Paroxysmal Nonreentrant Supraventricular Tachycardia Due to Simultaneous Fast and Slow Pathway Conduction in Dual Atrioventricular Node Pathways

456 lacc Vol. 10, No.2 DIAGNOSTIC STUDIES Paroxysmal Nonreentrant Supraventricular Tachycardia Due to Simultaneous Fast and Slow Pathway Conduction in Dual Atrioventricular Node Pathways SUNG SOON KIM, MD, FACC,* ROOP LAL, MD, FACC, RODOLPHE RUFFY, MD, FACC St. Louis, Missouri Electrophysiologic studies were performed on a 49 year old woman who hall paroxysmal nonreentrant supraventricular tachycardia due to simultaneous anterograde conduction through dual atrioventricular (AV) node pathways. Slow pathway conduction was inversely related to the preceding sinus cyclelength and fast pathway conduction was determined by the Hs-A interval (measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial electrogram). Major determinants of sustained simultaneous anterograde fast and slowpathway conduction duringsinus rhythm were 1) a retrograde unidirectional block in both fast and slow pathways, and 2) a critical conduction delay in the slow pathway and a long enough Hs-A interval to allow sequential conduction of impulse from both pathways. Flecainide was successful in preventing recurrences of the tachycardia by eliminating slow path. way conduction during long-term follow-up. (1 Am Coil Cardiol1987;lO:456-61) Simultaneous anterograde fast and slow pathway conduction has been reported in patients who have dual atrioventricular (AV) node pathways (1-3). This phenomenon was previously reported to occur primarily during rapid atrial pacing or premature atrial stimulation, whereas sustained simultaneous anterograde fast and slow pathway conduction was rarely observed during sinus rhythm (4-6), This report describes a case of paroxysmal nonreentrant supraventricular tachycardia due to sustained simultaneous anterograde fast and slow pathway conduction over dual AV node pathways, treated successfully with flecainide, We also attempt to define the electrophysiologic determinants of sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm. Case Report The patient was a 49 year old woman admitted to the hospital for elective rectal surgery. After an uneventful operation, paroxysmal supraventricular tachycardia and inter- mittent 2:1 AV block were observed during her recovery. The medical history included frequent episodes of palpitation for several years, lasting from a few minutes to V2 hour. The patient had no known cardiac disease and was taking no medication. Her cardiovascular examination, chest X ray film and M-mode and two-dimensional echocardiograms were normal. The 12 lead electrocardiogram (ECG) at rest was normal except for occasional' 'blocked atrial premature beats. " Review of the patient's arrhythmias. Twenty-four hour, ambulatory ECG monitoring after surgery showed multiple paroxysmal episodes of both narrow and wide QRS tachycardia with one P wave for two QRS complexes (Fig. IA). Additional rhythm strips revealed sinus rhythm with a very prolonged PR interval (0.6 second), alternating double ventricular responses and nonconducted P waves (Fig. IB), and sinus rhythm with occasional "blocked atrial premature beats" (Fig. l C). These features suggested a diagnosis of simultaneous fast and slow pathway conduction in dual AV node pathways. From the Jewish Hospital at Washington University Medical Center, Cardiology Division, 216 S. Kingshighway, SI. Louis, Missouri 63110. *Present address: Cardiology Division, Yonsei University College of Medicine, c.p.a. Box 8044, Seoul, Korea. Manuscript received August II, 1986; revised manuscript received December 17, 1986, accepted January 9, 1987. Address for reprints: Rodolphe Ruffy, MD, Jewish Hospital at Washington University Medical Center, Cardiology Division, 216 S. Kingshighway, SI. Louis, Missouri 63110. 1987 by the American College of Cardiology Electrophysiologic Studies After the patient provided written informed consent, electrophysiologic studies were performed using standard techniques with the patient in the postabsorptive, unmedicated state, Pacing techniques included incremental atrial pacing until the development of second degree AV node block, 0735-1097/87/$3.50

lacc Vol. 10. No.2 KIM ET AL. 457 :n: li: l ' t.- ' ;;- ~I - ~ ~ r-r-' :,,1 I 1-, ' \ ~,,!, ~ r. I - t; ".! : :,., -: r":'j _, 1_ l-. ' I! : " ~ ~'kt~-1 B '-! 1-4. I : l- :~ ".' ~ I '~ I d ~ i i' I :,..i '-". i i,!,i ', : : :. I!..,, I i 1-. i... I' j., ~ ;, : c ",..",. :.,.. r!' I " I I r ~1, I t " I I, '! ' ;., ; : :. t ',. : i i.. :.., '; ; - 1, -, Figure I. Noncontinuous electrocardiographic (ECG) stnps ot lead VI (A) and II (B,C). A, Each P wave is associated with two QRS complexes. Note the "bigeminal" distribution of the QRS complexes and the brief period of aberrancy in the second halfof the strip. B, Sinus rhythm with a long PR interval (0.6 second) followed by alternating (2: I) double ventricular responses as the sinus cycle length has shortened to 700 ms. The eleventh sinus P wave is blocked unexpectedly. C, Frequent "blocked atrial premature beats." See text for discussion and explanation. single atrial extrastimulation during atrial pacing at a cycle length of 500 ms and incremental ventricular pacing. Observations during sinus rhythm. During sinus rhythm all the clinically recorded arrhythmias and conduction abnormalities were observed. At a cycle length of ::::790 ms, Figure 2. Sustained simultaneous anterograde fast andslow pathway conduction shifting to sustained slow pathway conduction as the Hs-A interval decreased to 220 ms or less (asterisks). Shown from top to bottom are surface electrocardiographic (ECG) lead VI, intracardiac recordings from the high right atrium (HRA), bundle of His region (HBE) and right ventricular apex (RV) and time lines (T). A = atrial electrogram; Hf = His potential from fast pathway conduction; Hs = His potential from slow pathway conduction; V = ventricular electrogram. The Hs-A interval was measured from the H potential due to slow pathway conduction to the onset of the next atrial electrogram (A) at the His bundle level. On the ladder diagram, A, AV, HB, HP and V represent the atrium, the atrioventricular (AV) node, the His bundle, the His-Purkinje system and the ventricle, respectively. The solid and dashed linesrepresent fastandslow AV node pathway conduction, respectively. each atrial impulse was followed by two ventricular responses. The AH interval of the first QRS response (AHf) measured 110 to 130 ms and that of the second QRS response (AHs) measured 540 to 550 ms. A His potential was recorded before each QRS complex with a constant HV interval of 40 ms (Fig. 2). These findings were indicative of sustained simultaneous fast and slow AV node pathway conduction. The conduction pattern shifted to sustained exclusive slow pathway conduction as the Hs-A interval decreased from 250 to 220 ms (Hs-A intervals were measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial deflection observed from the His bundle electrogram). This decrease in Hs-A interval was the result of a shortening of the sinus cycle length from 790 to 770 ms and a slight increase in slow pathway conduction time from 540 to 550 ms. As the sinus cycle length decreased further to 740 ms, Wenckebach periodicity occurred in the slow pathway (Fig. 3). At sinus cycle lengths shorter than 700 ms, alternating (2: I) simultaneous fast and slow pathway conduction was observed. During such alternating conduction, facilitated conduction over the slow pathway after a long cycle resulted occasionally in a critically short Hf-Hs interval (measured between the two His potentials due to fast and slow pathway conduction of the same atrial impulse), producing block of the impulse below the His bundle (the seventh atrial impulse in Fig. 3). This concealed phenomenon, however, interfered with subsequent AV conduction, producing an inappropriately nonconducted sinus P wave, or pseudo-av block on the surface recording (Fig. IBand 3). In addition, sustained double ventricular responses to a single atrial impulse were on occasion limited by His-Purkinje refractoriness. Figure 4 depicts sustained simultaneous anterograde dual AV node pathway conduction induced by atrial pacing at a cycle length of 550 ms. However, only a single ventricular response with a short PR interval was observed until the Hf-Hs interval had lengthened beyond the effective refractory period of the His-Purkinje system as a result of deeremental conduction over the slow pathway. In this range of cycle lengths, the His-Purkinje effective refractory period VI,,--'\r-----..r--~', -"""\r-----..',---... r--- "I,r_---_./----v_---~r_---v_- T I I I I I I I I t I I I I I I I r I I I I I, I I I I I I I I Hs-A A AV HB -~~"--J, n;;~\:-:rip<--hil?i'_"'_hrir~~...--'--'-"'---t-:l~:...:..><'--~~--'-=--_+_:r~~'--~""77'o---'-"<><--t;;_;:, Hp --+=--+'-"'---+o'=-----\,.=--+'-"'--+=-----1-'-'''-------l,.,..,..-----+-'''''-----+'-'''-----+'"'''-- V_---L. L.-_...J..._--L-_----L...L- --J....L--...J- L.-...J--_

458 KIM ET AL. SIMULTANEOUS FAST ANDSLOWPATHWAY CONDUCTION JACC Vol. 10, No, 2 VI -v----"""'v,..------..r----"""'v~----""""\v V~--------V,..----------,v,..--~ A A A A A A ~--,~...----'f1 HRA --v;\ J h t------'4 II~-~ A Hs J HBE ijj:~ H~I1t A~tY;'--_--"N-\ '-_~f', ---IA~J'--_lo\- RV +----\I'-----i,I'-----v------v...,-----i1I'-------'v-------..v------,/,r- " T I I I 111 I I I t I I I I I r----iooo ms---l I I I I I, I I I I I I I I I Hs-A -r-----:;-:;-;::;--=-=r---:;:;~=r :;=...:...:.=_r_- ::;_;c~----.,-~=:_"_",,=-_r_-=-'-"-"t_--=-=c::_-r---- A-\-::-:-----'--::"::'::---\--:::----'-:7:= ~----''-=!:'::_= \o.::-~----\o-::= ~:''::---_+:_----C~--k-~~-k_~~~,.,.._-::c==- AV HB ---...;:.,,...---::=---''""r--~~~-.:=--\-:...::...,,~..:::..-,.- ;<""";;_::::_--;:-::::...:-:~~-_=~--t-=-;=-''--r_ HP V -----T-'-''---------r-'"-----\-=--------'P----'P-----\-~-=--------P'----r''' -L- '-- --'- ----'" ---J'-- ---' ---'- --Lcould be precisely measured to be 410 ms. On a surface ECG, this concealed phenomenon would have appeared as sustained exclusive fast pathway conduction. Sustained simultaneous fast and slow pathway conduction could also appear as exclusive slow pathway conduction with a long PR interval on the surface ECG because of His-Purkinje block after each fast AV node pathway conduction (Fig. 5). Finally, Figure 6 shows that the' 'blocked atrial premature beats" illustrated in Figure lc were, in fact, single AV node (slow-fast) echoes with an HA interval of 80 ms and a low to high atrial sequence occurring with or without a ventricular response. Sustained AV node reentrance, however, was not observed. Observations during programmed electrical stimulation. Incremental atrial pacing demonstrated alternating (2: 1) simultaneous fast and slow pathway conduction at pacing cycle lengths of 600,550 and 500 ms. Shorter pacing cycle lengths were associated with 1:1 exclusive fast AV node pathway conduction; at a cycle length of 350 ms, AV node Wenckebach periodicity occurred. Standard single atrial extrastimulation testing was impossible during sinus rhythm as well as during atrial pacing at cycle lengths of 600 and 500 ms because of intermittent anterograde slow pathway conduction. Modified single atrial extrastimulation was performed during atrial pacing at a cycle length of 500 ms. At this cycle length, alternating simultaneous anterograde fast and slow pathway conduction was associated with an AH J interval of 100 ms and an AHs interval of 550 ms with the Figure 3. Wenckebach periodicity in the slow pathway and 2: I simultaneousfast and slow pathway conduction. As the sinus cycle length decreased from 740 to 670 ms, Wenckebach periodicity occurred in the slow pathway, followed by 2: I simultaneous dual AV node pathwayconduction. The seventh atrial impulse produced two His bundle responses due to simultaneous fast and slow pathway conduction but the second ventricular response did not follow the slow pathway conduction because of a short Hf-Hs interval (410 ms). Note that the eighth sinus beat was blocked because of refractorinessof both pathways secondary to concealed conduction of the preceding slow pathway conduction. Abbreviations as in Figure 2. H,-Hs interval being 450 ms (Fig. 7). Atrial extrastimuli were delivered after fast pathway conduction. At A 1-A2 intervals :::::450 ms an H 2 response could not be elicited because the impulse (A J ) carried over the slow pathway always preempted the His bundle (Hs) (Fig. 7). At A,-A 2 Figure 4. Apparentexclusive fast pathway conduction. Atrial pacing at a cycle length of 550 ms was associated with alternating (2: I) simultaneousfast and slow pathway conduction. Termination of pacing was followed by sustained simultaneous dual AV node pathway conduction. However, the impulse carried over the slow pathway could not reach the ventricles because of His-Purkinje refractoriness until the Hf-Hs interval lengthened to 420 ms (asterisks). Note the intermittent rate-dependent left bundle branch block on the surface electrocardiogram (the second, fourth and last two QRS complexes). S = stimulation artifact; other abbreviations as in Figure 2. VI -,r----.,----,,.-----,---,,.-----""""ir-----'r----'/'-------..r--, T I I I I I I I I I I I I I I I I I,, I,, f, Hs-A 440 A 940 >----1000 ms---l I I I I I I I I Itt I I I I I 1 I I I, I I, 1 I I, I I I I I I It' t AV "- 500 70"" HB 430 520 HP 40 40 40 V

JACC VoL 10, NO.2 KIM ET AL. 459 HRA HBE RV T, 1 1 I I I 1 I I I I I I I I I I I I Hs-A.----=;;---''-'''-'''r--=:-'':...=.r--=::--='r---==--='T---;;-;:-;:--''-'-'T-----;:=--'''-''=r---;:;:~--=-==r---- A4r::-~=!...--~~~-~or;:_~~-4.,. ~=----4r::::_~~-4r::::_~=--~::: ~~-4 ::_- - AV HB -..,""7.=-"..,...,=-f-"-""7.::':::"-"'1~c=\r=-=..::...,---:;-;:;-;::-T"'-:-:=""...,..--,=--t='-==~"r""""":;::;;:;--t==~--=:;::---1~~:.., = 'f"~:;_""'t- Hp -A.""...---t"T,.;..-+=-:."""~~""..._---T'-"'------..-..,.,... ---F"----~,.. ---F"----,...,..,.. --'P"--l'i"l!'I'. ----\r c'a7"-_t_ V_.L..:!:>!.!L---l..~~--:::l~---L_~"'----_----l..-_~~_-L-_~"'----_-L-----'~~_L.-_~~ '' '''.:ll<..._~ Figure5. Apparent exclusive slow pathway conduction. After two sinus beats with double ventricular responses, each subsequent sinus beat was followed by a single ventricular response despite sustained simultaneous dual AV node conduction. This was initiated by a short Hs-Hf interval of 350 ms (asterisk) and perpetuated by a long-short sequence. Abbreviations as in Figure 2. intervals between 430 and 340 ms H)-H 2 intervals gradually shortened from 430 to 370 ms. At A)-A 2 intervals from 330 to 220 ms the H 1-H2 (H1-Hs) interval suddenly lengthened to 450 ms and remained constant, indicating the reappearance of slow pathway conduction of A) and block of A 2 in the fast pathway. No ventriculoatrial conduction was observed at any ventricular paced cycle lengths. Drug intervention. The intravenous administration of 2 mg of atropine sulfate decreased the sinus cycle length to 600 ms. Frequent single AV node reentrant echoes, with or without simultaneous ventricular responses, were observed. Alternating, but not sustained, simultaneous fast and slow pathway conduction was observed intermittently after atropine was given. Intravenous administration of digoxin (0.75 mg) and propranolol (0.15 mg/kg body weight) had no apparent effect on the phenomena described. The patient was ultimately treated with oral flecainide, 50 mg every 12 hours. This treatment resulted in apparent exclusive fast pathway conduction at rest and during exercise testing. There was no recurrence of nonreentrant paroxysmal supraventricular tachycardia or apparent slow pathway conduction for the next 16 months. At the last measurement, the ftecainide plasma level was 210 ng/m!. Determinants of fast and slow pathway conduction. Slow pathway conduction was inversely related to the preceding sinus cycle length (Fig. 8). The slow pathway developed Wenckebach periodicity at the unusually long cycle length of 740 ms indicative of very prolonged refractoriness. At sinus cycle lengths between 750 and 850 ms, stable slow pathway conduction was present with AHs intervals ranging from 500 to 570 ms (Hf-Hs interval 2:420 ms). At longer sinus cycle lengths (between 860 and 950 ms), the slow AV node pathway was capable of conducting impulses with shorter AHs intervals, ranging from 460 to 480 ms, resulting in critically short Hf-Hs intervals «420 ms) associated with block below the His bundle. At cycle lengths >950 ms, slow pathway conduction was no longer observed, probably because the conduction delay in the slow pathway was not sufficient to allow recovery of the distal common pathway HRA V A V v AHf,ll ~jh,flll H~~~ --8Il1~-...w.l'I~"'II------'li~I""'-+I"'----"I~~~~~- V V V V V v RV ----ill,-'-==-~t t---- '----""-----1r ~ 1---1000 ms---i HBE T 111111111111111111I11111111111111111111111111111111111111111111111111111111111111",,111"11111111"1,11,111111""11111111,,111,,1,,,,1,,,,1,11,1,,,,1,",1'11I1""1111111111111111""1'"11,,,,1",,1",,1,,,,1",,1""1""I""I" "I.J,,"I,",IJ Hs-Ae --,-=::--r--;::-:;;-~r-~;:;;::;----'---;::-;;-;;~---;:;-;:;:;:::--'-----'=:--lr-;::-;:;;:;::-:::':-- A~..,.-~~-k-~~I.,-~~---4""""":=::--J.,..,----~~4-'-'=-"'---J\o;-:-"'=".:'-:::-J- AV -~----'~~-----\r--=r-----r"'-----p'-----""r HB -~::---+=::--+=,.-----t-:;,;o;---+-----+--~r----\' HP -~!...-.-~!...-.4='----- =---------+---\-------\,--- V_-I.- -L..._-L... ---'- -1- ---'-_--'-_ Figure 6. Single AV node reentrant (slowfast) echoes with or without ventricular responses. The atrial sequence of the echo beat (Ae) was low to high and the H-Ae interval of 80 ms was fixed, whether associated with a ventricular response or not. This appeared as "blockedatrial premature beats" on the surface electrocardiogram (ECG) (arrow). The top tracing on this figure is surface ECG lead II. Hs-Ae = interval between Hs and Ae; other abbreviations as in Figure 2.

460 KIM ET AL. JACC Vol. 10, No.2 August 1987:456--61 Cf) ~ 400 I '" E 500 N I ~ 300 I 600 400 '"E ~ 300 <1: 200 100 Cycle Length' 500... o o 0 o 0 o... I I I 300 400 500 A I-A2 (rns ) Figure 7. Single atrial extrastimulation during atrial pacing at a cycle length of 500 ms. AI and HI are the right atrial and His bundle responses to the driven beats and Hs is the His bundle electrogram due to slow pathway conduction. Az and Hz are the right atrial and His bundle responses to atrial extrastimulation. The conduction curve suggests dual AV node pathways. See text for discussion. from prior activation through fast pathway. In contrast to slow pathway conduction, fast pathway conduction was determined by the Hs-A interval. This interval was a function of the preceding sinus cycle length and the slow pathway conduction time of the preceding atrial impulse (Fig. 2). Simultaneous anterograde fast and slow pathway conduction was present when the Hs-A interval was >220 ms. When the Hs-A interval measured ::;220 ms, the fast pathway was refractory. To have double ventricular responses to a single atrial impulse, the difference in conduction times between the fast and the slow pathways (Hf-Hs) had to be longer than the effective refractory period of the distal conducting system, including distal common pathway and His-Purkinje system. Figure 8. Effect of the preceding sinus cycle length (A-A) on slowpathwayconduction. A-Hs = slow pathwayconduction time; A-Hf = fast pathway conduction time; H-P = His-Purkinje. See text for discussion.... :.:.. 500 oap 0 0 A-Hs o A-Hs with H Pblock.. A-HI,,1 I I I I I I a 800 900 1000 1100 PRECEDING A-A (rns) The shortest Hf-Hs interval that allowed double ventricular responses was 420 ms (Fig. 4). Therefore, paroxysmal nonreentrant supraventricular tachycardia due to sustained simultaneous fast and slow pathway conduction during sinus rhythm was observed at sinus cycle lengths between 780 ms (Hs-A :::::240 ms, AHf 120 ms and Hf-Hs :::::420 ms) and 850 ms. Discussion Determinants of sustained simultaneous fast and slow pathway conduction. Simultaneous anterograde fast and slow pathway conduction has been observed during rapid atrial pacing or atrial extrastimulation in patients with AV node reentrant paroxysmal supraventricular tachycardia (1-3). In these patients simultaneous fast and slow pathway conduction was usually followed by a slow-fast reentrant echo or a reentrant tachycardia. A critical conduction delay as well as unidirectional retrograde block in the slow pathway have been postulated as major determining factors for this phenomenon (3). Csapo (4) and Sutton and Lee (5,6) reported four cases of dual AV node pathways in which sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm manifested itself as nonreentrant paroxysmal supraventricular tachycardia. It was suggested that nonreentrant supraventricular tachycardia was possible only when the refractory period of the distal conducting system was shorter than the shortest cardiac cycle length and unidirectional retrograde block was present in both fast and slow pathways (5). In our patient we were able to identify the electrophysiologic determinants of sustained simultaneous fast and slow pathway conduction. This conduction abnormality was maintained in a range of sinus cycle lengths associated with a critical conduction delay in the slow pathway and long enough Hs-A intervals to allow sequential conduction of impulse from both pathways. Although a discontinuous AV node conduction curve could not be demonstrated because standard programmed atrial extrastimulation could not be performed, the presence of two distinct AV node pathways was strongly suggested when modified extrastimulation testing was performed during atrial pacing at a cycle length of 500 ms. Also suggestive of dual AV node pathways was the observation of single AV node (slow-fast) echoes with or without a ventricular response. Despite the absence of ventriculoatrial conduction during ventricular pacing, the fast pathway was occasionally capable of retrograde conduction in our patient. This indicates that the reentrant circuit was confined to the AV node and that ventricular tissue was not necessary to produce reentrant echoes, in accordance with the observation of Wellens et al. (7). Because of the unreliable retrograde conduction properties of the fast pathway, our patient presented mainly with paroxysmal nonreentrant supraventricular tachycardia and

JACC Vol. 10, NO.2 KIM ET AL 461 had only rare single AV node reentrant echoes. Although such single echoes were possible, sustained AV node reentrance was not because of the unusually long refractory period of the slow pathway. The cycle length of the AV node echo was 640 ms (AH interval 560 ms, HA interval 80 ms), far shorter than the slow pathway block cycle length of 740 ms. Effects of antiarrhythmic agents. Previous investigators (4-6) have noted the unusual response to atropine sulfate and type I antiarrhythmic drugs such as ajmaline, procainamide and quinidine in patients who had nonreentrant paroxysmal supraventricular tachycardia due to sustained simultaneous conduction through dual AV node pathways. This response is probably related to the effect of such drugs on retrograde fast pathwayconduction. Our patient had more frequent single AV node reentrant echoes and no sustained simultaneous anterograde fast and slow pathway conduction after the administration of atropine, probably because the drug had improved retrograde fast pathway conduction to facilitate AV node reentrance (8). Flecainide, on the other hand, appeared to have prevented sustained simultaneous fast and slow pathway conduction by total elimination of slow pathway conduction. In patients who have a dual AV node pathway it is known that flecainide has a weak depressant effect on anterograde slow pathway conduction in addition to a marked depressant effect on the conductive properties of the retrograde limb (9,10). Because we did not repeat electrophysiologic studies during flecainide treatment' we have not confirmed that the effect of flecainide was limited to the AV node. It seems equally likely that normalization of the surface ECG may have occurred as a result of a flecainide effect on the His-Purkinje system. Because the conductive properties of the His-Purkinje system were demonstrably abnormal before flecainide administration, it is reasonable to hypothesize that flecainide, even in small amounts, may have further disabled the infra-hisian propagation of impulses occurring at relatively short coupling intervals, namely those carried over the slow pathway. Clinical implications. Simultaneous anterograde fast and slow pathway conduction may not be simply a rare electrophysiologic observation of academic interest only. In our case moderate changes in sinus rate and in fast or slow pathway conduction times resulted in a variety of ECG manifestations, simulating supraventricular and ventricular bigeminy, junctional premature beats and junctional tachycardia, ventricular tachycardia and unexplained sudden PR prolongation or unexpected (pseudo) AV block (4, II). These complex ECG manifestations could all be explained on the basis of intermittent or sustained simultaneous anterograde dual AV node pathway conduction, aberrant intraventricular conduction and concealed fast and slow pathway conduction. This recognition may also have important therapeutic implications, because the response of this type of arrhythmia to traditional type I drugs differs from the response of more common varieties of supraventricular tachycardia. In our patient, flecainide, a class IC drug, was successful in preventing recurrences of nonreentrant paroxysmal supraventricular tachycardia by maintaining apparent sustained fast pathway conduction during long-term follow-up. We thank Margie Galkowski for expert secretarial assistance and Roberta Rich and Mary Sorrells for preparation of illustrations. References L Wu 0, Denes P, Dhingra R, Pietras RJ, Rosen KM. New manifestations of dual A-V nodal pathways. Eur J Cardiol 1975;2:459-66. 2. Gomes JAC. Kang PS, Kelen G, Khan R, EI-Sherif N. Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide. Am J Cardiol 1980;46:677-84. 3. Lin FC, Yeh SJ, Wu D. Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways. Am Heart J 1985;109:963-70. 4. Csapo G. Paroxysmal nonreentrant tachycardia due to simultaneous conduction in dual atrioventricular nodal pathways. Am J Cardiol 1979;43: 1033-45. 5. Sutton FJ, Lee Yt,'. Supraventricular nonreentrant tachycardia due to simultaneous conduction through dual atrioventricular nodal pathways. Am J Cardiol 1983;51:897-900. 6. Sutton FJ, Lee yc. Paroxysmal nonreentrant tachycardia due to simultaneous conduction via dual atrioventricular nodal pathways. Am Heart J 1985;109:157-9. 7. Wellens HJJ, Wesdorp JC, Duren DR, Lie KI. Second degree block during reciprocal atrioventricular nodal tachycardia. Circulation 1976;53: 595-9. 8. Wu 0, Denes P, Bauernfeind R, Dhingra RC, Wyndham C, Rosen KM. Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia. Circulation 1979;59:779-88. 9. Hellestrand KJ. Nathan AW, Bexton RS, Spurrell RAJ, Camm AJ. Cardiac electrophysiologic effects of ftecainide acetate for paroxysmal reentrant junctional tachycardia. Am J Cardiol 1983;51:770-6. 10. Kim SS, Lal R, Ruffy R. Treatment of paroxysmal reentrant supraventricular tachycardia with ftecainide acetate. Am J Cardiol 1986;58: 80-5. I!. Rosen KM, Rahimtoola SH, Gunnar R. Pseudo A-V block secondary to premature nonpropagated His bundle depolarizations. Documentation by His bundle electrography. Circulation 1970;42:367-73.