Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man

Initiation of Two Distinct Forms of Atrioventricular Nodal Reentrant Tachycardia During Programmed Ventricular Stimulation in Man

RUEY J. SUNG, MD, FACC JANUARIUSZ L. STYPEREK, MD ROBERT J. MYERBURG, MD, FACC AGUSTIN CASTELLANOS, MD, FACC Miami, Florida

From the Electrophysiological Laboratories of Jackson Memorial Hospital and the Veterans Administration Hospital, and the Division of Cardiology, Department of Medicine, University of Miami School of Medicine, Miami, Florida. Manuscript received February 1, 1978; revised manuscript received April 11, 1978, accepted April 12, 1978. Adbess for reprints: Ruey J. Sung, MD, Division of Cardiology, University of Miami School of Medicine, PO Box 520875, Miami, Florida 33152.

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Ol 42 patients with supraventricuiar tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). in th&e patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventricuioatriai (V-A) conduction curves (V&, Al-A*) were smooth. Ventricular premature beats,.being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. in the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). in these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (VI-V2, Al-AZ) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. in both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction. The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atriai premature stimulation in two patients. in this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (Al-AZ, HI-Hz) were smooth. Atriai premature beats, conducted anterograde over the fast pathway, could activate the sfow pathway in a retrograde direction resulting in an atriai echo or sustained fast-slow form of A-V nodal reentrant tachycardia.

Recent electrophysiologic studies’-14 have suggested that atrioventricular (A-V) nodal reentry, related to the presence of dual A-V nodal pathways, is frequently responsible for the occurrence of paroxysmal supraventricular tachycardia in man. Using the techniques of intracardiac recordings and programmed atrial premature stimulation, most studies describe the induction of an atria1 echo or A-V nodal reentrant tachycardia in association with characteristic discontinuous A-V nodal conduction curves (Al-As, Hi-Hz). M*s-14 In contrast, limited information is available concerning the mechanisms of retrograde initiation of A-V nodal reentrant tachycardia during programmed ventricular stimulation in patients with dual A-V nodal pathways.15-ls

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During the study tricular tachycardia,

of eight patients with supraventwo distinct forms of A-V nodal

reentrant tachycardia were elicited during programmed ventricular stimulation; their initiation depended on differences in the electrophysiologic properties of fast and slow A-V nodal pathways during retrograde conduction. Patients

and Methods

Patients: Data of all patients studied in the electrophysiologic laboratories of Jackson Memorial Hospital and the Veterans Administration Hospital, Miami, Florida between July 1974 and June 1977 were reviewed. The following observations suggested the presence of dual A-V nodal pathways: (1) induction of discontinuous A-V nodal conduction curves (Ai-Az, Hi-Hs) during programmed atria1 premature stimulation3-6s-i4; or (2) induction of discontinuous ventriculoatrial conduction curves (Vi-Vs, Al-As) during programmed ventricular premature stimulation16T1a20; or both (1) and (2). Patients with manifest or concealed accessory A-V bypass tracts15,21~22 were excluded. Forty-two patients with episodes of supraventricular tachycardia were determined to have dual A-V nodal pathway conduction; in eight of these, sustained (non self-terminating) A-V nodal reentrant tachycardia could be elicited during programmed ventricular stimulation. These eight patients constituted the study population. Their ages ranged from 21 to 64 (mean 36.4) years. Protocol: After the patients gave informed consent, all cardiotonic and antiarrhythmic medications were discontinued 48 to 72 hours before the study. The study was performed with patients in a postabsorptive nonsedated state. With a conventional technique,23 the His bundle electrogram was obtained with a tripolar electrode catheter placed across the tricuspid valve, from which low septal right atrial activity was recorded as well. A hexapolar electrode catheter was introduced by way of an antecubital vein. The distal pair of electrodes was placed at the right ventricle for ventricular pacing, and the proximal two pairs were used for high right atria1 pacing and recording .21 The intracardiac electrograms were then displayed simultaneously with standard electrocardiographic leads I, II and Vi on a multichannel oscilloscopic photographic recorder (Electronics for Medicine, DR-16) and recorded at a paper speed of 100 mm/set, using a filter setting of 40 to 500 hertz. Programmed atria1 and ventricular stimulation consisted of extrastimulation and incremental pacing.21 During programmed extrastimulation, the high right atrium and the right ventricular endocardium were respectively stimulated at one or two cycle lengths (Al-Al or Vi-Vi) with use of a programmed digital stimulator (Biocelestronix, Miami Springs, Florida) that delivered stimuli (Sr and Sz) of 2 msec duration at approximately twice diastolic threshold. After every eighth spontaneous or paced beat (Ai or Vi), a single premature atria1 or ventricular beat (A2 or Vz) was delivered at progressively shorter coupling intervals (Al-A2 or Vi-Vz) until the effective refractory period of the atrium or the ventricle was encountered.21 Definitions: A-V conduction intervals and refractory periods were defined and measured as conventionally described.24 Ai, Hi and Vi were low septal right atrial, His bundle and ventricular responses, respectively, induced by the driving stimuli (Si); As, Hz and Vs were low septal right atrial, His bundle and ventricular responses, respectively, induced by the premature stimuli (Sz). Ae represented an atria1 echo phenomenon or atria1 reentry during A-V nodal reentrant tachycardia. The critical A-V nodal conduction time was the A-H interval required for the development of the

NODAL REENTRANT TACHYCARDIA-SUNG

ET AL.

atria1 echo phenomenon or A-V nodal reentrant tachycardia.s-a,a*is*‘4 The Ae-H/H-Ae ratio was used to compare anterograde with retrograde A-V nodal conduction time during the episode of A-V nodal reentrant tachycardia. The Ae-H interval was measured from the end of the low septal atria1 echo electrogram to the beginning of the His bundle potential and the H-Ae interval from the end of the His bundle potential to the beginning of the low septal atria1 echo electrogram.25 Electrophysiologic evidence for retrograde conduction over the A-V node-His-Purkinje system was based on the following observations: (1) Progressive prolongation of ventriculoatrial (V-A) conduction time was induced by gradual shortening of the ventricular premature coupling interval (Vi-V,) and incremental ventricular pacing (Vi-V#1,26,27; and (2) ventricular premature stimulation during tachycardia did not result in atrial preexcitation.13p27When discontinuous A-V nodal conduction curves (Al-As, Hi-Hz) and discontinuous V-A conduction curves (Vi-Vz, AI-AZ) were respectively induced during anterograde and retrograde conduction studies, the refractory periods of the fast and slow A-V nodal pathways in anterograde and retrograde directions were measured and defined as described by Denes3 and Wui6 and their co-workers. Briefly, the curve to the right of the discontinuity reflected the fast A-V nodal pathway conduction, and that to the left represented the slow A-V nodal pathway conduction. In discontinuous AI-AZ, Hi-H2 curves, the longest Ai-A2 interval at which As was blocked in the fast or the slow A-V nodal pathway was defined as the anterograde effective refractory period of the fast or the slow A-V nodal pathway, respectively. Similarly, in discontinuous Vi-Vs, Ai-Az curves, the longest Vi-V2 interval at which Vs was blocked in the fast or the slow A-V nodal pathway was defined as the retrograde effective refractory period of the fast or the slow A-V nodal pathway, respectively.

Results The pattern of the tachycardia circuit within the A-V node identified two distinct forms of A-V nodal reentrant tachycardia that could be induced during programmed ventricular stimulation in these eight patients: (1) the slow-fast form using a slow A-V nodal pathway for anterograde conduction and a fast A-V nodal pathway for retrograde conduction (Ae-H/H-Ae ratio greater than 1) (Cases 1 to 3); and (2) the fast-slow form having a tachycardia circuit in reverse of the former using a fast A-V nodal pathway for anterograde conduction and a slow A-V nodal pathway for retrograde conduction (AeH/H-Ae ratio less than 1) (Cases 4 to 8). The anterograde and retrograde A-V conduction patterns in these patients were then analyzed. Slow-Fast Form of A-V Nodal Reentrant Tachycardia (three patients) During programmed atria1 stimulation, dual A-V nodal pathway conduction was evident in all three patients. In two of these three patients, sustained A-V nodal reentrant tachycardia of the slow-fast form could be elicited after achievement of a critical A-V nodal conduction delay (A-H) during anterograde slow pathway conduction. The same form of A-V nodal reentrant tachycardia could also be elicited with ventricular premature depolarization (Vz) at short premature coupling intervals (Vi-V,) during programmed ventricular stimulation in these two patients.

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As illustrated in Figure 1, both the high right atrium and the right ventricle were driven at a cycle length of 650 msec. The Al-As, HI-Hs and Al-As, As-Hz curvea were diicontinuous because of a sudden increase in A-V nodal conduction time (As-Hz) at an atrial premature coupling interval (Al-As) of 460 msec (Fig. 1A). This reflected a failure of anterograde conduction over the fast A-V nodal pathway with resultant slow A-V nodal pathway conduction. The anterograde effective refractory periods of the fast and slow A-V nodal pathways

msec. 650

were 460 and 330 msec, respectively. The critical A-H interval that induced an atrial echo phenomenon was 310 msec. Sustained A-V nodal reentrant tachycardia of the slow-fast form could be induced between atrial premature coupling intervals of 360 and 340 msec. The corresponding Vr-Vs, Ar-Aa and Vr-Vs, Vs-As curves, in contrast, were smooth (Fig. 1B). Note that there was a progressive increase in V-A conduction time (Vs-As) as the ventricular premature coupling interval (VI-Vs) gradually shortened, a characteristic of retrograde conduction

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FIGURE 1. Case 1. A, A,-AZ, H,-H2 and A,-A2, AdO cwves duringhi@ right atrial (HRA) pacing at a cycle length (CL) of 650 msec. Note discontinuity due to a sudden increase in A-V nodat conduction time (AsH2) at a premature coupling interval (A,-A2) of 460 msec. Solid circles represent responses without atrial echoes; open circles represent responses with atrial echoes. (See text.) B, VI-V2. AI-A2 and VI-V2. VTAP curves during right ventricutar (RV) pacing at a cycle length (CL) of 650 msec. Solid ctrcles represent responses without ventricular echoes; open circle8 represent responses with ventricular echoes. Retrograde His bundle potentials (H-) are depicted as open triangles, Both V,-V2. A,-A2 and VI-V2, VTAp curves are smooth. Retrograds A-V nodal conduction time (H2-A2) ranges from 90 to 100 msec. Induction of sustained A-V nodal reentrant tachycardia of the slowfast form coincides with the ventricular echo zone between prematule coupling intervals (VI-V,) of 240 and 220 msec. LRA = low septal right atrium.

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FIGURE 2. Same case. Atrial premature stimulation with induction of the slow-fast form of A-V nodal reentrant tachycardia. In this and subsequent figures are shown eiectrocardiogaphic lead II (II), hi right atrtal (HRA) and His bundle electrographic (HBE) leads. S1 and Ss represent pacing and premature stimuli. and A and H atrial and His bundle electrograms, respectively. The high right atrium is driven at a cycle length (S&I interval) of 650 msec. A, an atria1 premature beat at a coupling interval (S,-S2) of 470 msec lengthens the A-H interval from 90 to 150 msec. B, an atrial premature beat at a coupling interval (S1S2) of 460 msec suddenly prolongs the A-H Interval to 290 msec, resuiting in disccmtlnuousA-V nodal conduction curves (Al-A2, HI-H2) (Fig. 1A). C, an atrial premature beat at a coupling interval (S&s) of 360 rnsec induces a sustained A-V nodal reentrant tachycardla of the slow-fast form upon achievement of an A-H interval of 340 msec (arrow). The Ae-HlKAe ratio Is greater than 1 during tachycardia. Ae = atrial echo phenomenon.

HI-Hz:660

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in the A-V node-His-Purkinje system. The retrograde His bundle potential (Hz) secondary to ventricular premature depolarization (Vz) could be recorded between ventricular premature coupling intervals (VI-Vz) of 320 and 200 msec. Retrograde A-V nodal conduction time (Hz-Az) ranged from 90 to 100 msec. Because the V-A conduction curve (VI-Vz, Al-As) was smooth and retrograde A-V nodal conduction time was relatively short, it was concluded that V-A conduction occurred exclusively by way of the fast A-V nodal pathway. Between ventricular premature coupling intervals (VI-V,) of 240 and 200 msec, sustained A-V nodal reentrant tachycardia of the slow-fast form, similar to that induced during programmed atria1 premature stimulation, could be elicited.

NODAL REENTRANT TACHYCARDIA-SUNG

The representative tracings corresponding to Figure 1, A and B, are shown in Figures 2 and 3. Note that the slow-fast form of A-V nodal reentrant tachycardia induced during both atria1 and ventricular premature stimulation had an Ae-HI H-Ae ratio of more than 1, indicating anterograde conduction over a slow A-V nodal pathway and retrograde conduction over a fast A-V nodal pathway (Fig. 2C and 30. Furthermore, shortening of the ventricular pacing cycle length (VI-VI) seemed to widen the tachycardia zone. As demonstrated in Figure 3D, when the ventricular pacing cycle length was decreased to 450 msec, a ventricular premature depolarization (Vz) at a relatively long coupling interval (VI-Vs) of 370 msec could readily elicit a sustained A-V nodal reentrant tachy-

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FKilJRE 3. Same case. Ventricular premature stimulation with induction of the slow-fast form of A-V nodal reentrant tachycardla. The right ventricle is &ken at a cycle length of 650 rnsec. A to C, ventricular premature beats (S2) at coupling intervals of 320, 250 and 240 rnsec induce retrograde atrial activation with a gradual prolongation of V-A conduction time (SrA2 interval = 230, 280 and 290 msec, respectively). The corresponding VI-V2, A,-A2 and V@J2, VTAP curves are smooth (Fig. 1B). Retrograde A-V nodal conduction time (HrA2) is 90 msec. In C, the ventricular premature beat (S2) elicits not only a ventricular echo phenomenon but also sustained A-V nodal reentrant tachycardia of the slow-fast form (errow). The Ae-HIl+Ae ratio is seater then 1 during tachycardia. D, when the ventricular pacing cycle length (S&) is decreased to 450 msec, a ventricular premature beat (Se) can induce sustained A-V nodal reentrant tachycardia of the slow-fast form (arrow) beginning at a coupling interval (S&J of 370 msec until V-A conduction fails at 230 msec (not shown). Abbreviations as in Figure 2.

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FfGURE 4. Case 2. Anterogrede duel A-V nodal pathway conduction during basic atrial pacing. S = stimulus. The first beat is of sinus origin with an A-H interval of 60 msec. The second and subsequent beats are responses to high right atrial pacing at a cycle length of 800 msec. Note a sudden increase in the A-H interval (250 msec) after the first atrial capture. Gradual prolongation of A-V nodal conduction time (A-H) is followed by the occurrence of en atrial echo (Ae) phenomenon (critical A-H interval = 280 rnse~ corresponding to the fourth atrial capture). me sixth atria1 capture is biooked in the A-V node. The occurrence of en atrial echo (Ae) phenomenon interferes with programmed atrial premature stimulation. Abbreviations as in Figure 2.

September 1979

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Volume 42

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ATFtlOVENTRlCULAR NODAL REENTRANT TACHYCARDIA-SUNG

ET AL.

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FKNRE 5. Seme case. Induction of lhe slow-fast form of A-V nodal reentrant tachycardii at a shorter ventricular pacing cycle length without verMcular premature stimulation. A and B, the right ventricle is driven at a cycle length of 800 msec. Ventricular premature beats (S2) at coupling intervals of 390 and 310 msec induce retrograde atrial activation with a gradual prolongation of V-A conduction time (&-A1 = 150 msec in both panels, STAP = 220 and 300 msec, in A and8, respectively). In each instance, ventriculoatrial activation is followed by a ventricular echo beat with an atrial echo (Ae). The corresponding VI-VP. AI-A2 and VI-V2, VTA2 curves are smooth, similar to those demonstrated in Figure 16. Retrograde A-V nodal conduction time(HrA2) is 100 msec. C, the right ventricular pacing cycle length is decreased from 800 to 500 msec. The third and fourth pacing stimuli not only capture the ventricle but also induce retrograde atrial activation. A sustained A-V nodal reentrant tachycardia of the slow-fast form Is elicited after termination of ventricular pacing (the fourth pacing stimulus). The Ae-H/KAe ratio is greater than 1 durlng tachycardla. Abbreviations as in Figure 2.

cardia of the slow-fast form. The tachycardia zone extended from the premature coupling interval (VI-V,) of 370 msec to 240 msec before V-A conduction failed (VI-V2 interval = 230 msec). In the remainingpatient (Fig. 4), the fast A-V nodal pathway appeared to have a long effective refractory period in an anterograde direction. At an atrial pacing cycle length of 800 msec, anterograde A-V nodal conduction immediately shifted from fast to slow A-V nodal pathway conduction. A gradual prolongation of anterograde conduction time (A-H) over the slow A-V nodal pathway then resulted in retrograde atrial activation (Ae) through the fast A-V nodal pathway interfering with programmed atrial premature stimulation. Neither continuous atrial pacing at various cycle lengths nor rapid atrial stimulation up to 250 beats/min could elicit an epi?ode of A-V nodal reentrant tachycardia. The right ventricle was then driven at a comparable cycle length of 800 msec. V-A conduction time (Vz-Az) progressively lengthened as the ventricular premature coupling interval (VI-V2) gradually shortened, suggesting retrograde conduction over the A-V node-His-Purkinje system (Fig. 5, A to C). Ventricular premature depolarizations (VZ) induced a ventricular echo phenomenon between premature coupling intervals (VI-V2) of 390 and 290 msec. Although an atria1echo (Ae) constantly occurred after the ventricular echo beats, no sustained A-V nodal reentrant tachycardia could be elicited. A retrograde His bundle potential (Hz) secondary to ventricular premature depolarization (V2) was also discernible between premature coupling intervals (VI-V,) of 390 and 290 msec. The V-A

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conduction curve (VI-V2, AI-AZ) was smooth, similar to that illustrated in Figure lB, and retrograde A-V nodal conduction time (HZ-AZ)was relatively short, ranging from 80 to 100msec. It was therefore concluded that the fast A-V nodal pathway was used for V-A conduction, and the slow A-V nodal pathway for anterograde conduction during the occurrence of a ventricular echo phenomenon (Fig. 5, A and B). Shortening of the ventricular pacing cycle length to 500 msec could in itself initiate sustained A-V nodal reentrant tachycardia of the slow-fast form (Ae-H/H-Ae greater than 1) without delivery of ventricular premature stimulation (Fig. 5C). Fast-Slow Form of A-V Nodal Reentrant Tachycardia (flve patients) In two of these five patients, A-V nodal conduction curves (AI-AZ, HI-Hz) were smooth during programmed atria1 premature stimulation. Nevertheless, atria1 premature depolarizations (AQ) at short coupling intervals (AI-AZ) resulted in the late appearance of an atrial echo (Ae) or sustained A-V nodal reentrant tachycardia of the fast-slow form. During programmed ventricular premature stimulation in these two patients, discontinuous V-A conduction curves (VI-V2, AI-AZ) suggesting retrograde dual A-V nodal pathways were present. However, demonstration of discontinuous V-A conduction curves (VI-VZ, AI-AZ) appeared to be dependent on cycle length.

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FIGURE 6. Case 4. A, At-As. HI-HP and AI-AZ. Atis curves during high right atrial pacing at a cycle length of 640 msec. Selid clrcks represent responses without atrial echoes, open circles represent responses wlth atria1 echoes. Both Al -AZ, HtH2 and Al-Hz. A&i2 curves are smooth. A-V nodal conduction tlms (Ads) Wgthens progressiveiy as the atrial premature coupling interval (AI-AZ) gadualiy shortens (see text). B, VI-V2, AI-A2 and VI-V2. VTAO curves during right ventricular pacing at a cycle length of 640 msec. Sdfd circles represent responses without ventricuiar echoes. Retrograde His bundle potentiais (H-) are depicted as open trlaglos. Both V,-V2, Al-As and VI-V2, VT-AZ curves are smooth. Retrograde A-V nodal rxndu&m time &-HP) ranges from 120 to 130 msec. No ventrlcui~ echo phenomenon or A-V nodalreentmnt tachycardia can ba inducsd. C, V,-V2. Al-A2 and VI-V2, &A2 cuves Uing ri@t ventria~lar pacing at a cycle iength of 500 msec. Note the discontinuitydue to a sudden increase in VA conduction time &-As) at a ventricular premabre coupling interval (VI-V,) of 450 msec. S&i cfrcles represent responses without ventricular echoes; open clrcfes represent responses with ventricular echoes. Retrograde His bundle potentials are depicted as open trlanglr. The curve to the right of discontinuity reflects retrograde fast A-V nodal pathway conduction, that to the left, retrograde slow A-V nodal pathway conduction. Retrograde slow A-V nodal pathway conduction time (HrA2) ranges from 300 to 330 msec. Induction of sustained A-V nodal reentrant tachycardia of the fast-slow form coincides wlth the entire retrograde slow A-V nodal pathway conduction curve. Abbreviations as in Figure 1.

As illustrated in Figure 6, A and B, both the high right atrium (HRA) and the right ventricle (RV) were driven at a cycle length of 640 msec. The Ai-AZ, Hi-H2 and Ai-As, Ae-Hs curves were smooth. There was a progressive increase in anterograde A-V nodal conduction’time (A-H) as the atrial premature coupling interval (Al-As) gradually shortened (Fig. 6A). The critical A-H interval that induced an atrial echo beat was only 160 msec. Sustained A-V nodal reentrant tachycardia of the fast-slow form could be induced between atrial premature coupling intervals (Al-As) of 350 and 330 msec (Fig. 6A). It was believed that the entire Al-As, Hi-H2 and Al-As, As-H2 curves reflected the fast A-V nodal pathway conduction, and its anterograde effective refractory period was 320 msec. The slow A-V nodal pathway had an effective refractory period longer than that of the fast A-V nodal pathway in an anterograde direction, and its exact value could not be measured. The corresponding Vi-Ve, Al-As and Vi-Ve, Ve-A2 curves were also smooth (Fig. 6B). There was a progressive increase in V-A conduction time (Vs-AZ) as the ventricular premature coupling interval (Vi-Vs) gradually shortened, a characteristic of retrograde conduction in the A-V nodeHis-Purkinje system. The retrograde His bundle potential (Hz) secondary to ventricular premature depolarization (VZ) could be recorded between premature coupling intervals (Vi-V,) of 360 and 270 msec. Retrograde A-V nodal conduction time (HZ-AZ) ranged from 120 to 130 msec. Because of the smooth V-A conduction curve (Vi-Ve, Al-Ae) and relatively sommlmr

short retrograde A-V nodal conduction time (Hz-As), it was concluded that the fast A-V nodal pathway was used exclusively for retrograde atrial activation during programmed ventricular premature stimulation at this selected pacing cycle length.

The ventricular pacing cycle length was then decreased from 640 to 500 msec in the same patient (Fig. 6C). At this pacing cycle length, a sudden increase in V-A conduction time (Vs-As) occurred between premature coupling intervals of 460 and 450 msec resulting in discontinuous V-A conduction curves (Vi-Vs, Al-As). This indicated a failure of retrograde conduction over the fast A-V nodal pathway with resultant slow A-V nodal pathway conduction. The curve to the right of discontinuity reflected retrograde fast A-V nodal pathway conduction and to the left, retrograde slow A-V nodal pathway conduction. The retrograde effective refractory period of the fast A-V nodal pathway was 450 msec and that of the slow A-V nodal pathway 220 msec. V-A conduction time (Vr-AZ) of both the retrograde fast and slow A-V nodal pathway conduction curves showed characteristic progressive lengthening as the ventricular premature coupling interval (VI-Vs) gradually shortened (Fig. 6C). The retrograde His bundle potential (He) secondary to ventricular premature depolarization (Vs) could be recorded between premature coupling intervals (Vi-V2) of 350 and 230 msec. Retrograde A-V nodal conduction time (He-As) was relatively long (300 to 330 msec), thus confirming that the slow A-V nodal pathway was used for retrograde atrial

1971

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ATRlOVENTRlCULAR NODAL REENTRANT TACHYCARDIA-SUNG

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activation after the sudden increase in V-A conduction time (Vz-AZ). Throughout the entire retrograde slow A-V nodal pathway conduction curve (VI-VS, AI-AZ), a ventricular premature depolarization (Vz) could elicit not only a ventricular echo phenomenon but also sustained A-V nodal reentrant tachycardia of the fast-slow form. The representative tracings corresponding to Figure 6, A to C, are shown in Figures 7,8 and 9. Note that the fast-slow form of A-V nodal reentrant tachycardia induced during both atria1 and ventricular premature stimulation had an Ae-HI H-Ae ratio of less than 1, indicating anterograde conduction over a fast A-V nodal pathway and retrograde conduction over a slow A-V nodal pathway (Fig. 7B and 9, B to D). In the other three patients, discontinuous A-V nodal conduction curves (Al-As, HI-Hz) suggestive of the presence of dual A-V nodal pathways were evident

during programmed atria1 premature stimulation. However, no atria1 echo phenomenon or A-V nodal reentrant tachycardia of either form could he elicited. During programmed ventricular stimulation, two of the three patients had discontinuous V-A conduction curves (Vi-Vs, Al-As) suggesting dual A-V nodal pathways in

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SI-A1:130

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FIGURE 7. Same case. Atrial premature stimulation with induction of the fast-slow form of A-V nodal reentrant tachycardia. The high right atrium is driven at a cycle length (S1-S1) of 640 msec. The A-V nodal conduction time (A-H) lengthens progressively as the atrial premature coupling interval (S,-Ss) gradually shortens. The corresponding AI-As, HI-HP and Al-As, As-H2 curves are smooth (Fig. 6A). A, an atrial premature beat at a coupling interval (S,-S2) of 400 msec lengthens the A-H interval from 70 to 180 msec and elicits the late appearance of an atrial echo (Ae) (arrow). Note that the anterogradelretrograde A-V nodal conduction time ratio (A-H = 130 msec/H-Ae = 250 msec) is less than 1. 6, an atrial premature beat at a coupling interval of 350 msec elicits not only an atrial echo (Ae) phenomenon but also a sustained fast-slow form of A-V nodal reentrant tachycardia (arrow). The Ae/H/H-Ae ratio is less than 1 during tachycardia, indicating anterograde conduction over a fast A-V nodal pathway and retrograde conduction over a slow A-V nodal pathway. Abbreviations as in Figure 2.

1978

The Amerksn

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FfQURE 8. Same case. Ventricular premature stimulation without induction of A-V nodal reentrant tachycardia of either form. The right ventricle is driven at a cycle length (S1S2) of 640 msec. A and B, ventricular premature beats (Ss) at coupling intervals (St-S2) of 360 msec and 270 msec progressively lengthen V-A conduction time (S,A1 = 130, f&-As = 250 and 350 msec, respectively) without inductlon of a ventricular echo phenomenon cr A-V nodal reentrant tachycardia. Retrograde A-V nodal conduction time (&-As) is 130 msec. Abbreviations as in Figure 2.

the retrograde direction. Sustained A-V nodal reentrant ,tachycardia of the fast-slow form could be induced after a shift from retrograde fast to retrograde slow A-V nodal pathway conduction, similar to that illustrated in Figures 6C and 9, A to D. In the remaining patient, a prolonged V-A conduction time (VI-AI) before ventricular premature stimulation suggested retrograde conduction over a slow A-V nodal pathway. Induction of the fastslow form of A-V nodal reentrant tachycardia by ventricular premature beats (Vz) was associated with a smooth V-A conduction curve (Vi-V2, Ai-AZ). As illustrated in Figure 10, both the high right atrium and the right ventricle were driven at a cycle length of 650 msec. The AI-Az, HI-Hr and Al-Az, AZ-HZcurves were discontinuous because of a sudden increase in A-V nodal conduction time (AZ-He)at an atrial premature couplinginterval (AI-Az) of 340 msec (Fig. lOA). This reflected a failure of anterograde conduction over the fast A-V nodal pathway with resultant slow A-V nodal pathway conduction. The anterograde effective refractory period of the fast A-V nodal pathway was 340 msec. A further decrease in the atria1 premature coupling interval (AI-AZ) did not induce an atria1 echo phenomenon or A-V

Volume 42

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FfGURE 9. Same case. Ventricular prernatue stimulation with induction of the fast-slow form of A-V nodal reentrant tachycardia. The right ventricle is driven at a cycle length (S&) of 500 rnsec. A, a ventricular premature beat (Ss) at a coupling interval (S&J of 460 msec lengthens V-A conduction time (!&-AZ) from 180 to 200 msec. B, a ventricular premature beat (Ss) at a coupling interval (St-.$) of 450 rnsec suddenly increases V-A conduction to 380 msec, resulting in discontinuous V-A conduction curves (VI-Vs, AI-As) (Fig. 6C) and induction of a sustained A-V nodal reentrant tachycardia of the fast-slow form (arrow). C and D, ventricular premature beats (Ss) at coupling intervals (St-Sp) of 350 and 230 msec further progressively lengthen V-A conduction time (&-As) to 420 and 540 msec, respectively, and induce sustained A-V nodal reentrant tachycardia of fhe fast-slow form (arrow). Retrograde A-V nodal conduction time (HTAP) is 300 and 330 msec, respectively. Note the Ae-H/H-Ae ratio is less than 1 during tachycardia. Abbreviations as in Figure 2.

NODAL

REENTRANT

mser,

ET AL.

nodal reentrant tachycardia. The determination of the anterograde effective refractory period of the slow A-V nodal pathway was limited by atrial refractoriness. Premature atrial stimulation at a shorter atrial pacing cycle length of 450 msec and rapid atria1 stimulation up to 250 beats/min also failed to elicit an atria1 echo phenomenon or A-V nodal reentrant tachycardia. In contrast, the corresponding Vi-Vs, Ai-Az and Vi-Vz, Vz-A2 curves were smooth (Fig. 10B). Note the relatively long V-A conduction time during basic ventricular driving (Vi-Al = 310 msec) and the progressive increase in V-A conduction time (Vs-As) as the ventricular premature coupling interval (VI-V,) gradually shortened, characteristic of retrograde conduction by way of the A-V node-His-Purkinje system. The retrograde His bundle potential (Hz) secondary to ventricular premature depolarization (Vs) could be recorded between ventricular premature coupling intervals (Vi-Vs) of 310 and 290 msec. Retrograde A-V nodal conduction time (Hz-As) ranged from 270 to 280 msec. Because of the smooth V-A conduction curve (Vi-V2, Al-As) and relatively long retrograde A-V nodal conduction time, it was concluded that the slow A-V nodal pathway was used exclusively for V-A conduction. The retrograde effective refractory period of the slow A-V nodal pathway was 280 msec. The fast A-V nodal pathway had a retrograde effective refractory period longer than that of the slow A-V nodal pathway and its exact value could not be measured. Between ventricular premature coupling intervals (Vi-V,) of 470 to 290 msec, ventricular premature depolarizations (Vz) constantly elicited sustained A-V nodal reentrant tachycardia of the fast-slow form. The representative tracings corresponding to Figure 10, A and B, are shown in Figures 11 and 12. Note that the A-V

nodal reentrant tachycardia inducedduring ventricular premature stimulation had an Ae-H/H-Ae ratio of less than 1, indicating anterograde conduction over a fast A-V nodal pathway and retrograde conduction over a slow A-V nodal pathway (Fig. 12, A to C). The fast-slow form of A-V nodal reentrant tachycardia could also be triggered by a decrease in the ven-

msec, FIGURE 10. Case 6. A, AI-As. HI-H2 and A,-A2, As-H2 curves during high right atrial pacing at a cycle length of 650 msec. Note discontinuity due to a sudden increase in A-V nodal conduction time (A&12) at a premature coupling interval of 340 msec. SoEd circles represent responses without atrial echoes. No atrial echo phenomenon or A-V nodal reentrant tachycardia can be induced (see text). B, VI-V2. AI-A2 and VI-V2, V2-A2 curves during right ventricular pacing at a cycle length of 650 msec. Solld circles represent responses without ventricufar echoes; open d&es represent responses with ventricular echoes. Retrograde His bundle potentials (H-) are depicted as open trlangles. Both VI-Vs. Al-A:, and VI-Vs. VrAs curves are smooth. Note the relatively long V-A ccnduction time duing basic cklving (VI-A1 = 310 msec). Retrograde A-V nodal conduction time (HTA2) ranges from 270 to 280 msec. Induction of sustained A-V nodal reentrant tachycardia of the fast-slow form coincides with the entire ventricular echo zone between premature coupling intervals (V,-V2) of 470 and 290 msec. Abbreviations as in Figure 1.

TACHYCARDIA-SUNG

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The Amerfcan Journal ot CARDlOLOGY

Vahrmc, 42

411

ATRIOVENTRICULAR

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NODAL REENTRANT TACHYCARDIA-SUNG

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AL FIGURE 11. Same patient. Atrial premature stimulation without induction of A-V nodal reentrant tachycardia of either form. The high right atrium was driven at a cycle length (Sf-S,) of 650 msec. A, an atrial premature beat at a coupling interval (S&) of 350 msec lengthens the A-H interval from 70 to 130 msec. 6, an atrial premature beat at a coupling interval (S,-S,) of 340 msec suddenly increases the A-H interval to 210 msec, resulting in discontinuous A-V nodal conduction curves (AI-AZ, H,-H2) (Fig. lOA). No atrlal echo phenomenon or A-V nodal reentrant tachycardia can be induced by further shortening of the atrial premature coupling interval (S1-Sr). Abbreviations as in Figure 2.

FIGURE 12. Same case. Ventricular premature stimulation with induction of the fast-slow form of A-V nodal reentrant tachycardla. The right ventricle is driven at a cycle length of 650 msec. V-A conduction time is relatively long during basic driving (VI-A, = 310 msec). A to C. ventricular premature beats (Sz) at coupling intervals of 470, 400 and 300 msec induce retrograde atrial activation with a progressive prolongation of V-A conduction time ($-A* = 330,360 and 450 msec, respectively). The corresponding VI-Vs, Al-As and VI-VP, VTAl curves are smooth (Fig. 1OB). In each instance, retrograde atrial activation is followed by development of a ventricular echo phenomenon and inductionof SustaiMd A-V nodal reentrant tachycardia of the fast-slow form (arrow). Retrograde A-V nodal conduction time (Hz-As) is 270 msec (C). The Ae-H/H-A8 ratio is less than 1 during tachycardia. Abbreviations as in Figure 2.

tricular pacing cycle length in three of the five patients. Two examples are shown in Figure 13, A and B. This response indicated that cycle length shortening, possibly by facilitating retrograde block in the fast A-V nodal pathway and prolonging retrograde conduction time in the slow A-V nodal pathway, favored the initiation of the fast-slow form of A-V nodal reentrant tachycardia in these patients.

Discussion Dual A-V nodal pathway conduction: Both animal and human experiments have demonstrated that the A-V node can undergo functional longitudinal dissociation into two conducting pathways differing in electrophysiologic properties.3-6>g-14Jep2s-a1 These two A-V nodal pathways converge proximally as well as distally to form proximal and distal common pathways. An atrial or ventricular premature impulse may thus induce a reentry mechanism utilizing one pathway for anterograde conduction and the other pathway for 412

September 1976

The Amerkan

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retrograde conduction, or vice versa, with initiation of an atrial or ventricular echo phenomenon or sustained A-V nodal reentrant tachycardia. Induction of sustained A-V nodal reentrant tachycardia during programmed ventricular stimulation has rarely been observed in man.15J6Js It occurred in 8 of our 42 patients with paroxysmal supraventricular tachycardia associated with dual A-V nodal pathway conduction. Two distinct forms of A-V nodal reentrant tachycardia could be clearly differentiated-the slowfast form using a slow A-V nodal pathway for anterograde conduction and a fast A-V nodal pathway for retrograde conduction (Ae-H/H-Ae > l), and the fastslow form with a tachycardia circuit of the reversed direction (Ae-H/H-Ae Q 1). In this study we demonstrated that both forms of A-V nodal reentrant tachycardia can be elicited from the atria as well as from the ventricles. The fast-slow form of A-V nodal reentrant tachycardia frequently presents as a “permanent” form of

Volurna 42

ATRIOVENTRICULAR

NOOAL REENTRANT TACHYCARDIA-SUNG

ET AL.

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FIGURE 13. Same case. induction of the fast-slow form of A-V nodal reentrant tachycardia with ventricular pacing at shorter cycle lengths without delivery of ventricular premature stimulation. S represents the ventricular pacing stimulus. A, the right ventricle is driven at a cycle of 450 msec. The fourth and flfth pacing stimuli not only capture the ventricle but also induce V-A conduction with a relatively long V-A conduction time (X? msac and 350 msec, respectively [in parentheses]), suggesting retrograde conduction over a slow A-V nodal pathway. After the ffflh pacing stimulus, a sustained A-V nodal reentrant tachycardia of the fast-slow form is initiated (arrow). The Ae-H/H-Ae is less than 1 during tachycardia. 6, the right ventricle Is driven at a cycle length of 490 msec. l-l- indicates retrograde His bundle potentials. The three pacing stimuli all capture the ventricle and Induce V-A conduction. There is an atypical Wenckebach periodicity of the V-A conduction time (140, 210 and 420 msec, respectively [in parentheses]), followed bydevelopment of a sustained A-V nodal reentrant tachycardia of the fast-slow form (arrow). The Ae-H/H-Ae ratio is less than 1 durlng tachycardia. The sudden increase In V-A conduction time corresponding to the third ventricular captured beat is believed to be due to a failure of retrograde conduction over the fast A-V nodal pathway (retrograde unidirectional block) with resultant conduction over the slow A-V nodal pathway.

supraventricular tachycardia.7 It resembles, electrocardiographically, an ectopic atria1 tachycardia and probably occurs more commonly in children than in adults.7 Using the technique of atrial and ventricular premature stimulation,Coumel et al.7v32 postulated A-V nodal reentry as the underlying mechanism. Of note, Satake et al20 could demonstrate the occurrence of both anterograde and retrograde dual A-V nodal pathway conduction in the same patient, and Wu et a1.16documented the association of sustained A-V nodal reentrant tachycardia of this form with discontinuous V-A conduction curves (VI-Vs, Al-As). During programmed atrial premature stimulation, recording of the His bundle potential illustrated that a sudden increase in A-V nodal conduction time (A-H) is the cause of discontinuity in the anterograde A-V conduction pattern. This suggested that failure of an anterograde fast A-V nodal pathway is followed by conduction by way of an anterograde slow A-V nodal pathway.5-6ts-14However, during programmed ventricular premature stimulation, delineation of the exact routes of V-A conduction is frequently handicapped by the difficulty and uncertainty in recording a retrograde His bundle potential.21*26*27 In our laboratories, we routinely identify His bundle deflections of sinus beats after delivery of each ventricular premature stimulation and, accordingly, adjust the position of the recording electrode catheter whenever it is necessary.Registration of the retrograde His bundle potential at short ventricular premature coupling intervals33*34 in these eight patients was of value in helping to delineate which A-V nodal pathway was utilized for V-A conduction and, more importantly, provided significant information pertaining to the understanding of the mechanisms of ventricular echo phenomenon and retrograde initiation of A-V nodal reentrant tachycardia in man.

A-V nodal reentrant tachyeardia initiated during programmed atria1 premature stimulation: The

slow-fast form of A-V nodal reentrant tachycardia may be elicited by an atria1premature beat if the fast A-V nodal pathway has an anterograde effective refractory period longer than that of the slow A-V nodal pathway. Its occurrence is associated with discontinuous anterograde A-V nodal conduction curves (Al-As, HI-HZ) and requires achievement of a critical A-V nodal conduction delay (A-H) with failure of anterograde conduction by way of the fast A-V nodal pathway and resultant conduction by way of the slow A-V nodal pathway (Fig. 14A).3-69g-14 On the other hand, initiation of the fastslow form of A-V nodal reentrant tachycardia during atria1premature stimulation is only possible when the slow A-V nodal pathway has an anterograde effective refractory period longer than that of the fast A-V nodal pathway. In this situation, the anterograde effective refractory period of the slow A-V nodal pathway cannot be measured, and all the atrial impulses will be exclusively conducted over the fast A-V nodal pathway in the anterograde direction, thus producing a smooth A-V nodal conduction curve (Al-A2, HI-Hs). The critical A-V nodal conduction delay (A-H) required for induction of an atria1echo phenomenon or A-V nodal reentrant tachycardia, or both, may be only minimal because it will be within the range of anterograde conduction time of the fast A-V nodal pathway (Fig. 14B). Ventricular echo phenomenon and A-V nodal reentrant tachycardia initiated during programmed ventricular stimulation: In addition to the

proposed mechanism of intraventricular reentry involving the His-Purkinje system,35v36 a ventricular echo phenomenon may occur as a result of delayed retrograde conduction of a ventricular premature depolarization within the A-V node.1gT2a31 The presence of dual A-V

September 1979

The American Journal of CARMOLCGY

Volume 42

413

ATRIOVENTRICULAR

AI

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NODAL REENTRANT TACHYCARDIA-SUNG

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ET AL.

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FIGURE 14. Diagrammatic representation of induction of two different forms of A-V nodal reentrant tachycardia (RT) during programmed atrial (A and B) and ventricular (C, D and E) premature stimulation. A, B, C, D and E correspond to Figures 2C, 78, 3C, 12A and 9B. respectively (see text). At = atrium; AVN = A-V node; V = ventricle. AI and VI are basic atria1 and ventricular drives, respectively. A2 and V2 are atrial and ventricular premature complexes, respectively. Ae and Ve represent atrial and ventricular echoes, respectively. Type I and Type II RT = the slow-fast and fast-slow form, respectively, of A-V nodal reentrant tachycardia.

nodal pathways differing in electrophysiologic properties in a retrograde direction favors the occurrence of the ventricular echo phenomenon. If the slow A-V nodal pathway has a retrograde effective refractory period longer than that of the fast A-V nodal pathway, V-A conduction proceeds exclusively over the fast A-V nodal pathway during programmed ventricular premature stimulation, producing a smooth V-A conduction curve (VI-V2, AI-AZ). At critical premature coupling intervals, a ventricular premature beat, being blocked retrograde in the slow A-V nodal pathway, is conducted over the fast A-V nodal pathway in the retrograde direction and may, in turn, activate the slow A-V nodal pathway in the anterograde direction, resulting in a ventricular echo beat. This ventricular echo phenomenon, when perpetuated, leads to the slow-fast form of A-V nodal reentrant tachycardia, using the fast A-V nodal pathway for retrograde conduction and the slow A-V nodal pathway for anterograde conduction (Fig. 14C). If the slow A-V nodal pathway has a retrograde effective refractory period shorter than that of the fast A-V nodal pathway, V-A conduction proceeds either exclusively over the slow A-V nodal pathway or over the

414

September 1978

fast A-V nodal pathway at long premature coupling intervals but over the slow A-V nodal pathway at short premature coupling intervals. In the former situation, exclusive V-A conduction over the slow A-V nodal pathway produces a smooth V-A conduction curve (VI-V2, Al-AZ). In the latter situation, failure of retrograde propagation over the fast A-V nodal pathway followed by a shift in conduction in a retrograde direction over the slow A-V nodal pathway results in a sudden increase in V-A conduction time and, subsequently, discontinuous V-A conduction curves (VI-V2, AI-AZ). In both situations, a ventricular premature beat, being blocked retrograde in the fast A-V nodal pathway, is conducted over the slow A-V nodal pathway in a retrograde direction, and may, in turn activate the fast A-V nodal pathway in an anterograde direction, resulting in a ventricular echo beat. This ventricular echo phenomenon, when perpetuated, leads to the fast-slow form of A-V nodal reentrant tachycardia using the slow A-V nodal pathway for retrograde conduction and the fast A-V nodal pathway for anterograde conduction (Fig. 14, D and E). A decrease in the ventricular pacing cycle length seems to facilitate initiation of either type of A-V nodal reentrant tachycardia. This is because a shorter ventricular pacing cycle length tends to prolong retrograde conduction time in one A-V nodal pathway and may simultaneously lengthen the retrograde effective refractory period in the other A-V nodal pathway (development of retrograde unidirectional block).37 Widening of the ventricular echo zone or self-induction (requiring no ventricular premature stimulation) of A-V nodal reentrant tachycardia of either form may thus be observed at shorter ventricular pacing cycle lengths (Fig. 3D, 5C and 13, A and B). Electrocardiographic differentiation: In the slow-fast form of A-V nodal reentrant tachycardia, the retrograde P wave usually coincides with the QRS complex, hardly discernible from the surface electrocardiogram.15p3sThis is because the retrograde fast A-V nodal pathway is used for retrograde atria1 activation at a time when the impulse is also being transmitted in an anterograde direction to the ventricles. In contrast, when the slow A-V nodal pathway is used for retrograde atria1 activation, as in the fast-slow form of A-V nodal reentrant tachycardia, the retrograde P wave is inscribed far behind the QRS complex. Differential diagnosis between the fast-slow form of A-V nodal reentrant tachycardia and reciprocating tachycardia using the A-V node-His-Purkinje system for anterograde conduction and a concealed accessory A-V bypass tract for retrograde conduction (concealed Wolff-Parkinson-white syndrome) then becomes necessary because the retrograde P wave in the latter situation is also inscribed after the QRS complex. Our previousz2 and current observations indicate that the fast-slow form of A-V nodal reentrant tachycardia has an R-P interval longer than that of the P-R interval, whereas in reciprocating tachycardia related to a concealed accessory A-V bypass tract, the R-P interval is shorter than the P-R interval. Long and short R-P intervals during the

The American Journal ol CAFtDlOLOGY Volume 42

ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA-SUNG

tachycardia, under these circumstances, reflect retrograde atria1 activation through a slow A-V nodal pathway and a fast conducting A-V bypass tract, respectively. However, cardiotonic or antiarrhythmic medications, such as digitalis, propranolol, quinidine or procainamide, and physiologic alterations, such as hypoxia and ischemic processes, may influence the conduction properties of both the A-V node and the accessory bypass tract. Consequently, the characteristics described for each type of tachycardia may be ob-

ET AL.

scured. Electrophysiologic study with intracardiac recordings may be necessary for delineating the underlying mechanisms in certain patients. Acknowledgment We express our appreciation to Dr. Henry Gelband for critical review of the manuscript, to Mr. Francisco GarciaMantes for technical assistance and to Mrs. Patricia Zenos and Mrs. Vivian Hixon for the secretarial work.

References 1. Bigger JT Jr, Doldreyer BN: The mechanism of supraventricular tachycardia. Circulation 42:673-686, 1970 2. Goldreyer BN, Bigger JT Jr: Site of reentry in paroxysmal supraventricular tachycardia in man. Circulation 43:15-26, 1971 3. Denes P, Wu D, DNngra RC, et d: Demonstration of dual A-V nodal pathways in patfents wfth paroxysmal supraventricutar tachycardii. Circulation 48549-555, 1973 4. Wu D, Denes P, Dkingra RC, et al: The effects of propranolol on induction of A-V nodal reentrant paroxysmal tachycardia. Circulation 50:665-677, 1974 5. Wu D, Wyndam CRC, Arm&y-Leon R, ef al: The effects of ouabain on induction of atrioventricular nodal reentrant paroxysmal supraventricular tachycardia. Circulation 52:201-207, 1975 a.Denes P, Wu D, Dhfngra RC, et al: Dual atrioventricular nodal pathways. A common electrophysiological response. Br Heart J 37:1069-1076, 1975 7. Coumel P: Junctional reciprocating tachycardias. The permanent and paroxysmal forms of A-V nodal reciprocating tachycardias. J Electrocardiol 6:79-90, 1975 a. Weffens HJJ, Durae DR, Uem KL, et al: Effect of digitalis in patients with paroxysmal atrioventricular nodal tachycardia. Circulation 52:779-768,1975 9. Wu D, Denes P: Mechanisms of paroxysmal supraventricular tachycardia. Arch Intern Med 135437-442, 1975 10. Neuss H, w M, spies HF: Effects of heart rate and atropine on “dual A-V conduction”. Br Heart J 37: 1216-1227, 1975 11. Touboul P, Huerta F, Porte J, et al: Reciprocal rhythm in patients with normal electrocardiogram: evidence for dual conduction pathways. Am Heart J 91:3-10, 1976 12. Bfawf JK, de Soyza N. Kane JJ, et al: Atrioventricular conduction patterns in patients with paroxysmal supraventricular tachycardia. Am Heart J 91:287-291.1976 13. Barold SS, Coumel P: Mechanisms of atrfoventricular junctional tachycardia. Role of reentry and concealed accessory bypass tracts. Am J Cardiol 39:97-106. 1977 14. Josephson ME, Kastor JA: Supraventricular tachycardia: mechanisms and management. Ann Intern Med 87:346-354, 1977 15. Wellens HJJ, Durrer D: The role of an accessory atrioventricular pathway in reciprocal tachycardia. Observations in patients with and without the Wolff-Parkinson-White syndrome. Circulation 52:58-72,1975 16. Wu D, Denes P, Amat-y-Leon F, et al: An unusual variety of atrioventricuiar nodal reenby due to refrograds dual atrioventricular nodal pathways. Circulation 5650-59, 1977 17. Denes P, Wu D, Amat-y-Leon F, et al: The determinants of atrioventricular nodal reentrance wlth premature atrial stimulation in patients with dual A-V nodal pathways. Circulation 58:253-259, 1977 18. Sung RJ, Castellanos A, Styperek J, et al: Initiation of an unusual form of A-V nodal reentrant tachycardia by atrial and ventricular premature stimulation (abstr). Circulation 56:Suppl lll:lll-105, 1977 19. Schullenfaurg RY, Durrr D: Ventricular echo beats in the human heart elicited by induced ventricular premature beats. Circulation 11~337-347, 1969 20. Satake S, HefJlma K, Sakamoto Y, et ak Demonstration of bidirectional dual A-V nodal pathways in the same patient. J Electro-

cardiol 10:71-76, 1977 21. Sung RJ, Cadellanos A, Malton SM, et al: Mode of initiation of reciprocating tachycardia during programmed ventricular stimulation in the Wolff-Parkinson-White syndrome. With reference to various patterns of ventriculo-atrial conduction. Am J Cardlol 40~24-31, 1977 22. Sung RJ, Befband H, Castellanos A, et al: Clinical and electrophysiological observations in patients with concealed accessory A-V bypass tracts. Am J Cardfol40:839-847, 1977 23. Scherlaa BJ. Lau SH. HeHant RH. et al: Catheter techniaue for recording His bundle activity in. man. Circulation 39: i3-18, 1969 24. Castellanos A Jr, .Castlllo CA, Agha AS, et al: His bundle electrograms in patients with short P-R intervals, narrow QRS complexes, and paroxysmal tachycardias. Circulation 43:667-878. 1971 25. AkMar M, Datnato AN, BatsMrd WP. ef al: A comparative analysis of antand retrogade conduction patterns in man. Circulation 52786-778.1975 28. Wellens HJJ, Durrer D: Patterns of ventriculo-atrial conduction in Wolff-Parkinson-White syndrome. Circulation 49:22-31, 1974 27. Svenaon RH, Miller HC, Gallagher JJ, et al: Electrophysiological evaluation of the Wolff-Parkinson-White syndrome: problems in assessing antwade and retrograde conduction over the accessory pathway. Circulation 52552-582, 1975 28. Rosenbluuth A: Ventricular “echoes”. Am J Physiol 195:53-60, 1958 29. Moe OK, Preston JB, Burfkigfon H: Physiologic evidence for a dual A-V transmission system. Circ Res 4:357-375, 1958 30. Men&z C, Han J, Garcia de Jafon PD, et al: Some characteristics of ventricular echoes. Circ Res 16:562-581, 1965 31. Mender C, Moe OK: Demonstration of a dual A-V ncdal conduction system in the isolated rabbit heart. Circ Res 19:378-393, 1966 32. Cwmel P, Cabrol C, Fabiato A, et al: Tachycardie permanente par rhythme reaproque. I. Preuves du diagnostic par stimulation auriculaire et ventriculaire. Arch Mal Coeur 60: 1830-1849, 1967 33. Castlllo CA, Castellanos A Jr: Retrograde activation of the His bundle during intermittent paired ventricular stimulation in the human heart. Circulation 43:1079-1092. 1970 34. Castellanos A, Sung RJ, Ghahramani A, et al: The retrograde His bundle deflection: its recognition and value In the analysis of tachyarrhythmias induced by stimulation on the T wave. Eur J Cardfol4:295-302, 1976 35. Akhtar M, Damato AN, Batsford WP. et al: Demonstration of reentry within the His-Purkinje system in man. Circulation 50: 1150-1162.1974 36. Akhtar Mi Damato AN, Ruskin JN, et al: Characteristics and coexistence of two forms of ventricular echo phenomena. Am Heart J 92:174-182, 1976 37. Denes P, Wu D, Dhlngra RC, et al: The effects of cycle length on cardiac refractory periods in man. Circulation 49:32-41, 1974 38. Wu D, Denes P, Amat-y-Leon F, et al: Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventriculartachycardii. Am J Can.90141:1045-1051, 1978

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