit during supraventricular tachycardia and on occasion may be capable of anterograde conduction. The electrophysiologic criteria used to establish the mechanisms of supraventricular tachycardia in the laboratory in&de: (1) mode of initiation of the tachycardia, with particular attention to the requisite site of conduction delay because slow conduction is a hallmark of the reentrant circuit; (2) atria1 activation sequence and P wave contour during the tachycardia; (3) requirement of the atria or ventricles, or both, to initiate and sustain the tachycardia; (4) effect of bundle branch block on the tachycardia; (5) the effects of pharmacologic or physiologic maneuvers, or both, during the tachycardia; and (6) the effect of electrical stimulation during the tachycardia. Of these six observations only the last is inaccessible to the clinician.

Editorials published by the Journal reflect the views of the authors and do not necessarily represent the views of the Journal or of the American College of Cardiology l

May 22,1978

The American Journal of CARDIOLOGY

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Many of the remaining observations are available from the surface electrocardiogram and can be used by the clinician to characterize the tachycardia. Although analysis of the surface electrocardiogram cannot provide as detailed and specific data as those obtained in the electrophysiology laboratory, a substantial amount of diagnostically important information is obtainable. Observations at the Onset of the Tachycardia If the clinician is fortunate enough to observe the onset of the tachycardia several important observations can be made. If the tachycardia is initiated (or, for that matter, terminated) by an early atria1 or ventricular premature depolarization, reentry is the likely mechanism. Recent evidence has shown that under specific experimental conditions tachyarrhythmias can result when premature stimuli cause oscillatory afterpotentials to reach threshold.6 These arrhythmias do not require conduction delay. However, the role of such “triggered automaticity” in tachycardia in man has not been established. Thus, if one can demonstrate that the initiation of the tachycardia by an atria1 premature depolarization depends on achieving a critical degree of P-R prolongation, then the reentry must involve the A-V conducting system because this is the site of the conduction delay. This finding suggests that the mechanism of the tachycardia is either A-V nodal reentry or A-V reentry involving a concealed bypass tract. Neither sinus nodal reentry, intraatrial reentry nor automatic atria1 tachycardia requires A-V delay for its initiation. Analysis of the P wave configuration of the initial and subsequent beats of the tachycardia is also useful. If the P wave of the initiating atrial premature depolarization is identical to subsequent P waves during the tachycardia, automatic atrial tachycardia is likely.7s In most cases of reentrant supraventricular tachycardia, the initiating atrial premature depolarization will not come from the same area that is depolarized by the impulse as it activates the atria after exiting the reentrant circuit. Finally, if an atria1 premature depolarization initiates the tachycardia and the first atrial complex of the tachycardia is not conducted, then reentry utilizing a concealed bypass tract is ruled out and A-V nodal reentry becomes an extremely unlikely possibility. The basis for these conclusions is that (1) ventricular depolarization is necessary for the impulse to reach the ventricular insertion of the bypass tract, and (2) it is very difficult for reentry to be sustained in the A-V node in the presence of A-V nodal block. Observations During the Tachycardia Several important clues can be gleaned from the surface electrocardiogram during the tachycardia.

Foremost among these are data obtained from the P wave configuration and the position of the P wave relative to the QRS complex during the tachycardia when the P wave is clearly seen. Thus: 1. Absence of a visible P wave during the tachycardia strongly suggests A-V nodal reentry because it implies simultaneous atria1 and ventricular activation. This


May 22,187s

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relation can occur only if the reentrant circuit is confined within the region of the A-V node. A similar relation can occasionally be noted during an automatic His bundle tachycardia. However this arrhythmia is most often nonparoxysmal and related to specific events such as digitalis toxicity, myocardial infarction or open heart surgery. The presence of a bypass tract functioning in retrograde manner is excluded because ventricular depolarization must activate the retrograde limb of the circuit (bypass tract) before the retrograde P wave can appear; thus, atria1 and ventricular activation cannot be simultaneous9 2. Inverted (retrograde) P waves in the inferior leads with an R-P interval less than one half the R-R interval are found in either A-V nodal reentrant supraventricular tachycardia (approximately 3Q percent of patients with A-V nodal reentry) or reentry utilizing a concealed bypass tract (100 percent of these patients will demonstrate this pattern).l 3. Patients with retrograde P waves and long R-P intervals (R-P interval greater than one half the R-R interval) usually have an atypical, and often incessant, form of A-V nodal reentry.lOJl 4. Patients with a P-R interval appropriate for the rate of tachycardia have either sinus nodal reentry, if the P wave is identical to the sinus P wave, or atria1 tachycardia (automatic or reentrant), if the P wave is different from the sinus wave but not retrograde.1~2~3~7 In our patients with supraventricular tachycardia we found a greater incidence of concealed bypass tracts than that reported by Wu et a1.l Approximately 50 percent of our patients with retrograde P waves and a short R-P interval during the tachycardia had concealed bypass tracts (unpublished observations). We have found the P wave configuration in lead I during the tachycardia helpful in analyzing the mechanism of the arrhythmia. We have found that a negative P wave in lead I, if discernible, is diagnostic of a left-sided bypass tract as confirmed with atrial mapping. Because the vast majority of patients with a concealed bypass tract have left-sided A-V connections, including all of Wu’s patients and ours, a negative P wave in lead I assumes major diagnostic significance. The relation of P waves to the QRS complex during the tachycardia provides another valuable diagnostic clue. In patients with concealed extranodal bypass

tracts A-V block or A-V dissociation is impossible, and the presence of either rules out a concealed bypass tract because both the atria and ventricles are requisite components of the reentrant circuit. The presence of A-V dissociation with an atria1 rate slower than the junctional rate has been reported with A-V nodal reentry12Js but is most commonly observed with nonparoxysmal junctional tachycardia. Sinus nodal reentry, automatic atria1 tachycardia and intraatrial reentrant tachycardia may all exist in the presence of A-V block because neither the A-V node nor the distal conducting system is part of the reentrant circuit. On the other hand, A-V block is extremely uncommon in patients with A-V nodal reentry although a few cases of the lat-

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ter, predominantly ported.gJ3

with infra-His block, have been re-

Functional bundle branch block is quite uncommon in supraventricular tachycardia except in tachycardias using a concealed bypass tract. As Wu et a1.l noted, it is only in patients with the latter condition that the initiating atria1 premature depolarization encroaches on His-Purkinje refractoriness resulting in bundle branch block. Bundle branch block is much less common in the presence of A-V nodal reentry because initiation of the tachycardia usually occurs during anterograde slow pathway conduction and thus the critical HI-HZ interval defining His-Purkinje refractoriness is not reached at the initiation of the tachycardia. We too have noted a similar large incidence of bundle branch block during tachycardias utilizing a concealed bypass tract. In our experience, aberration of the left bundle branch block type during supraventricular tachycardia has, with a single exception, occurred in patients with bypass tracts. If both normal and aberrant conduction are observed in the same recording, a change in the cycle length of

the tachycardia and R-P interval with the development of bundle branch block provides a diagnostic clue to the mechanism of the tachycardia. When supraventricular tachycardia utilizes a concealed bypass tract, bundle branch block ipsilateral to the side of the tract will prolong the cycle length of the tachycardia as a result of prolonged ventriculoatrial conduction time.r4 This occurs because the impulse must travel over the contralateral bundle branch, then through the contralateral ventricular muscle to the ventricular insertion of the bypass tract in the blocked ventricle. This produces a larger reentrant circuit and slower conduction within that circuit. Pharmacologic and physiologic maneuvers can also be useful in determining the mechanism of the tachycardia. For example, the production of A-V block by carotid sinus pressure or other vagomimetic maneuvers with persistence of the tachycardia rules out the participation of the concealed bypass tract and makes A-V nodal reentry most unlikely. On the other hand, abrupt termination of a tachycardia by these maneuvers suggests that either the sinus node or the A-V node is involved; thus, one should consider a possible diagnosis of sinoatrial nodal reentry, A-V nodal reentry or A-V reentry utilizing a concealed bypass tract. As discussed, the P wave contour and its relation to the QRS complex during the tachycardia can help distinguish the former from the latter two mechanisms. Therapeutic Implications of the Electrophysiologic Study In patients with recurrent paroxysmal supraventricular tachycardia the electrophysiologic studies can provide major clinical benefits. Aside from establishing the mechanism of the tachycardia, such studies can aid in determining appropriate therapy.i5J6 Treatment of recurrent supraventricular tachycardia is often frustrating; multiple antiarrhythmic agents are often tried alone or in combination with a variable degree of both

success and intolerable side effects. The ability to initiate and terminate predictably an arrhythmia provides the electrophysiologist with an objective means of assessing drug efficacy. The methodology of such studies can be summarized briefly. After demonstrating that the tachycardia can

be reproducibly initiated and terminated, a temporary electrode pacing catheter is left in the heart, and on sequential days multiple drugs are studied singly and in combination. At the end of this trial a single drug or drug combination that is most effective-that is, one that either prevents initiation or aids termination-is chosen for outpatient management. Thus the physician can choose on an objective basis the drugs most likely to be successful in the treatment of this arrhythmia. Antiarrhythmic

therapy needs to be individualized

because patients with the same arrhythmia mechanism can respond differently to antiarrhythmic agents. This is of particular importance in patients with concealed bypass tracts, especially those in whom anterograde preexcitation can be produced with atria1 pacing. Patients in whom anterograde conduction down the bypass tract can occur are susceptible to life-threatening ventricular responses during atria1 flutter and fibrillation. In these patients digitalis, a drug often utilized successfully for various types of reentrant supraventricular tachycardias, may prove disastrous by producing A-V nodal block and decreasing bypass tract refractoriness, thus facilitating rapid conduction down the bypass tract resulting in ventricular fibrillation.17J8 Patients potentially at risk for this complication can be identified from observations during the tachycardia. As noted in our laboratory and reported by Wu and others,1T4*5*gJ4 all patients with supraventricular tachycardia utilizing concealed bypass tracts have P waves after the QRS complex during the tachycardia. Thus, any patient whose P wave follows the QRS complex during supraventricular tachycardia, particularly when a negative component is noted in lead I, should probably undergo electrophysiologic testing. In addition to determining the efficacy of various antiarrhythmic drugs, electrophysiologic studies can evaluate the potential therapeutic benefits of a pacemaker or surgery in the case of bypass tracts. In patient8 who are refractory to drugs, but in whom atria1 or ventricular stimulation, or both, can terminate the tachycardia, permanent pacemakers, either atria1 or ventricular, have been employed to terminate the arrhythmia on demand by the patient.4J2Jgy20 The arrhythmia is terminated when an appropriately timed impulse penetrates the reentrant circuit resulting in a collision of circulating wavefronts. Who should undergo electrophysiologic study? Many electrophysiologists believe that patients with frequent recurrent episodes of paroxysmal supraventricular tachycardia, particularly those most likely to have concealed bypass tracts, should be evaluated with electrophysiologic studies. Such studies could avoid multiple readmissions or emergency room visits resulting from unsuccessful therapy. Furthermore, the ability to diagnose a free wall bypass tract through ex-

May 22, 1978

The American Journal of CARDIOLOGY

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tensive electrophysiologic evaluation raises the possibility of surgically curing a disabling or life-threatening arrhythmia.4 Both the extensive electrophysiologic evaluation and surgical therapy for arrhythmias should be done only in the centers that are best equipped and most experienced in these procedures. We have found such electrophysiologic evaluation invaluable in the management of patients referred with “intractable” supraventricular tachycardias. The therapeutic regimens selected on the basis of these studies have yielded rewarding results in 12 of 15 patients followed up for 6 to 15 months (unpublished observations). Conclusion Modern electrophysiologic techniques have permitted differentiatiation of the arrhythmia once called “paroxysmal atria1 tachycardia” into several electro-

physiologically distinct arrhythmias. The rational approach to therapy of an arrhythmia depends on knowledge of the mechanism of the arrhythmia. Certain clinical clues are available to help elucidate these mechanisms. They include P wave contour and the relation of the P wave to the QRS complex of the tachycardia, the presence of bundle branch block and its effect on the tachycardia and the effect of A-V dissociation on the tachycardia. Other clinical data, including the rate of tachycardia, incidence of organic heart disease and age and sex of the patient, are not specific enough to diagnose the mechanism of the arrhythmia, although patients with concealed bypass tracts do seem to be younger, have a lesser incidence of organic heart disease and tend to have faster rates of tachycardia.l It is in patients with recurrent disabling arrhythmias that electrophysiologic studies offer important data for making therapeutic decisions.

References 1. Wu D, Denes P, Amat-y-Leon F, et al: Clinical, eiectrocardiographic and eiectrophysiologic observations in patients with paroxysmal sqraventriculartachycardia. Am J Cardioi 41:1045-1051, 1978 2. Wu D, Denes P: Mechanisms of paroxysmal supraventricular tachycardia. Arch intern Med 135:451-442, 1975 3. Josephson ME, Kastor JA: Supraventricular tachycardta: mechanisms and management. Ann intern Med 87:346-358, 1977 M, Svenscn RH, et al: Woiff-Paddnso+Whiie 4. Gaiiaghar JJ, GiM syndrome-The problem, evaluation, and surgical correction. Circulation 51:767-785, 1975 5. Siama I?, Ceutnai P, Bouvrain Y: Les syndromes de WPW de type A inapparent ou latent en rythme sinusei. Arch Mai Coeur 66: 629-639.1973 6. Wit AL, Cranefieid W: Triggered activity of cardiac muscle fibers of the simian mitral valve. Circ Res 38:85-98, 1976 7. Goidreyer BN, Gaiia&er JJ, Dameto AN: The electrophysioiogic demonstration of atriai ectopic tachycardia in man. Am Heart J 85:205-215, 1973 6. Scheinmen MM, Basu D, Hoiiaobq M: Eiectrophysioiogic studiis in patients with persistent atriai tachycardla. Circulation 50: 266-273.1974 9. Weiiens HJJ, Durrer D: The role of an accessory atrioventricuiar pathway in reciprocal tachycardia. Circulation 52:58-72, 1975 10. Coumei P: Junctional reciprocating tachycardias. The permanent and paroxysmal forms of A-V nodal reciprocating tachycardias. J Electrocardiography 879-90, 1975 11. Wu D, Denes P, Amat-y-Leon F, et al: An unusual variety of atrioventrtcuiar nodal m-entry due to retroqade dual atrioventricuiar nodal pathways. Am J Cardiol 56:50-59. 1977


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The American Journal of CARDiDLDGY

12. Haft JI: Treatment of arrhythmias by intracardiac electrical stimulation. Prog Cardlovasc Dis 16:539-561, 1974 13. Weiiens HJJ, Wesderp X, Duren DR, ef al: second degree block during reciprocal atrioventricular nodal tachycardia. Circulation 53:595-599.1976 14. Pritchett ELC, Tonken AM, Dugan FA, et al: Ventricuioatriai conduction time during reciprocating tachycardia with intermittent bundle-branch block in Wolff-Parkinson-White syndrome. Br Heart J 38:1058-1064.1976 15. Wu D, Wyndham CR, Denes P, et al: Chronic eiectrophysloiogicai study in patients with recurrent paroxysmal tachycardia: a new method for developing successful cral an&rhythmic therapy, chap 2 1. In, Reentrant Arrhythmias (Kuibertus HE, ed). Baltimore, University Park Press, 1977, p 294-311 16 Wu D, Amat-y-Leon F, Simpson Jr RJ, et al: Electrophysiologicai studies with multiple drugs in patients with atrioventricular reentrant tachycardias utilizing an extranodal pathway. Circulation 56:727-736,1977 17 Sellers Jr TD, Bashore TM, Gallagher JJr Digitalis in preexcitation syndrome. Circulation 56260-267, 1977 18. Weiiens HJ, Durrer D: Effect of digitalis on atrioventricular conduction and circus movement tachycardias in patients with the Wolff-Parkinson-White syndrome. Circulation 47:1229-1233, 1973 19. Moss AJ, Rivers Jr RJ: Termination and inhibition of recurrent tachycardias by implanted pervenous pacemakers. Circulation 50:942-947,1974 20. Kahn A, Merris J, Citron P: Patient-initiated rapid atriai pacing to manage supraventricular tachycardla. Am J Cardlol38:200-204, 1976

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Paroxysmal supraventricular tachycardia: an electrophysiologic approach.

EDITORIALS Paroxysmal Supraventricular Tachycardia: An Electrophysiologic Approach * MARK E. JOSEPHSON, IWladelphia, MD, FACC Pennsylvania The...
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