Electrophysiologic characteristics of concealed bypass tracts: Clinical and electrocardiographic correlates

Electrophysiologic Characteristics of Concealed Bypass Tracts: Clinical and Electrocardiographic Correlates

ARDESHIR FARSHIDI, MD MARK E. JOSEPHSON, MD, FACC LEONARD N. HOROWITZ, MD,’ FACC

Philadelphia, Pennsylvania

Twelve of 60 consecutiveiy studied patients undergoing eiectrophysioiogic study for paroxysmal supraventricuiar tachycardia had atrioventricuar (A-V) bypass tracts functioning as the retrograde limb of the reentrant circuit. None had evidence of preexcitation in the surface eiectrocardiogram, but in two patients anterograde preexcitation could be produced by pacing from the coronary sinus. in ail 12 patients with concealed bypass tracts the retrograde atriai activation sequence or effect of left bundle branch block aberration during the tachycardia, or both, confirmed the iefl-sided bypass tract. A negative P wave in lead I during the tachycardia was also diagnostic of a left-sided bypass tract. Dual A-V nodal pathways were found in five patients with concealed bypass tracts but were unrelated to the development of the tachycardia. When compared with supraventrtcuiar tachycardia due to A-V nodal reentry, clinical findings suggestive of a concealed bypass tract included: (1) P wave following the QRS complex (12 of 12 versus 12 of 40), (2) negative P wave in lead I during the tachycardia, and (3) bundle branch block aberration during the tachycardia (8 of 12 versus 3 of 40). Other characteristics of patients with concealed bypass tracts that were of less value in individual cases were shorter cycle lengths of tachycardia, younger patient age and lesser incidence of organic heart disease.

Intracardiac stimulation and recording techniques have led to the recognition that bypass tracts functionally silent during sinus rhythm, and therefore clinically unsuspected, are frequently responsible for cases of supraventricular tachycardia.i-l2 Recently several series of patients with supraventricular tachycardia utilizing such concealed bypass tracts have been describede-ls; however, the clinical setting and electrocardiographic correlates have not been emphasized. Material and Methods From the Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. This work was supported In part by grants from the American Heart Association, Southeastern Pennsylvanla Chapter, Philadelphia, Pennsylvania and by Grant HL 14807 from the National Institutes of Health, Bethesda, Maryland. Manuscript received November 28,1977; revised manuscript received February 8, 1978, accepted February 8, 1978. Address for reprints: Mark E. Josephson, MD, 668 White Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104. Recipient of Career Development lnvestigatorship, American Heart Association, Southeastern Pennsylvania Chapter. l

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Sixty patients with paroxysmal supraventricular tachycardia underwent electrophysiologic evaluation between January 1972 and August 1977. Patients were studied in the nonsedated postabsorptive state after informed consent was obtained. Antiarrhythmic drugs were withheld for 24 hours before each study. Standard electrode catheters (1 cm interelectrode distance) were inserted percutaneously through femoral or antecubital veins, or both, and advanced under fluoroscopic control to positions in the right atrium, atrioventricular (A-V) junction to obtain a His bundle electrogram, right ventricle and, in 49 cases, the coronary sinus. When stimulation and recording were required from the same catheter a quadripolar electrode catheter was utilized with the proximal pair of electrodes used for recording and the distal pair of electrodes for stimulation. Stimulation was performed with a constant current source. Multiple intracardiac electrograms were simultaneously displayed with two or three surface electrocardiograms on a switch beam oscilloscope (Electronics for Medicine DR 16) and recorded on magnetic tape (Honeywell 56OOC). Subsequently data were retrieved on photographic paper at speeds of 100 to 400 mm/set.

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Case no.

Data

A@‘(Y)

!

60 M 39 M 35 F 60 F 70 M 65 M 58 M 17F 62 M

10 11 12

63 F 25 M 18F

: 3 4 6 7

TRACTS-FARSHIDI

ET AL

complex; (4) similar V-A intervals during the tachycardia and ventricular pacing at the same rate of the tachycardia; (5) prolongation of the cycle length and V-A conduction time during supraventricular tachycardia by the development of bundle branch block ipsilateral to the bypass tract; and (6) the ability to preexcite the atrium with ventricular premature depolarizations during the tschycardia without affecting the His bundle electrogram. This latter finding is of particular value in identifying patients with tachycsrdia utilizing a septal bypass tract; in such cases the retrograde activation sequence during supraventricular tachycardia is normal and bundle branch block does not influence the cycle length or V-A conduction. Criteria used for A-V nodal reentry have been previously reported.5

TABLE I Patient

BYPASS

Cardiac Diagnosis Cardiomyopathy None MVP None None None MVP MVP Old inf-post MI, CAD MVP None None

Results

CAD = coronary artery disease; Inf-post MI = inferoposterior myocardial infarction; MVP = mitral valve prolapse.

The following specific phenomena were evaluated to determine the mechanisms of supraventricular tachycardia:

(1) the mode of initiation of the tachycardia with particular attention to site of conduction delay appearing requisite for the development of the arrhythmia; (2) the requirement of the atria or ventricles, or both, to initiate the tachycardia; (3) the atria1 activation sequence and relation of the P wave to the QRS complex at the onset of and during the tachycardia; (4) the influence of bundle branch block, spontaneous or induced, on the cycle length and ventriculoatrial (V-A) conduction time during the tachycardia; and (5) the effect of atria1 or ventricular stimulation, or both, during the tachycardia. Criteria used to diagnose supraventricular tachycardia using a concealed A-V bypass tract included: (1) initiation of the tachycardia in the absence of or not requiring a critical degree of A-V nodal conduction delay; (2) requirement of the ventricles to initiate and sustain the tachycardia; (3) abnormal retrograde atria1 activation sequence during the tachycardia with the earliest onset of atria1 activation following the QRS

Twelve of the 60 patients (20 percent) met criteria for the presence of an atrioventricular (A-V) bypass tract functioning as a retrograde limb during supraventricular tachycardia (Table I). Four patients had echocardiographic and clinical evidence of mitral valve prolapse, six had no heart disease, and two had clinically significant organic heart disease. In 2 of the 12 patients with concealed bypass tracts anterograde ventricular preexcitation could be demonstrated by atrial pacing from the coronary sinus near the atria1 insertion of the bypass tract although no electrocardiographic evidence of preexcitation was noted during sinus rhythm. No evidence of anterograde ventricular preexcitation could be demonstrated in the remaining 10 patients with any method of atria1 stimulation. Mode of lnltiation of Supraventricular Tachycardia Programmed atria1 and ventricular stimulation initiated supraventricular tachycardia in all patients. During anterograde stimulation, supraventricular tachycardia typically developed after some degree of

FIGURE 1. Case 1. Initiation of supraventrrcular tachycardia in the absence of A-V nodal delay. The figure is organized from top to bottom as follows: Electrocardiographic leads I (I), II (2) and VI and electrograms from the high right atrrum (HRA), coronary sinus (CS), His bundle (HBE) and right ventrrcular apex (RVA) and time (T) scale A, f-l and V = atrial, His bundle and ventricular electrograms, respectively S = stimulus artifact An atrial premature depolarization (S, arrow) delivered from the coronary sinus at a coupling interval of 380 msec results in supraventrcular tachycardia. The A-H interval of the sinus complex and the premature complex are identical. Note that the earliest retrograde activation during the tachycardia is recorded from the coronary sinus See text for further discussron.

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A-V delay was induced. In two patients, however, no A-V delay was required; the tachycardia occurred either with a spontaneous change in the cycle length or during relatively late atria1 premature depolarizations delivered from the coronary sinus (Fig. 1). In one patient a His premature depolarization initiated supraventricular tachycardia. In all patients supraventricular tachycardia could be initiated with rapid ventricular pacing or programmed ventricular stimulation, or both, in the absence of V-A conduction delay (Fig. 2). In each instance the V-A in-

terval and the retrograde atria1 activation sequence during ventricular stimulation were similar to those during the tachycardia. In seven patients ventricular premature depolarizations delivered at long coupling intervals (more than 75 percent of the paced cycle length) resulted in retrograde atrial activation over both pathways producing an atrial fusion complex.13J4 When conduction proceeded solely over the bypass tract, supraventricular tachycardia was initiated. Thus, the initiation of supraventricular tachycardia during ventricular stimulation depended upon the development

FIGURE 2. Case 1. Initiation of supraventricular tachycardia by ventricular pacing. Pacing from the right ve&ricular apex (S, arrow) at a cycle length of 400 msec initiates supraventricular tachycardia. Retrograde atrial activation during ventricular pacing and supraventricular tachycardia is the same. Abbreviations as in Figure 1.

FIGURE 3. Case 3 Termination of supraventrlcular tachycardia by an atrial premature depolarization Supraventricular tachycardia is present. After the fourth complex of supraventricular tachycardia, an atrial premature depolarization is introduced from the coronary sinus at a coupling interval of 3 10 msec (S, arrow), which terminates the supraventricular tachycardia by creating atrioventricular nodal block 3 = electrocardiographic lead Ill; other abbreviations as in Figure 1.

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of retrograde tem.

block in the normal A-V conducting

sys-

Effects of Stimulation During Supraventricular fachycardia

Rapid atria1 or ventricular pacing (cycle lengths 250 to 500 msec) as well as programmed atrial or ventricular extrastimuli were able to terminate the tachycardia in each patient. In 10 patients termination was produced by A-V nodal block and was independent of the stimulation site, for example, atria or ventricles (Fig. 3). In contrast, in two cases termination of supraventricular tachycardia with ventricular premature depolarizations was produced with retrograde block in the bypass tract alone or simultaneously with retrograde block in the A-V node (Fig. 4). In each of the 12 patients right ventricular stimulation during supraventricular tachycardia could preex-

T

ET AL

cite the atria at a time when the His bundle was depolarized and therefore refractory (Fig. 5). In no instance was left ventricular stimulation necessary to demonstrate this phenomenon. In two patients spontaneous termination was observed and resulted from progressive conduction delay and then block in the A-V node. Thus, as with termination of supraventricular tachycardia by programmed stimulation, spontaneous termination resulted from block in the anterograde limb of the reentrant circuit, that is, the A-V node. V-A conduction never changed during supraventricular tachycardia despite variations in A-V conduction produced with atria1 stimulation. Electrophysiologic Findings During Supraventricular Tachycardia P wave configuration and atria1 activation: In each of the 12 patients with concealed bypass tracts the

I

FIGURE 4. Case 1. Termination of supraventricular tachycardia by block in both normal and accessory atrioventricular (A-V) pathways in response to ventricular premature depolarizations. A, two ventricular premature depolarizations capture the atrium without interrupting anterograde conduction over the normal A-V conduction system. The second ventricular premature depolarlzatlon (S2) preexcltas the atrium early enough to produce prolongation of A-V nodal conduction B, the second ventricular premature depolarization (Sp) terminates the tachycardia by blocking in both normal and accessory A-V pathways. Abbreviations as in Figure 1.

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FIGURE 5. Case 1. Retrograde atrial preexcitation and normalization of the QRS complex by a ventricular premature depolarization during supraventricular tachycardia During supraventricular tachycardia with left bundle branch aberration, a ventricular premature depolarization is introduced in the right ventricular apex (S, arrow) and conducts in retrograde fashion to the atrium after the His bundle has been depolarized in anterograde manner. This also results in normalization of the QRS complex with concomitant shortening of ventriculoatrial conduction time and cycle length (from 425 to 372 msec). Abbreviations as in Figure 1.

P wave was negative in lead I of the surface electrocardiogram during supraventricular tachycardia (Fig. 6, Table II), a finding that is considered diagnostic of left atria1 orgin of atria1 depolarization.15-I8 In each of the patients atria1 depolarization (the earliest intracardiac or surface electrocardiographic recording) appeared shortly after the QRS complex with an R-P/R-R ratio of less than 0.5 (Table II). The earliest onset of retrograde atria1 activation was recorded in the coronary sinus. Functional bundle branch block during supraventricular tachycardia: Eight patients manifested bundle branch block during supraventricular tachycardia: seven at the onset and one during the arrhythmia. Five had aberration of both the left and right

NSR

I

bundle branch block type. The cycle length and V-A conduction time during supraventricular tachycardia with left bundle branch block were longer than during supraventricular tachycardia with a normal QRS complex or with right bundle branch block (Table II). In patients manifesting functional bundle branch block at the initiation of the tachycardia, the presence and type of bundle branch block depended on the Hi-Hz interval preceding the onset of the arrhythmia. In three patients with continuing bundle branch block during the tachycardia, ventricular premature depolarizations or ventricular pacing were able to normalize the QRS complex, allowing analysis of the effect of the bundle branch block on V-A conduction (Fig. 5). H-V prolongation was associated with the development of left

SVT

FIGURE 6. P wave configuration during supraventricular tachycardia with left-sided atrioventricular bypass tracts. During supraventricular tachycardb (SVT) negative P waves are seen in lead I (arrows) after the QRS complex in a patient with a left-sided bypass tract. aVF = electrocardiographic lead aVF; NSR = normal sinus rhythm; other abbreviations as in Figure 1.

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bundle branch block in four of six patients and contributed to the prolongation of the cycle lengths of the tachycardia. Associated A-V nodal dual pathways: In five patients (Cases 1,6,8,10 and 12) dual A-V nodal pathways were demonstrated. In three (Cases 1,6 and 8) the slow A-V nodal pathway functioned as the anterograde limb during supraventricular tachycardia, whereas in Patients 10 and 11 the fast pathway was utilized as the anterograde limb of the reentrant circuit.1sy2cA second, slow A-V nodal pathway was also demonstrated during supraventricular tachycardia when atria1 or ventricular premature depolarizations, which were blocked in the fast pathway, conducted in anterograde fashion (Fig. 7). Associated arrhythmias: In 6 of the 12 patients with concealed retrograde bypass tracts, rapid atria1 or ventricular pacing, or both, during supraventricular tachycardia induced sustained atria1 flutter or fibrillation, or both. In each case the flutter or fibrillation spontaneously converted to the supraventricular tachycardia or sinus rhythm. Concealed Bypass Tract Versus A-V Nodal Reentry

The characteristics of supraventricular tachycardia utilizing the concealed bypass tract (12 patients) were compared with those of supraventricular tachycardia due to A-V nodal reentry (40 patients) (Table III). The remaining eight patients had sinus nodal reentry (five patients) or intraatrial reentry (three patients). The following electrocardiographic features appeared to characterize suprauentricular tachycardia utilizing a concealed bypass tract (Table III): (1)

Rapid rate of supraventricular tachycardia. The average cycle length of supraventricular tachycardia was 337 f 32 (mean f standard error of the mean) msec and that due to A-V nodal reentry was 395 f 25 msec. (8) The P wave followed the QRS complex with an R-P/R-R ratio

ET AL

TABLE III Comparison of Supraventricular Tachycardia Utilizing Concealed Bypass Tracts With A-V Nodal Reentrant Tachycardia SVT-CBT

Average tachycardra cycle length (msec) Negative P wave in ECG lead I P wave following QRS Functional bundle branch block Induced atria1 fibrillation Patients’ age (yr) Male/female ratio Organic heart disease

337 f 32*+ 12 of 12 (100%)” 12 of 12 (100%)’ 8 of 12 (66%)’ 6 0’4;2~5CX~)’ 2/l 2 of 12’

S/T-AVNR

385 f 25’

0 of 40 (0%) 12of40(30%) 3of40(8%) 1 o;fOi21$) 1 5/l 13of40

P <0.05. + Mean f standard error of the mean A-V = atrioventricular; ECG = electrocardrographic; SVT-AVNR = supraventricular tachycardia due to A-V nodal reentry; SVT-CBT = supraventricular tachycardia utilizing a concealed bypass tract l

less than or equal to 0.5 in all patients with supraventricular tachycardia using a concealed bypass tract whereas it did so in only 12 of 40 patients (30 percent) with A-V nodal reentry. (3) A negative P wave in lead I during supraventricular tachycardia was seen in all patients in which the arrhythmia utilized a retrograde concealed bypass tract but was not seen in any patient with A-V nodal reentry. (4) The incidence of functional bundle branch block was significantly greater in patients with supraventricular tachycardia utilizing a concealed bypass tract than in those with tachycardia secondary to A-V nodal reentry (8 of 12 versus 4 of 40). (5) There was a much greater incidence of induced atrial flutter or fibrillation in patients with concealed bypass (6 of 12 versus 1 of 40). Although differences existed in age, sex and the incidence of organic heart disease, too much overlap existed to make any of these variables useful in a differential diagnosis of the mechanism of

TABLE II Electrophyslologic Data on 12 Patients With Supraventrlcular Tachycardia Utilizing Concealed Bypass Tracts

Cy;;TL;ne;

of P Wave ECG lead I

Early LA

AVNFRP (m=)

Negatrve Negative Negative Negative Negative Negative

+

310 370

120 100 100

: :

350 290 370

100 Zl

Negative

:+

335 400

120 110

Negative Negative

+

340 310

100 90

Negative

:+

360 350

Normal QRS

W’ h LBEB

:

330 300

420 355

310 300

110 120

3 4 0

350 260 330 370

370 410 380

340 260 330 370

;:

335 340

-

1:

340 350

400 -

345 +LAHB -

::

360 380

-

-

Case no

With RBBB

Dual A-V Nodal Pathways Fast Pathway Slow Pathway (anterograde) (anterograde) +

-

. -

‘+ + +

+ = present; - = absent; . . = not recorded. A-V = atrioventricular; AVN-FRP = atrfoventricular nodal functional refractory per&; early LA = atrial depolarization noted first in coronary slnus (left atrial) electrode; ECG = electrocardiogram; LAHB = left anterior hemiblock; LBBB = left bundle branch block; RBBB = right bundle branch block; SVT = supraventrrcular tachycardia.

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supraventricular tachycardia. The mean A-H intervals and functional refractory period of the A-V node in patients with supraventricular tachycardia utilizing a concealed bypass tract were shorter than those in a normal population (95 and 420 msec, respectively).21922 Discussion Incidence and clinical features: The use of programmed stimulation and endocardial mapping has provided evidence of multiple mechanisms for the arrh-ythmia termed paroxysmal supraventricular tachycardia.23-25 In a suprisingly high proportion (20 percent) of patients with clinical supraventricular tachycardia and no manifestation of preexcitation in the surface

electrocardiogram an atrioventricular bypass tract was utilized as the retrograde limb during the tachycardia. These patients are younger and have a lesser incidence of clinically significant heart disease than patients with A-V nodal reentrant supraventricular tachycardia. Electrocardiographic correlates: Several electrocardiographic and clinical features distinguish patients with supraventricular tachycardia utilizing a concealed bypass tract. These may be helpful in the differential diagnosis of supraventricular tachycardia. In contrast to most patients with A-V nodal reentry tachycardia all patients with supraventricular tachycardia utilizing a concealed bypass tract demonstrated retrograde P waves. Moreover, these P waves were negative in lead I, a diagnostic feature of left-sided by-

FIGURE 7. Demonstration of dual atrioventricular (A-V) nodal pathways during supraventricular tachycardia. A, an atrial premature depolarization (S) delivered in the coronary sinus (CS) at a coupling interval of 210 msec prolongs the A-H interval from 110 msec to 170 msec. B, an atrial premature depolarization (S) delivered at a slightly shorter coupling interval (200 msec) prolongs the A-H interval to 295 msec, suggesting block in a fast A-V nodal pathway and anterograde conduction through a slow A-V nodal pathway. The fast A-V nodal pathway Is utilized as the antemgrade limb of the tachycardia, and retrograde conduction occurs over the left A-V bypass tract. See text for further discussion. Abbreviations as in Figure 1.

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pass tracts. Confirmation of this clinical clue was provided by endocardial atria1 mapping, which demonstrated a left-sided bypass tract in all of our patients. The average rate of supraventricular tachycardia incorporating a concealed bypass tract is faster than that of A-V nodal reentry tachycardia despite the longer reentry circuit in the former. Functional bundle branch block during the tachycardia is also very common in these patients. Both the rapid rate and large incidence of bundle branch block in patients with tachycardia using bypass tracts have a common explanation. We believe that both are related to relatively enhanced A-V nodal conduction and a short functional refractory period of the A-V node, which allows the His-Purkinje system to be engaged at shorter HI-HZ intervals than in normal subjects and specifically shorter intervals than in patients with A-V nodal reentry tachycardia. The functional refractory period of the A:V node allows the impulse to encounter a partially refractory bundle branch, producing the electrocardiographic abnormality. This does not happen in patients with A-V nodal reentry because most have dual A-V nodal pathways and the tachycardia is initiated only after a “jump” in HI-H2 intervals as conduction proceeds along the slow pathway1%20,2%24; th erefore the relative refractory period of the His-Purkinje system is never encroached upon. The relative refractory periods of the His-Purkinje system in patients with concealed bypass tracts fall within the normal limits previously noted.zl We therefore believe that both the rapid rate of the tachycardia and functional bundle branch block are the result of a shortened A-V nodal functional refractory period. As noted by previous authors,1-8 the presence of functional bundle branch block ipsilateral to the site of the bypass tract (in this case left bundle branch block) provides information important to making the diagnosis of an accessory pathway. During left bundle branch block the cycle length of the tachycardia and, more specifically, V-A conduction time during the tachycardia are prolonged. The explanation of this phenomenon is that the left bundle branch block necessi-

TRACTS-FARSHIDI

ET AL

that the impulse first pass through the right ventricle and then slowly by muscle conduction reach the ventricular end of the bypass tract in the left ventricle before retrograde conduction, and hence circus movement tachycardia, can ensue. Thus, the reentry circuit is lengthened and the conduction time within the ventricular component of the circuit is prolonged. As noted by Spurrel12” and Wellens and their co-workers, ventricular stimulation during supraventricular tachycardia can induce or abolish the bundle branch block enabling the investigator to analyze the effects of the block on the tachycardia. This procedure was useful in three of our patients. Although delayed anterograde input to the A-V bypass tract might explain the normal P-R interval and QRS pattern in the surface electrocardiogram in patients with left-sided bypass tracts, unidirectional block was demonstrated in 10 of our 12 patients by atria1 pacing at the site of the bypass tract. It is unclear why all concealed bypass tracts in our series and most previously reported are left-sided.l-g Implications: The recognition of supraventricular tachycardia associated with concealed A-V bypass tracts is suggested by rapid heart rate, presence of functional bundle branch block and a discrete P wave following the QRS complex by an interval less than half the R-R interval. The observation of a negative P wave in lead I is virtually diagnostic of this type of supraventricular tachycardia. As newer specific antiarrhythmic drugs become available and the place of surgical therapy of refractory supraventricular tachycardia becomes established, the diagnosis of supraventricular tachycardia utilizing a concealed bypass tract assumes even greater significance.

tatBS

Acknowledgment We gratefully acknowledge the support and editorial comments of John A. Kastor, Chief of the Cardiovascular Section. We also thank Marie Coscia for preparation of the manuscript, Ralph Ianuzzi for photographic assistance, and Kathleen Sundra, Blanche Douglas and Karen Resko for technical assistance.

References Spurrell RAJ, Klrkler DM, Sowton E: Concealed bypass of the atrioventricular node in patients with paroxysmal supraventricular tachycardias revealed by intracardiac stimulation and Verapamil. Am,J Cardiol 33590-595, 1974 , Tonkln AM,.Gallagher JJ, Svenson RH, et al: Antegrade block in accessory pathways with retrograde conduction in reciprocating tachycardia. Eur J Cardiol 3:143-152, 1975 News H, Schlepper M, Thormann J: Analysis of re-entry mechanisms, in three patients with concealed Wolff-Parkinson-White syndrome..Circulation 51:75-81. 1975 Slama R, Coumel PH, Bouvrlan Y: Lqs syndrome de Wolff Parkinson White de type A inapparents ou latents en rhythm sinusal Arch .Mal Coeur Vaiss 66:639-653, 1973 Wellens HJ, Durrer D: The role of an accessory atrio-ventricular pathway in reciprocal tachycardia: observations in patients with and without the Wolff-Parkinson-White syndrome. Circulation

52:58-72, 1975 6 Gallagher JJ, Glfberl M, Sveneon RH, et al: Wolff-Parkinsor+White syndrome. The problem, evaluation and surgical correction. Circulation 51:767-785, 1975 7. Coumel PH, Altuel P: Reciprocating tachycardia in overt and latent pre-excitation. Influence of functional bundle branch block on the rate of the tachycardia. Eur J Cardiol 1.423-436, 1974 8 Sung RJ, Castellanos A, Gelband H, et al: Mechanism of reciprocating tachycardia induced during sinus rhythm in concealed Wolff-Parkinson-White syndrome. Circulation 54338-344, 1976 9 Sung RJ, Gelband H, Castellanos A, et al: Clinical and electrophysiologic observations in patients with concealed accessory atrioventricular bypass tracts. Am J Cardiol40:839-847, 1977 10. GllleHe PC: Concealed anomalous cardiac conduction pathways: a frequent cause of supraventricular tachycardia. Am J Cardiol

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40:646-652, 1977 11. Wu D, Denes P, Amat-Y-Leon F, et al: Clinical, electrocardiographic and electrophysiological observations in patients with paroxysmal supraventricular tachycardia (abstr) Am J Cardiol 39 264, 1977 12 Coumei P, Attuei P, Motti G, et al: Les tachycardies junctionnelles paroxystiques. Evaluation du point de jonction inferieur de r&&&r Demembriment des soidisant rhythmes reciproques intra-ncdeaux. Arch Mal Coeur 66: 1255-1266, 1975 13. Sung RJ, Casteiianos A, Maiion SM, et al: Mode of initiation of reciprocating tachycardia during programmed ventricular stimulation in the Wolff-Parkinson-White syndrome. Am J Cardiol 40: 24-31, 1977 14. Svenson RH, Miller HC, Gallagher JJ, et al: Electrophysiological evaluation of Wolff-Parkinson-White syndrome Circulation 52: 552-562, 1975 15. MacLean WAH, Karp RB, Kouchoukos NT, et al: P waves during ectopic atrial rhythms in man. A study using atrlli pacing with fixed electrodes. Circulation 54:426-434, 1975 16. Harris BC, Shaver JA, Gray S, et al: Left atrial rhythm Experimental production In man Circulation 37:1000-1014, 1966 17. Massumi R, Tawakkoi AA: Direct study of left atriai P waves. Am J Cardiol 20:331-340, 1967

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ia 19.

20 21. 22.

23. 24. 25. 26

Mtrowski hll:Ectopic rhythms originating in the left atrium. Am Heart J 74:229-306,1967 Denes P, Wu D, Dhingra R, et al: Demonstrabon of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Crrcuiatron 48:549-555, 1973 Rosen KM, Mehta A, Miller RA: Demonstration of dual atrioventricular nodal pathways in man Am J Cardiol 33:291-294, 1974 Denes P, Wu D, Dhingra R, et al: The effects of cycle length on cardiac refractory periods in man Circulation 49.32-41, 1974 Akhtar M, Damato AN, Batsford WP, et al: A comparative analysis of antegrade and retrograde conduction pattern in man Circulation 52:766-776, 1975 Josephson ME, Kastor JA: Supraventricuiar tachycardia: mechanisms and management. Ann Intern Med 67:346-356, 1977 Wu D, Denes P: Mechanisms of supraventricular tachycardia Arch Intern Med 135.437-442, 1975 Baroid SS, Coumei P: Mechanrsms of atrioventricular junctional tachycardia Am J Cardioi 39:97-106, 1977 Spurreii RAJ, Kirkier DM, Sowton E: Retrograde invasion of the bundle branches producing aberration of the QRS complex during supraventricular tachycardia studied by programmed electrical stimulation. Circulation 50:487-495, 1974

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