effects of bundle branch block on experimental a-v reentrant tachycardia

8
Effects of bundle branch block on experimental A-V reentrant tachycardia Fernando Amat-y-Leon, M.D., F.A.C.C.’ Alison Blasdell, B.S. * * Steve Teague*** Kenneth M. Rosen, M.D., F.A.C.C.**** Pablo Denes, M.D., F.A.C.C.***** Chicago, Ill. Most cases of ventricular preexcitation reflect the presence of an anomalous A-V pathway, which may be located in either the right or left A-V rings, or within the atrioventricular septum.‘-” In patients with preexcitation, circus movement paroxysmal tachycardias (PSVT) usually involve the normal pathway as antegrade limb, and anomalous pathway as retrograde limb.‘-” In patients with circus movements involving retro- gradely conducting anomalous pathways, it has been suggested that development of functional bundle branch block ipsilateral to the anomalous pathway produces a slowing in the rate of parox- From the Cardiology Section, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, and West Side Veterans Administration Hospital, Chicago, Illinois. Supported in part by National Institutes of Health grant HL18794.01, United States Public Health Service training grant HL-05879-06, Basic Institutional Support West Side Veterans Administration Hospital (MRIS No. 18281, Veterans Administration grant 0363-01, and Chicago Heart Association grant A76-59, Chicago, Illinois. Received for publication Oct. 3, 1977. Accepted for publication Nov. 2, 1977. Reprint requests: Fernando Amat-y-Leon, M.D., Cardiology Section, University of Illinois Hospital, P.O. Box 6998, Chicago, Ill. 60680. *Research Associate, West Side Veterans Administration Hospital; Assistant Professor of Medicine, Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago. **Graduate Student in Physiology and Biophysics at the University of Illinois Medical Center. ‘**Senior Medical Student, Abraham Lincoln School of Medicine, University of Illinois. ****Professor of Medicine and Chief, Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medi- cine. **‘**Associate Professor of Medicine, Cardiology Section, Abraham Lincoln School of Medicine, Univemity of Illinois College of Medicine, Chicago. 62 July, 1978, Vol. 96, No. 1 ysmal tachycardia.6-‘0 It has been additionally suggested that the presence or absence of this slowing during bundle branch block could be used as a diagnostic sign for lateralization of anoma- lous pathways.6-12 Recently, Pritchett and co-workers,*3 further elucidated this phenomenon. They studied 15 patients with left free wall anomalous pathways, three patients with right free wall anomalous pathways, and four patients with presumptive septal preexcitation. Ventriculo-atria1 conduction times were increased during paroxysmal tachy- cardia when functional bundle branch block occurred ipsilateral to the location of an anoma- lous pathway. Contralateral functional bundle branch block did not affect V-A conduction during PSVT in these patients. In patients with septal anomalous pathways, neither right or left bundle branch block appeared to affect V-A conduction times during PSVT. Since the occurrence and lateralization of functional bun- dle branch block could not be controlled in the above study, it was not possible to look at the effects of both right and left bundle branch in all patients. In the present study, we extend the observa- tions of Prichett and colleagues13 by systemati- cally examining the effects of ipsilateral and contralateral bundle branch block on experi- mented A-V reentrant paroxysmal tachycardia in dogs. The experimental model utilized an anom- alous pathway simulator so that the effects of bundle branch block could be examined utilizing multiple anomalous pathway locations in the same dog. 0002-8703/78/0196-0062$00.80/O 0 1978 The C. V. Mosby Co.

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Effects of bundle branch block on experimental

A-V reentrant tachycardia

Fernando Amat-y-Leon, M.D., F.A.C.C.’ Alison Blasdell, B.S. * * Steve Teague*** Kenneth M. Rosen, M.D., F.A.C.C.**** Pablo Denes, M.D., F.A.C.C.***** Chicago, Ill.

Most cases of ventricular preexcitation reflect the presence of an anomalous A-V pathway, which may be located in either the right or left A-V rings, or within the atrioventricular septum.‘-” In patients with preexcitation, circus movement paroxysmal tachycardias (PSVT) usually involve the normal pathway as antegrade limb, and anomalous pathway as retrograde limb.‘-” In patients with circus movements involving retro- gradely conducting anomalous pathways, it has been suggested that development of functional bundle branch block ipsilateral to the anomalous pathway produces a slowing in the rate of parox-

From the Cardiology Section, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, and West Side Veterans Administration Hospital, Chicago, Illinois.

Supported in part by National Institutes of Health grant HL18794.01, United States Public Health Service training grant HL-05879-06, Basic Institutional Support West Side Veterans Administration Hospital (MRIS No. 18281, Veterans Administration grant 0363-01, and Chicago Heart Association grant A76-59, Chicago, Illinois.

Received for publication Oct. 3, 1977.

Accepted for publication Nov. 2, 1977.

Reprint requests: Fernando Amat-y-Leon, M.D., Cardiology Section, University of Illinois Hospital, P.O. Box 6998, Chicago, Ill. 60680.

*Research Associate, West Side Veterans Administration Hospital; Assistant Professor of Medicine, Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago.

**Graduate Student in Physiology and Biophysics at the University of Illinois Medical Center.

‘**Senior Medical Student, Abraham Lincoln School of Medicine, University of Illinois.

****Professor of Medicine and Chief, Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medi- cine.

**‘**Associate Professor of Medicine, Cardiology Section, Abraham Lincoln School of Medicine, Univemity of Illinois College of Medicine, Chicago.

62 July, 1978, Vol. 96, No. 1

ysmal tachycardia.6-‘0 It has been additionally suggested that the presence or absence of this slowing during bundle branch block could be used as a diagnostic sign for lateralization of anoma- lous pathways.6-12

Recently, Pritchett and co-workers,*3 further elucidated this phenomenon. They studied 15 patients with left free wall anomalous pathways, three patients with right free wall anomalous pathways, and four patients with presumptive septal preexcitation. Ventriculo-atria1 conduction times were increased during paroxysmal tachy- cardia when functional bundle branch block occurred ipsilateral to the location of an anoma- lous pathway. Contralateral functional bundle branch block did not affect V-A conduction during PSVT in these patients. In patients with septal anomalous pathways, neither right or left bundle branch block appeared to affect V-A conduction times during PSVT. Since the occurrence and lateralization of functional bun- dle branch block could not be controlled in the above study, it was not possible to look at the effects of both right and left bundle branch in all patients.

In the present study, we extend the observa- tions of Prichett and colleagues13 by systemati- cally examining the effects of ipsilateral and contralateral bundle branch block on experi- mented A-V reentrant paroxysmal tachycardia in dogs. The experimental model utilized an anom- alous pathway simulator so that the effects of bundle branch block could be examined utilizing multiple anomalous pathway locations in the same dog.

0002-8703/78/0196-0062$00.80/O 0 1978 The C. V. Mosby Co.

Poser :o:

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Frg. 1. Schematic representation of the seven anomalous pathway Iocations. Anterior, lateral, and postcr~t: mews o+’ the heart are shown. Anomalous pathway locations, both atria! and ventricular, are represented by closed cxdes. AR = anterior right; LR = lateral right; AL = anterior left; LL = left lateral; PL = pasterior left; S = posterior septum; PR = posterior right; RA = right atrium; L4 = left atrium.

Seventeen mongrel dogs weighing from 14 to 24. kilograms were premeditated with morphine sulfate (2 mg./Kg. intramuscularly) and anesthe- tized with Nembutal (30 mg./Kg. intravenously). Ventilation ‘was maintained with endotracheal intubation and a Harvard Respirator. Autonomic blockade was achieved by bilateral cervical vagot- onny and propranolol administration (1 mg./Kg. intravenously). The chest was opened through a

and the heart suspended in a

Close pairs of plunge bipolar electrodes (Teflon coated stainless steel wires of 0.003 inch diameter) were positioned at seven contiguous atria1 and ventricuiar sites around the A-V ring in order to simulate the atria1 and ventricular insertions of anomalous pathways. The following anomalous pathway sites were utilized (Fig. 1): (1) anterior right (AR) at the right atrial appendage and underdying right ventricular outflow tract; (2) posterior right (PR) at the posterior right atrium and contiguous right ventricle (just to the right of the intra-atrial and intraventricular grooves); (3)

): at a midpomt between AR and Et; (4) septum (S): at the posterior a~trioventric- ular septum (the atrial septal site was reached by plunging electrodes throu the posterior free wall of the right atrium a kxiging them. in the posterior septum-the co onding ve?;tpicuiar septum was reached by ~~~~~~~~ electrodes through the posterior i~terve~t~~~~ar septum and lodging them I to 2 cm. deep in the post,e.rior septum); (5) anterior left (AL): at the left atria% appendage and underlying left vectriclcle; (6) posterior left (PL): at the posterior left atrium just above the coronary sinus and the adjacent left ventricle; (7) left lateral ILL): at midpoint between AL and PL. Special attention was paid to positionjng the efectrodes close to xhe A-V ring at a distance of 1 cm.

A 5F bipolar electrode catheter was ktroduce into the left carotid artery the non-coronary cusp of t bundle recordings.li His b potentiaEs were validated by atria1 and Standard e~~~t~~cardi~~r His bundle elec-trograms, right ai.-&! electro-

Amat-y-Leon et al.

Table I. Cycle length of A-V reentrant PSVT with and without bundle branch block (mean + SEM in msec.)

AP site

AR LR PR

S PL LL AL

Control (N = 7)

281.5 z!z 8.3 276.5 + 9.4 266 I 8 271 + 10.5 277 I 11 289 k 10.5 286 5 10.5

RBBB (N = 7)

318 f 9.5 303 + 12 289 I!z 9.3 273.5 i 11 276 f 10 285 + 10 286.5 i 11

P

< 0.001 < 0.001

< 0.01 NS NS NS NS

Control (N = 10)

281.5 zk 7.4 275 + 9 267.5 t 5 273.5 i 8 275 i 6.7 269 i 9 280 + 7.5

LBBB (N = 10) P

281 +8 NS 274 t 6.4 NS 261 k9 NS 278 -c 6.5 NS 309 t 6.3 < 0.001 307 +- 7.7 < 0.01 312.5 If- 7.6 < 0.001

Abbreviations: AP = anomalous pathway; RBBB = right bundle branch block; LBBB = left bundle branch block; AR = anterior right; LR = lateral right; PR = posterior right; S = septum; PL = posterior left; LL = lateral left; AL = anterior left; NS = non-significant; P = P value.

grams, local ventricular electrograms, and stim- ulus artifacts were simulataneously displayed on an oscilloscope and recorded on a multichannel recorder (Electronics for Medicine DR-8, White Plains, N. Y.) at paper speeds of 100 and 200 mm. /sec.

The electronic anomalous pathway simulator was schematically depicted in a previous publica- tion.16 Local electrograms recorded from the ventricle were preamplified by a multichannel recorder, and filtered and differentiated by input circuitry. The resulting signal was used to trigger a crystal controlled digital timer, programmable to a specific pathway delay between 1 and 999 msec. When the preset time was reached, the timer triggered a pulse generator adjusted to deliver an above-threshold stimulus to the atria1 stimulating electrodes. Thus, the relevant fea- tures of this anomalous pathway simulator include ability for ventricular sensing, retrograde conduction with programmable conduction time, and atria1 stimulation.

recording catheter. This interval reflected intra- atria1 conduction time from the atria1 stimulation site to the low septal right atrium. (2) A-H interval, from the first high frequency deflection on the low septal right atria1 electrogram to the His bundle electrogram. This interval reflected A-V nodal conduction time. (3) H-V, interval, from the His bundle electrogram to the first high frequency deflection of the local ventricular elec- trogram recorded from the tested ventricular sensing site. This interval reflected conduction time from the His bundle to the sensing site. (4) V,-S interval, from the sensed ventricular electro- gram to the stimulus artefact. This interval was 100 msec., reflecting programmed delay of the anomalous pathway simulator.

Experimental protocol

A-V reentrant tachycardias were induced in each of the dogs at all seven sites with a programmed anomalous pathway conduction time of 100 msec. This conduction time was chosen since it allowed induction of paroxysmal tachycardia with a cycle length comparable to that seen in patients with Wolff-Parkinson-White syndrome and PSVT. Recordings were obtained during each tachycardia at a paper speed of 100 mm./sec. The following subintervals were mea- sured: (1) S-A interval, from the stimulus artefact to the first high frequency electrogram of the low septal right atrium recorded from the His bundle

After control values were obtained, right bundle branch block was produced in seven of the dogs by inserting a needle through the right ventricular wall and traumatizing the second portion of the right bundle branch.17 Similarly in another group of 10 dogs, left bundle branch block was induced by traumatizing the main left bundle branch with a needle introduced through the left ventricular wall at the apex of the heart.‘? A-V reentrant tachycardia was again induced in all dogs at all sites after a stable bundle branch block was produced. Measurements of tachy- cardia cycle length and subintervals were deter- mined.

At the termination of each experiment the heart was excised and the exact location of the plunge wires were verified. Lugol’s solution was used to identify the intraventricular conducting system and to verify the interruption of the traumatized bundle branch.

All the intervals given represent the average of

64 July, 1978, Vol. 96, No. 1

2. Induced A-V reentrant tachycardia (PSVT). Representative example from the anterior right L-.a.:on before (Panel A) and after (PaneE B) right bundle branch block was produced. Shown are electrocardiographic Leads I, II, XII. HBE = His bundle recordings; RA = right atrial. electrogram; V, = local ventricular ekctro- gram; S - stimulus artifact. Paper speed is 100 mm./sec. and time intervals are at 1 sec. Values for the direrent components of the cycle length (CL) of supraventricular tachycardia before and after RBBB are sbov~ in PFW right colwnn.

10 consecutive measurements. Statistical analysis was performed using the Student t test for paired data, and analysis of variance.

cardias (Table I). The effects of right bundle branch block on the cycle length of A-V re-entrant tachycardias in seven dogs at all sites is presented in Table I. Cycle length of tachycardias was significantly increased only with the three right-sided anomalous pathway locations, increasing by a mean of 37 + 3 msec. (I? < .OOl) with the anterior right site, by 2’7 i: 3 msec. (P < .001) with the lateral right site, and by 23 t 4 msec. (P < .01) with the posterior right site. Cycle length of tachycardias utilizing septal and left-sided pathways were not significantly changed. Fig. 2 is a representative

example of one of the experiment:< conducted with an anterior right anomalous pathway.

The effects of left bundle branch block on the cycle length of A-V w-entrant tad~ycardias in 10 dogs at all sites is presented in Table I. After left bundle branch block, cycle length. of PS’VT was significantly increased only with the three left- sided pathway locations, increasing by a mean of 34 t 2.6 msec. (P < ,001) wit.h the ;>oi;terior left site, by 38 I 4.6 msec. (P < .E) Gth the left lateral site, and by 32.5 k 3.3 msec:. iP < .OO1) with the anterior left site. Cycle length of tachy- cardias utilizing septaP and right-sided loca.tions were not significantly changed. Fig. 3 is a repre- sentative example of one of the experiments

a left lateral anomalous path-

The cycle length of .A-V reen-

Amat-y-Leon et al.

Left taterai (LL)

CL of PSVT 280

VL-S 100

S-A 48

A-H 105

H-q 35

II

IJi

HBE

CLaf PSVT 315

v L-s 100

S-A 40 A-H 75

H-V, too

Fig. 3. Induced A-V reentrant tachycardia. Representative example from the left lateral location before (Panel A) and after (Panel B) left bundle branch block was produced. Values for the different components of the cycle length of PSVT are shown in the right column.

trant PsVT in these experiments, is the sum of the following subintervals: S-A, A-H, H-V,, and anomalous pathway delay (V,-S). Any significant change in cycle length of PSVT, should be explainable on the basis of changes in subinter- vals.

Mean H-V, intervals during tachycardia before and after right and left bundle branch block are presented in Table II. With right bundle branch block, H-V,> interval significantly increased with tachycardia utilizing the three right sites. H-V, increased by a mean of 48 % 2.4 msec. with the anterior righit location (P < .OOl), by a mean of 32 +- 4 msec. with the lateral right (P < .OOl), and by a mean of 23 f 4 msec. with the posterior right location (P < .OOl). There was no signifi- cant differences in H-V, with septal and left sites. With left bundle branch block, H-V, interval was

66

significantly increased with tachycardia utilizing the three left-sided sites. Thus, H-V,, increased by a mean of 50 + 4.6 msec. with the posterior left location (P < .OOl), by a mean of 42 * 5 msec. in the left lateral (P < .OOl), and by 42.5 t 5 msec. in the anterior left (P < .OOl). His Purkinje conduction time (conventional H-V interval) was not altered by either right or left bundle branch block. Therefore, the changes in H-V, represented increases in intraventricular conduction time.

There were compensatory decreases in A-H intervals for the increases in H-V, with bundle branch block occurring ipsilateral to anomalous pathway location. Thus, with right bundle branch block, A-H decreased by 8.5 -+ 3.2 msec. (P < 0.05), 14 t 2.6msec. (P < 0.05), and8 f 2.6 msec. (P < 0.05) with tachycardias respectively utilizing the right anterior, lateral, and posterior

July, 1978, Vol. 96, No. 1

AR 39.5 t 3 87 t3 < 0.001 37.5 i 2.4 37 t 2.5 NS LR 37 z 2.4 69 +5 < 0.001 34.5 I 2 35 i-2 NS PR 40 k 2.4 63 it 4.7 < 0.00: 38 13 38 t 2.6 NS

5 40 i- 2.7 43.5 t 4.6 NS 37.5 t 3 42.5 I? 5 ph’s PL 37 It 1.5 43 t 1.8 NS 35.5 i 3 86.6 2 .5 c: 0.001 LL 41 27 3.5 48 k 3.4 NS 38 22 80 t 2.6 < 0.51 AL 40 23 36.5 + 7 NS 36.5 + 2.5 79 i 3.6 < 3.8’91

Kbbreviations: AP = anomalous pathway; RBBB = right bundle branch block; LBBB = left bundle branch biock; NS = ran-signiilcant; P = P

sites. ith left bundle branch block, A-H decreased by 12 t msec. (P < 0.05), 15 -+ 5

13 i 4 msec. (P < 0.05) eetively, utilizing the left

posterior, lateral, and anterior sites. S-A intervals did not change significantly after either right or left bundle branch block.

In patients with preexcitation, A-V reentrant taehycardias (PSVT) usually reflect circus move- ment with the normal pathway as antegrade limb, and the anomalous pathway as retrograde !imb.‘-5 The cycle length of the tachycardia is determined by A-V nodal conduction time, His Purkinje conduction time, conduction through ventricular muscle, anomalous pathway conduc- tion, and intra-atria1 conduction.

It has been suggested that the development of functional bundle branch block during PSVT ipsilateral to the location of an anomalous pathway results in lengthening of the cycle length of PSVT.“-‘” This lengthening is thought to be due to an increase in the size of the reentrant pathway ‘by addition of transseptal conduction time. Coumel and associates6-8 has suggested that the presence or absence of this lengthening in cycle iength could be Iused as a sign for lateralization of anomalous pathway location. Thus, in 1972, Coumel and Waynberger” reported a patient with left ventricular preexcitation and A-V reentrant PSVT in whom the development of functional Beft bundle branch block was accompanied by an increase in PSVT cycle length of 20 msec. PSVT cycle length was not changed by functional right bundle bran& block. This observation was later corroborated other reports from Slama, Coumel, and uvraln7 in 1973, Coumel and .Attuels in 1974, Spurrell and colleague@ in 1974, and Neuss and S~hlepper’~ in 1975. This phenom-

hirnerican Heart Jcmrnnl

enon has also been used to redict an locate concealed retrogradeiy $o~d~~~~~~ anomalous pathways.6-1”

More recently, Pritcbett and co-wo!‘kt?rs’.’ have extended these observations by analyzing t. changes in V-A ~o~d~~tio~ during episodes of A reentrant paroxysmal tachyrardla ;hihen func- tional bundle branch block develops. They reported 15 patients with left free wall anomalous pathways, three patients with right. free wail anomalous pathways, and four pa&r&s with septal preexcitation. Ven~ric~lo”a-~r~~.l ~5~~~~~~~0~

times were prolonged during A-V reentrant tachyeardia when fn~~t~o~~~ bundle branc developed ipsilateral to the location of an anom- alous pathway. Functional bun ie bl-an& block contralateral to anomalous pathway, did not prolong V-A time. In patients with seytal anoma- lous pathways, neither bundle branch block altered V-A time during PSQT.

Our results s~bstalltiated these c!inical obser- vations. e utilized a canine model of pree tion with an anomalous ~atb~~a~~ simulator acterized by ~~idire~tio~~l conduct&on (v ulo-atrial), p~o~ammab~e con &on time and predetermined location along -, A-V ring. A-V reentrant ta~~ly~ardias were easily iinduced using the normal pathway for antegrade co~d~~t~o~ and the anomalous pathway (simulat,or) for retrograde conduction. Following ~x~el~me~ta~~y induced bundie branch block ipsifaterai to anom- alous pathway locations, cycle length of reentrant PSVT was si~~~~~a~~~~ increased, experimental bundle branch block ~~j~~~~~a~e~a~ to anomalous pathway location, cycie len PSVT was not changed. Cycle length of utilizing septai’ anomalous pat cl-ranged by either right or left bu.ndIe branch block.

To further understand these resuits, one can

67

Amat-y-Leon et al.

look at the determinants of PSVT cycle length with our experimental model. PSVT cycle lengths equals the sum of the following subintervals: (1) S-A, conduction time from the atria1 stimulating electrode to the low septal right atrium (from His bundle catheter). This was a function of anoma- lous pathway atria1 site and independant of cycle length. This was unchanged by experimental bundle branch block. (2) A-H, from low septal right atrium to the His bundle electrogram, a measure of A-V nodal conduction time. This was partially a function of conduction times in the rest of the circuit. (3) H-V,, from His bundle electrogram to the onset of the ventricular elec- trogram at the ventricular sensing electrode (close to the A-V ring). This was a function of ventricular site and independent of cycle length. H-V, encompassed H-V (from His bundle electro- gram to the onset of ventricular activation), and V-VL, conduction time from onset of ventricular activation to the ventricular sensing site. (4) V,-S, from ventricular sensing site to the atria1 stimulus. This was a programmed function in this series of experiments and was 100 msec.

In these experiments, bundle branch block ipsilateral to an anomalous pathway location significantly increased H-V, during PSVT. Con- tralateral bundle branch block had no significant effect. When analyzed, it was demonstrated that the increase in H-VL, reflected an increase in V-V, and not H-V. The lack of change in H-V was consistant with prior experimental work, which demonstrated that conduction times in both bundle branches, to the onset of ventricular activation in the ipsilateral chamber were essen- tially equa1.‘8-20 The increase in V-V, with bundle branch block ipsilateral to an anomalous path- way, reflected change in sequence of ventricular activation. Ventricular activation was initiated in the contralateral ventricle, proceeded across the ventricular septum, and then invaded the ipsilat- era1 ventricle. The change in V-V, with bundle branch block ipsilateral to an anomalous path- way, thus reflected primarily the addition of transseptal conduction time. With bundle branch block, contralateral to an anomalous pathway, the activation sequence of the ventricle with the anomalous pathway, was essentially unchanged, since its bundle branch was intact, resulting in no change in V-V,.

The magnitude of increase of V-V, with ipsilat- era1 bundle branch block during PSVT was

similar for both right bundle branch block (range of 23 to 48 msec.) and left bundle branch block (range of 42 to 50 msec.). It is interesting to note that our values correlated very closely with calcu- lated transseptal conduction times of 40 msec. reported in dogs by Lewis and Rothschild”’ and of 30 to 40 msec. as reported by Wilson and Hermann22-23 in 1920, and of 40 msec. reported by Rodriquez and Sodi-Pallares’” in 1952.

The failure of H-V, (and of necessity V-V,) to increase cycle length of PSVT with septal anom- alous pathways suggested that the septal location (postero-basal) sensed ventricular activation ar- riving simultaneously from both ventricles, so that delay in the input of one or the other ventricle did not increase V-V,. This is presum- ably the reason for the clinically observed failure of bundle branch block to increase V-A conduc- tion time, during spontaneous PSVT in patients with septal anomalous pathway.

In previous work16 utilizing the anomalous pathway simulator, we demonstrated that A-H interval was a function of programmed anoma- lous pathway delay (V,-S). As programmed V,-S was decreased, A-H increased. This reflected a compensatory increase in A-V nodal conduction time, as the cycle length of PSVT was decreased due to the decrease in V,-S. In the present study, the decrease in A-H during PSVT with bundle branch block ipsilateral to anomalous pathway site, was compensatory for the increase in V-V,, which presented itself to the A-V node as a total increase in retrograde conduction time (increase of H-V, with a fixed V,-S of 100 msec.). The decrease in A-H was of small enough magnitude, so that it only partially offset the in- crease in H-V,, with resultant increase in cycle length of PSVT with ipsilateral bundle branch block.

Although in our experimental model, increase in intraventricular conduction time was respon- sible for the slowing in cycle length of PSVT, it is worth emphasizing that in patients with PSVT and functional bundle branch block, a detailed analysis of subintervals is necessary.13 For instance, it is possible that the decrease of A-H might be of such magnitude to completely offset the lengthening in ventriculo-atria1 conduction time, resulting in no change in cycle length of PSVT. Changes in H-V might also occur with functional bundle branch block complicating PSVT in patients.”

68 July, 1978, Vol. 96, No. I

The effects of bundle branch block on experi- mental A-V reentrant tachycardia (PSVT) were studied in 17 dogs using an anomalous pathway simulator (APS). The APS was a programmable digital electronic circuit with ability for ventric- ,glar sensing, retrograde conduction with pro- grammable conduction time, and atrial stimula- :ion. Close bipolar electrodes were positioned at seven contiguous atria1 and ventricular sites (V,) along the A-V ring, these being; anterior, lateral, and posterior right (AR, LR, PR), septal (S), and posterior, lateral and anterior left (PL, LL, AL). Right (R) (seven dogs) and left (L) (IO dogs) bundle branch block (B B) were produced with transcardiac needle. After BBB, cycle length :CL) of A-V reentrant PSVT was significantly mcreased only with ipsilateral sites. Thus, with RBBB, CL of PSVT increased by 37 + 3 msec., 27 it 3 msec., and 23 i 4 msec. (P < O.OOl), at AR, LR, and PR sites respectively. With LBBB, CL of PSVT increased only with left-sided sites Thus, CL increased by 34 + 2.6 msec., 38 i 4.6 msec., and 32 +- 3.3 msec., (P < 0.001) with PL, LL, and AL sites, respectively. PSVT CL and septal site did not change significantly after ,either R or LBBB. The increase in CL was explicable in terms of corresponding increases in intraventricular conduction time (H-V,). There were slight compensatory decreases in A-H inter- vals for the increases in H-V,,. These studies confirm findings suggest.ed by clinical electro- ohysiologica! observation.

We are indebted to Ms. Lore U. Foley for her secretarial assistance.

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Boineau, J. P.: Moore, E. N., Spear, J. F., and Sealy, W. C.: Basis of static and dynamic electrocardiographic variations in Wolff-Parkinson-White syndrome, Am. J. Cardiol. 3232, 1973. Durrer, D., and Wellens, H. J.: The Wolff-Parkinson- White syndrome anno 1973, Eur. J. Cardiol. 1:347, 1974. - Gallagher, J. J., Gilbert, M., Svenson, R. H., Miller, H., Sealv. W. C.. Kasel!. J.. and Wallace, A. G.: Wolff- Par&son-White syndrome. The problem, evaluation, and surgical correction, Circulation 51:767, 1975. Durrer, D.: Schoo, L., Schuilenburg, R. M., and Wellens, H. J.: The role of premature beats in the initiation and the termination of supraventricufar tachycardia in the Wolff-Parkinson-White syndrome, Circulation 36:644, 1967. Wellens, 1% J.: Contribution of cardiac pacing to our understanding cjf the Wolff-Parkinson-White syndrome, Br. Heart J. 37:231, 1975.

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Coume:, P., and lvaynberger, !&. ;ed ,,a &,cardies oar rythme reciproque au tours du syndrome de Wolz- Parkinson-White, Coeur Med. Intene I li :77, 197%. Slama, R., Coumel, P., and Bouvrain, U.: Les syndromes de Wolff-Parkinson-White de type A inapparents ou Patents en rythme sinusal, Arch. Ma!. Coeur 66:639, ‘373. Coumel, P., and Actuel, P.: Reciprocating tachycardia in overt and latent preexcitation, Eur. J. Cardiol. 3 :423, 1974. Spurreh, R. A., Krikler, D. M., and Sowcon, E.: Retro- grade invasion of the bundle branches producing aberra- iion of the QRS complex during supravent;icu!ar tachy- cardia studied by programmed electrical stimulation, Circulation 56487, 1974. Neuss, H., Schlepper, M., and Thormann. J.: Analysk of reentry mechanisms in three patients with concealed Wolff-Parkinson-White syndrome, Circi&?.ion 5 i ~7.5, T.975. Wellens, H. J., and Durrer, D.: The role of an accessory atrio-ventricular pathway in reciprocal tachycardia, Circulation 52:58, 1975. Barold, S.S., and Coumel, P.: Mechanisms of atrio- \entricuiar junctional tachycardia. Role of reentry and concealed accessory bypass tracts, Am. J. Cardiol. 39:S’i, 1377. Dritchett, E. L., Tonkin, A. M., Dugan, F. A., Wahace, A. G., and Ga!lagher, J. J.: Vent&&-at,tial conduction time during reciprocating tachycardia with intermittent bundle branch block in Wohf-Parkinson-White syn- drome, Br. Heart J. 361058, 1976. Scherlag, B. J., Helfant, R. H., and Damato, A. N.: A catheterization technique for His bundle stimulation and recording in t,he intact dog, J. AppI. Physioi. 2 ‘968. Scherlag, B. J., Kosowsky, B. D., and Damato, A. E.: .A technique for ventricular pacing from the His bundle of the intact heart, J. Appl. Physiol.. 22:5&I. 1967. Teague, S., Denes, P., Amat-y-Leon, F., sad Rosen, K. ‘%I.: Effect of anoma!ous pathway location on rate cf canine experimental A-V reentrant tachycardia, Am. J. ?hysiol. 233:H44, 1977. Xosenbaum, M. B.; Elizari, M. U., and T;azzari, J.: Los HemibIoqueos, Buenos Aires, 1967, Paidos, p. 93. Rosen, K. 1 M. Rahimtooia, S. H.. Sinno, M. Z.: and Gunnar, R. M.: Bundle branch and ventricular activa- tion in man, Circuiation 43:193, 1971. Yenes, P., Wu, D., Dhingra, R., Amat-y-Leon, F,, Wynd- ham, C., and Rosen, K. M.: Electrophyshological observa- tions in patients with rate dependent bundle branch block, Circulation 5 1:244, 1975. Narula, 0. S., Javier. R. P., Samef, P., and Maramba, L.: SigniEcance of His and left bundle recordings from the left heart in man, Circulation 42:385; 3970. YAewis, T., and Rothschild, M. A.: The excitatory process h the dog’s heart. Part il. The -ventricles, Phil. Tr. R. Sot. B. 2iitT181, 1915. W&on. 1”. N.. and Hermann. G. R,: Bun&e branch block and arborization. biock, Arch Intern Msd. 26~153, iszo. “Wilson, F. N., and Hermann, G. R.: An experimental study of incomplete bundle branch block and of the refractory period of the heart of the dog, Heart 1921. Rodriquez, ,M. I., and Sodi-Pallares, I)., The mechanism sf complete and incomplete bundle brar~h block, A&X. HEART 3. 4&715, 1952.