Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

J. ELECTROCARDIOLOGY, 9 (4) 1976 357-363

Case Studies: Right Atrial Versus Left Atrial Echo Zones: A Proposed New Criterion for Determining the Atrial Site of Retrograde Preexcitation BY ANDREW MORRIS, M.D., KEITH COHN, M.D. AND MELVIN M. SCHEINMAN, M.D.

The n a t u r a l history of patients with the Wolff-Parkinson-White syndrome (WPW) is still incompletely understood. It is known, for example, that the electrocardiographic abnormalities m a y disappear with time, but the relationship between this finding and subseq u e n t r i s k of t a c h y a r r h y t h m i a s is unknown. 1-~ Furthermore, there are no studies available concerning the incidence and mechanism(s) of a r r h y t h m i a s in these patients. Reported herein are results of a study of a patient who initially showed capability of antegrade conduction through an accessory p a t h w a y b u t s u b s e q u e n t l y a p p a r e n t l y lost such capacity and yet clearly used the accessory pathway as part of a reentrant circuit during bouts of supraventricular tachycardia (SVT). A new criterion for distinguishing the atrial site of retrograde preexcitation is proposed as a result of the study.

SUMMARY In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent s u p r a v e n t r i c u l a r t a c h y c a r d i a (SVT) developed but never s u b s e q u e n t l y s h o w e d antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250-450 msec after atrial depolarization) or coronary sinus depolarization (250-550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde preexcitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade b y p a s s c o n d u c t i o n . S t i m u l a t i o n o f the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.

CASE REPORT A 38 year old m a n was referred for study to San Francisco General Hospital in December 1974 because of recurrent bouts of SVT that w e r e u n r e s p o n s i v e to a n t i a r r h y t h m i c therapy. The patient used alcohol to excess b u t was in excellent health until 1966 when he consulted his private physician because of palpitations. The initial ECG (August 23, 1966) showed an ectopic atrial r h y t h m and Type A WPW v (Fig. 1). In 1970, the patient was hospitalized on three different occasions because of left ventricular failure and SVT. Between 1970 and 1975, many 12-lead ECGs and rhythm strips were obtained that showed either a normal QRS or left bundle branch block p a t t e r n ; no d e l t a w a v e s w e r e e v e r detected after 1966 (Fig. 2). Of note is the identical rate of the tachycardia in 1970 and 1972 regardless of the type ofintraventricular conduction pattern present. Cardiac catheterization in October 1974 at another hospital revealed evidence of severe left ventricular decompensation (left v e n t r i c u l a r end-diastolic p r e s s u r e 28 m m Hg); left v e n t r i c u l o g r a p h y s h o w e d an e n l a r g e d , d i f f u s e l y hypokinetic left ventricle, b u t coronary art e r i o g r a p h y revealed no abnormalities. Int r a c a r d i a c electrophysiologic studies at this time showed prolongation of t h e infranodal

From the Medical Service, San Francisco General Hospital, the Department of Medicine and the Cardiovascular Research Institute, University of California, San Francisco, and the Department of Medicine, Pacific Medical Center, San Francisco, California. This study was performed during Dr. Scheinman's tenure as an American Heart Association Teaching Scholar in Cardiology. Supported in part by grant GM 16496 from the National Institutes of Health, Bethesda, Maryland. Reprint requests to: Melvin M. Scheinman, Department of Medicine, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110. 357

358

MORRIS

ET AL

I " " : :-

~-t..;~

.~

-

-.i

'

L~

. . . . . . . . . .. .. .. .

-~::I~ . . . . ~:

12/8/70

'i

.

~

~

~, ~ ,

-'o'V#~ ~ '; § ::

IHi,,tI~I~:Hq!I..[I--~L

_v3m I.t I r'~!4 I

c.

i~i ' ~ '

:i

!J:~: ~ i

...:.L Z - : L t ~

: :~ ~

i~.

:

:;:: i:::~I ~t::t!:~ !J ~:[i :~II

9/70

T-s

] i i:~i!i:l

2/28/74

.

:

:::

.

.

:, :

.

.

.

.

::~! ~,I :~! !!~]

~ ; ~::!:;

Fig. 2 Fig. 1 Fig. 1. ECG obtained in 1966 showing an ectopic atrial pacemaker (left atrial rhythm?) at a rate of 75/min with a P-R interval of 0.14 sec and a delta wave directed anteriorly consistent with a Type A WolffParkinson-White syndrome (WPW) pattern. This was the only ECG showing the WPW pattern. Fig. 2. Representative electrocardiographic tracings from 1966 to present. Standard leads I, III, AVF and lead V1 are shown in each panel. A, 12/8/70: The ventricular complex is narrow and the P-R interval is normal (0.16). B, 5/9/72: Supraventricular tachycardia (SVT) at 145/min with QRS morphology identical to that noted in A. C, 9/70: SVT at 145 min with left bundle branch block (LBBB). Of note is the identical ventricular rate recorded in B and C (see Discussion). D, 2/28/74: SVT at 128 beats/min; LBBB pattern. All bouts of recorded SVT with LBBB were associated with the slower ventricular rates except for that noted in C. ues. Atrial rate was gradually increased by conduction t i m e (HV 75 msec), and a t r i a l either high right atrial or coronary sinus pacpacing up to a r a t e of 150 b e a t s / m i n proing. The spontaneous atrial cycle length was duced A-V n o d a l W e n c k e b a c h c o n d u c t i o n scanned by progressively p r e m a t u r e stimuli b u t did not r e s u l t in a n y changes in t h e H-Q from high r i g h t a t r i u m or coronary sinus. i n t e r v a l or a l t e r a t i o n of the QRS morpholAtrial pacing was used in similar fashion to ogy. Full a n t i a r r h y t h m i c doses of p r o c a i n e t e r m i n a t e bouts of induced SVT. The intraamide, q u i n i d i n e , propranolol, or digitalis cardiac electrograms and X, Y, and Z leads of did not p r e v e n t r e c u r r e n c e of SVT, and t h e the F r a n k orthogonal lead system were dispatient was referred to us for furplayed simultaneously on an oscilloscope and t h e r evaluation. recorded (Electronics for Medicine, DR-12, A h e x a p o l a r e l e c t r o d e c a t h e t e r was inWhite Plains, NY). Ventricular pacing was serted into the right femoral vein and posinot carried out because the p a t i e n t was being tioned across the tricuspid valve to record His evaluated for possible insertion of a permabundle potentials, s Another quadripolar n e n t atrial radiofrequency p a c e m a k e r , and c a t h e t e r was inserted into a right antecubital informed consent for v e n t r i c u l a r pacing was vein and positioned initially against the high not obtained prior to the study. lateral right atrial wall in order to pace the atrium. The distance between electrodes was 1 cm, and the distal electrode pair was used to RESULTS deliver electric impulses, whereas the proxiGraded Increases in Atrial Rate. Control remal pair was used for recording the r i g h t cordings showed a spontaneous sinus cycle atrial electrogram from the mid-right atrium. length between 640 and 660 msec with an The quadripolar catheter was subsequently A-V nodal conduction time (A-H) of 75-90 r e p o s i t i o n e d and i n s e r t e d into t h e l a t e r a l msec and an i n f r a n o d a l c o n d u c t i o n t i m e coronary sinus for left atrial recording and (H-Q) of 55-62 msec. Graded increases in the pacing. Electric pulses were delivered via a paced atrial rate (either from the high right p r o g r a m m e d s t i m u l a t o r (Bloom Associates, a t r i u m or coronary sinus) up to a cycle length Philadelphia, PA) and were 1 msec in duraof 300 msec produced gradual increases in the tion w i t h c u r r e n t a m p l i t u d e set at two to A-H i n t e r v a l u n t i l Wenckebach conduction t h r e e times the atrial diastolic threshold valJ. E L E C T R O C A R D I O L O G Y ,

V O L . 9, N O . 4, 1 9 7 6

ATRIAL

ECHO

occurred. Atrial pacing, however, failed to produce any changes in the H-Q interval or the QRS contour in the surface ECG leads.

Progressive Atrial Premature Depolarizations. The spontaneous atrial cycle was scanned with progressively premature atrial depolarizations from the high right a t r i u m or the coronary sinus. The relative and effective refractory periods of the A-V node were 480 and 250 msec, respectively, whereas the effective refractory period of the a t r i u m was 200 msec. Late diastolic atrial premature depolarizations from the high right a t r i u m t h a t fell outside the relative refractory period of the A-V node failed to produce SVT (Fig. 3), whereas premature high right atrial stimulation with AtA2 intervals between 250 and 450 msec regularly induced SVT with a cycle length of 435 msec (Fig. 4). During sinus beats, the higher right atrial electrogram preceded the low r i g h t a t r i a l e l e c t r o g r a m (Fig. 3), but changes in both the P wave contour in the surface leads and the interatrial activation sequence were observed during SVT (Figs. 4 and 5). Progressive left atrial premature depolarization (coronary sinus) resulted in a

P

'

J

~

P

ZONES

359

broader echo zone (250-550 msec) with very late atrial premature depolarizations capable of inducing SVT without prolongation of A-V nodal conduction (A-H) time (Fig. 5). This f i n d i n g excludes an A-V nodal r e e n t r a n t mechanism for the SVT2 -12 In addition, during the tachycardia, the atrial electrogram from the coronary sinus clearly preceded the a t r i a l e l e c t r o g r a m recorded from the low r i g h t a t r i u m ( F i g . 5). T h e v e n t r i c u loatrial conduction time during multiple induced bouts of SVT was always 240 msec. Atrial premature depolarizations from either the coronary sinus or high right atrial pacing sites failed to produce any change in the H-Q interval or delta waves in the surface leads. Thus, a l t h o u g h both r i g h t and left a t r i a l pacing failed to produce a n y evidence for antegrade conduction through an accessory pathway, ventriculoatrial bypass conduction was operative during the SVT.

DISCUSSION Retrograde Preexcitation. The presence of and capacity for a n t e g r a d e conduction via an anomalous p a t h w a y were clearly apparent on

v

';,,

H.R.A, i,|

!,I , i

,

HRA L

, ,

~

~,

J

15o

H.B.E.I~-'~Ij~

k,

't ,

,~

/,,'

,

!

t

AQ

15oi1.

!~r"~

k,

!

v,

'

P

I ,

I

,

',

' 9

:

r

pI

,

,

,

I !

T AQ

p

'

r

"

55

240

'

I

.

,L

, "

' k, H '3

A-~,~,

A~ "2y2

A' H'v'

Fig. 4

Fig. 3 Fig. 3. Simultaneous recordings of surface leads X, Y, and Z of the Frank orthogonal system, high right atrial (HRA), and His bundle electrograms (HBE). Numbers represent observed intervals recorded in milliseconds. An HRA premature depolarization (A~) induced 580 msec after a spontaneous sinus depolarization (A1) occurs outside the atrioventricular (A-V) nodal relative refractory period since the P-R or AQ intervals of the induced beat are identical with those of the spontaneous atrial depolarization (the His spike is not well visualized), and fails to result in SVT. Both the induced HRA or spontaneous atrial depolarization result in a normal sequence of atrial activation in that atrial activation occurs earlier in the higher right atrial position (HRA) compared with HBE. St = stimulus. Fig. 4. Simultaneous recordings of surface leads X, Y, and Z, HRA, and HBE. An atrial premature depolarization induced 450 msec following A1 results in prolongation of A-V nodal conduction time (A-H = 140) and a bout of SVT ensues. During tachycardia, there are clear-cut changes in P wave contour (P1) and the low right atrial electrogram A~ occurs slightly earlier than that from the HRA. The almost simultaneous occurrence of the atrial electrogram in HRA and HBE lead areas during tachycardia is probably due to the mid-right atrial position of the HRA lead. HRA depolarizations induced at A~A2 intervals of 250-450 msec regularly resulted in SVT. See Fig. 2 and 3 for abbreviations. J. E L E C T R O C A R D I O L O G Y ,

V O L . 9, NO. 4, 1 9 7 6

360

M O R R I S ET A L

P

,

i

" ""~

,

','~

_

~ " '

Antegrade

'

Z

St,

,

8o,

, '--

_ _

LA Slo;:k RA

LA

RV

LV

LV

RA

LA

RV

LV

N] A2-- 4180

,, C.S.E. I

RA

1

20

A

B

RV

C

Fig. 6

Fig. 5 Fig. 5. Simultaneous recordings of X, Y, and Z surface leads, HBE, and the lateral coronary sinus (CSE). A late induced atrial premature depolarization from the coronary sinus produces no change in A-V nodal conduction time (A~I-h = 80 msec) and initiates a bout of SVT. Spontaneous atrial depolarizations are associated with near simultaneous atrial activation recorded from HBE and CSE. During SVT, the atrial electrogram in CSE precedes that from HBE by 20 msec. The QRS configuration heart rate and atrial morphology during tachycardia is identical with that recorded in Fig. 4. See Fig. 2 and 3 for abbreviations. Fig. 6. Schematic representation of the components of the reentry circuit and mechanism of the SVT. RA = right atrium, LA = left atrium, RV = right ventricle, LV = left ventricle, AV = atrioventricular node, AP = accessory pathway. Solid lines indicate antegrade impulses in atria and ventricles. Dotted lines indicate retrograde ventriculoatrial (V-A) conduction in the bypass tract. Time interval represents observed atrioventricular (A-V) nodal (A-H) conduction times. A: Atrial premature depolarizations induced late in the atrial diastolic cycle from high right atrium fail to result in ventricular atrial conduction because the return impulse meets a refractory bypass tract (see Fig. 3). B: Earlier high right atrial premature depolarizations induced within the relative refractory period of the A-V node produce sufficient A-V nodal delay (A-H = 140 msec) to allow for recovery of bypass tract and retrograde V-A conduction (see Fig. 4). C: LA depolarizations induced late in the atrial diastolic cycle produce earlier bypass activation and recovery allowing for return of the ventricular impulse to atrium even without any change in A-V nodal conduction time (Fig. 5).

a single 12-lead ECG obtained in 1966. All subsequent ECGs failed to reveal evidence of antegrade preexcitation. In addition, graded increases in the paced atrial r a t e during two s e p a r a t e studies and p r e m a t u r e a t r i a l depolarizations from either the high right a t r i u m or th e coronary sinus failed to show any evidence of ant e gr ade conduction t h r o u g h the anomalous pathway. Although t he r e was a p p a r e n t f a i l u r e of a n t e g r a d e conduction, ventriculoatrial conduction was clearly present and mu s t have been a component limb of t h e r e e n t r a n t circuit. The SVT noted in our pat i ent was most likely r e e n t r a n t in origin because the tachycardia could be induced and t e r m i n a t e d by atrial pacing. 13 The mechanism of t he observed tachyarrhythmia could conceivably be due to 1) sinoatrial nodal r e e n t r y , 14-18 2) i n t e r a t r i a l reentry, ls'19 3) A-V nodal reentry, ~12 or 4) retrograde r e e n t r y via a n accessory A-V pathway. 2~ Sinus node r e e n t r y

was excluded because the P wave morphology on the surface ECG and t he sequence of interatrial activation were m a r k e d l y different during t h e t a c h y c a r d i a c o m p a r e d w i t h si nus r h y t h m . A t r i o v e n t r i c u l a r nodal r e e n t r y was excluded because 1) the tachycardia could be induced by at ri al p r e m a t u r e depolarizations without associated prolongation of t he A-H interval, and 2) there was no reciprocal relationship between A-H and v e n t r i c u l o a t r i a l c o n d u c t i o n t i m e s d u r i n g t h e i n d u c t i o n of SVTs. Similarly, the induction of t he tachycardia by late atrial p r e m a t u r e depolarizations (clearly outside t he relative refractory period of the atrium) and the constant retrograde ventriculoatrial conduction time during induced t a c h y c a r d i a regardless of t he preceding A~A2 would m a k e i n t e r a t r i a l r e e n t r y very unlikely, is It is recognized t h a t ventricular s t i m u l a t i o n is necessary for absolute proof of i nt act v e n t r i c u l a r conduction, but t he presence of discrete echo zones, the sequence J. ELECTROCARDIOLOGY, VOL. 9, NO. 4, 1976

ATRIAL ECHO ZONES

of atrial activation during the tachycardia, and the constant ventriculoatrial conduction time make intact retrograde ventriculoatrial conduction virtually a certainty. Atrial prem a t u r e depolarizations from either the high right atrium or the coronary sinus occurring w i t h i n the A-V nodal effective r e f r a c t o r y period failed to initiate the SVT and provided evidence for A-V node involvement in the reentrant circuit. In addition, the observation that the atrial electrogram from the lateral coronary sinus preceded that from the low r i g h t a t r i u m d u r i n g t h e t a c h y c a r d i a is strongly suggestive of left-sided retrograde p r e e x c i t a t i o n . 2~ In A-V n o d a l reentry, for example, one would have anticipated t h a t r e t r o g r a d e atrial depolarizations would result in initial activation of the low a t r i a l s e p t u m , w i t h t h e low r i g h t a t r i a l electrogram preceding that from the coron a r y sinus. 26'27 The sequence of activation found in our p a t i e n t d u r i n g t a c h y c a r d i a strongly supports retrograde conduction t h r o u g h a left-sided bypass.

Antegrade Conduction Within the Bypass. Regardless of the site of atrial stimulation, impulses spread through the atria to reach both the atrial end of the bypass tract as well as the normal A-V node His axis. As just noted, no evidence of antegrade A-V bypass conduction to the ventricles was apparent. 23'24'28 Either antegrade A-V bypass '~block" existed or such conduction was masked. The latter is possible if 1) antegrade A-V bypass conduction always encountered a refractory ventricle, or 2) the accessory p a t h w a y engaged intramyocardial or subendocardial ventricular sites resulting in "silent" ventricular preexcitation. 6 The former explanation appears unlikely because at increased paced atrial rates, which would be expected to r e s u l t in dec r e a s e d v e n t r i c u l a r r e f r a c t o r i n e s s , 29 A-V W e n c k e b a c h conduction occurred w i t h o u t evidence of antegrade preexcitation. The latter is excluded by the fact that some years previously, s p o n t a n e o u s a n t e g r a d e b y p a s s conduction with a typical Type A W P W pattern was apparent. Although interatrial block is a recognized m e c h a n i s m for a n t e g r a d e bypass conduction failure, 2a'24'a~ this mechanism was excluded because neither right atrial nor left atrial stimulation resulted in ventricular preexcitation. Atrial p r e m a t u r e depolarization induced very late in the atrial cycle during coronary sinus (or left atrial) stimulation resulted in a bout of SVT. Such impulses were conducted t h r o u g h the A-V node ( a p p r o x i m a t e l y 80 msec) and His-Purkinje system (60 msec) and returned to the left atrium (240 msec) to find the left atrium excitable after a total delay of J. ELECTROCARDIOLOGY, VOL. 9, NO. 4, 1976

361

approximately 380 msec. In contrast, spontaneous sinus impulses or p r e m a t u r e atrial depolarizations induced very late in the atrial cycle during right atrial stimulation presumably returned to the left atrium after a similar delay but failed to result in SVT. Atrial refractoriness could not have been the limiting factor in failure of t h e s e i m p u l s e s to traverse the reentrant p a t h w a y because the atrial effective refractory period was only 200 msec and the patient would be expected to remain in continuous SVT. More likely, atrial impulses invaded the accessory p a t h w a y but were blocked in it. The discrepancy between antegrade and retrograde conduction is due to either marked differences in antegrade vs. retrograde refractoriness of the bypass tract al or to " m i s m a t c h e d impedance. T M The relationship of the associated myocardiopathy w i t h f a i l u r e of a n t e g r a d e c o n d u c t i o n is uncertain.

Differing Echo Zones. The echo zone for induction of SVT was shorter for high right atrial stimulation t h a n that for left atrial stimulation. This difference can best be explained by analyses of the probable p a t h w a y s utilized in the tachycardia circuit, illustrated diagrammatically in Fig. 6. As outlined earlier, atrial impulses engage both the atrial end of the bypass tract and the A-V node His axis. Regardless of the precise site of antegrade bypass block, ventriculoatrial retroconduction will fail if it meets a refractory bypass tract (Fig. 6A). However, retroconduction is possible if the conduction time from atrium to the bypass tract (via the A-V-Hisventricular axis) exceeds the s u m of the conduction times from a t r i u m to the blocked b y p a s s a r e a plus t h e effective r e f r a c t o r y period of the bypass (Figs. 6B and 6C). We hypothesize that left atrial stimulation, because of its proximity to the bypass tract, results in earlier activation and recovery of this pathway, thus allowing return conduction of late left atrial p r e m a t u r e depolarizations. On the other hand, similarly timed late atrial p r e m a t u r e d e p o l a r i z a t i o n s from t h e high right atrium would be expected to result in later activation (and recovery) of the bypass tract with the r e t u r n i n g impulse m e e t i n g bypass refractoriness. Retroconduction to the left atrium is, however, possible with earlier high right atrial premature depolarizations only if A-V nodal delay is sufficently long to allow for bypass recovery of excitability. Reentry in our patient was, therefore, critically dependent on the interplay between A-V conduction time vs conduction time from the site of atrial stimulation to the atrial end of the bypass tract. Clearly, if interatrial conduction time re-

362

MORRIS ET AL

mains reasonably constant regardless of the site of atrial stimulation, then conceivably differences in echo zones between the atria may prove to be additional useful criteria for differentiation of the atrial site of bypass insertion. The atrial chamber with the widest echo zone would be expected to be closest to the site of bypass insertion. If only high right atrial pacing were utilized in this study, then the pattern of SVT induction would have fulfilled all the criteria for A-V nodal r e e n t r y 2 -12 Coronary sinus stimulation clearly excluded this possibility and allowed for diagnosis of retrograde activation of an A-V nodal bypass tract. Other i n v e s t i g a t o r s 19-12 h a v e suggested, on the basis of right atrial pacing studies, t h a t the most common m e c h a n i s m for SVT is A-V nodal reentrance. Our own observations plus those of Narula, 33 who showed evidence for isolated retrograde preexcitation in approximately 15% of 124 patients studied by vent r i c u l a r pacing, and Spurrell et al, 3a who found evidence of isolated retrograde pree x c i t a t i o n in 5 of 13 p a t i e n t s w i t h SVT, suggest t h a t retrograde A-V nodal bypass tracts m a y be a more frequent cause of SVT t h a n previously believed.

Clinical Applications. This study is of interest from several standpoints. The demonstration of failure of antegrade bypass conduction in a patient who initially showed this capacity but now uses his accessory p a t h w a y for retrograde ventriculoatrial conduction during SVT supports the observations of Wellens a n d Durrer. 35 Clearly, p a t i e n t s with this syndrome who lose the e l e c t r o c a r d i o g r a p h i c manifestations of antegrade conduction are still susceptible to bouts of SVT because the capacity for retroconduction may still be intact. 25'3a In addition, t h e i n t r o d u c t i o n of newer surgical techniques for patients with WPW and intractable SVT requires precise localization of the bypass tract. 27,36,37 Investigators have emphasized the importance of changes in the ventricular rate in patients w i t h WPW in w h o m i n t e r m i t t e n t b u n d l e branch complexes develop during SVT as a criterion for distinguishing right- from leftsided bypass tracts. 25'3~ In patients with left-sided bypass tracts, for example, the vent r i c u l a r response to SVT with left bundle branch block complexes might be expected to be slower t h a n the response to SVT with normal v e n t r i c u l a r complexes. This criterion is valid if the reentry p a t h w a y involves conduction over all or part of the bundle branches. A reentry circuit t h a t is completed proximal to the site of bundle branch conduction delay would not be expected to show this phenomenon. In our patient the ventricular rate

d u r i n g SVT a s s o c i a t e d w i t h left b u n d l e branch block was identical to t h a t showing a narrow QRS complex (Fig. 2). Variations in conduction times due to drugs, changes in autonomic tone, or other u n k n o w n factors may have affected the ventricular rate. Comparison of the initial atrial electrograms from the right a t r i u m and left a t r i u m during SVT is a u s e f u l t e c h n i q u e for d i s t i n g u i s h i n g bypass sites; nevertheless, Gallagher et a127 found t h a t the atrial electrogram recorded from the os of the coronary sinus m a y precede the right atrial electrogram during SVT in patients with posterior septal bypass tracts. Our observations suggest possibly an additional criterion for differentiation of rightand left-sided bypass tracts: stimulation of the a t r i u m to which the accessory p a t h w a y is connected should produce a wider echo zone t h a n t h a t for the opposite a t r i u m . Theoretically, the echo zones from right and left a t r i a l s t i m u l a t i o n should be identical in patients with septal bypass fibers. F u r t h e r experience, of course, is necessary before this finding can be used as a criterion for differentiating the atrial site of ventriculoatrial activation. Acknowledgment: We are indebted to Dr. Charles Sheptin for referring this patient for study and for kindly allowing us to review all the previous electrocardiograms and rhythm strips.

1.

2. 3.

4. 5.

6. 7.

REFERENCES NADAS, A S, DAESCHNER, C W, ROTH, A AND BLUMENTHAL,S L: Paroxysmal tachycardia in infants and children; study of 41 cases. Pediatrics 9:167, 1952 ORINIUS,E: Pre-excitation. Studies on criteria, prognosis and heredity. Acta Med Scand (Suppl) 465:1, 1966 VERKMAN,N L AND LAMB, L E: The WolffParkinson-White electrogram. A follow-up study of five to twenty-eight years. N Engl J Med 278:492, 1968 FLENSTED-JENSEN, E: Wolff-Parkinson-White syndrome. A long-term follow-up of 47 cases. Acta Med Scand 186:65, 1969 FIARDINA,A C V, EHLERS, K H AND ENGLE, M A: Wolff-Parkinson-White syndrome in infants and children. A long-term follow-up study. Br Heart J 34:839, 1972 DURRER, D AND WELLENS, H J: The WolffParkinson-White syndrome. Anno 1973. Eur J Cardiol 1:347, 1974 ROSENBAUM,F F, HECHT, H H, WILSON, F N AND JOHNSTON, F D: Potential variations of thorax and esophagus in anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome). Am Heart J 29:281, 1945 J. ELECTROCARDIOLOGY, VOL. 9, NO. 4, 1976

ATRIAL ECHO ZONES

8. SCHERLAG,B J, LAU, S H, HELFANT, R H, BERKOWITZ, W D, STEIN, E AND DAMATO, A N: Catheter technique for recording His bundle activity in man. Circulation 39:13, 1969 9. GOLDREYER, B N AND BIGGER, J T, JR: Site of r e e n t r y in p a r o x y s m a l s u p r a v e n t r i c u l a r tachycardia in man. Circulation 43:15, 1971 10. GOLDREYER, B N, WEISS, M B AND DAMATO, A N: Supraventricular tachycardia initiated by sinus beats. Circulation 44:820, 1971 11. GOLDREYER, B N AND DAMATO, A N: The essential role of atrioventricular conduction delay in the initiation of paroxysmal suprav e n t r i c u l a r t a c h y c a r d i a . C i r c u l a t i o n 43: 679,1971 12. WU, D, DENES, P, DHINGRA, R, KHAN, A AND ROSEN, K M: The effects of propranolol on induction of A-V nodal reentrant paroxysmal tachycardia. Circulation 50:665, 1974 13. DURRER, D, SCHOO, L, SCHUILENBURG, R M AND WELLENS, H J J: The role of premature beats in the initiation and the termination of supraventricular tachycardia in the WolffParkinson-White syndrome. Circulation 36:644, 1967 14. NARULA, O S: Sinus node re-entry. A mechanism for supraventricular tachycardia. Circulation 50:1114, 1974 15. PAULAY, K L, VARGHESE, P J AND DAMATO, A N: Sinus node reentry. An in vivo demonstration in the dog. Circ Res 32:455, 1973 16. PAULAY, K L, VARGHESE, P J AND DAMATO, A N: Atrial rhythms in response to an early atrial premature depolarization in man. Am Heart J 85:323, 1973 17. CHILDERS,R W, ARNSDORF, M F, DE LA FUENTE, D J, GAMBETTA, M AND SVENSON, R: Sinus nodal echoes. Clinical case report and canine studies. Am J Cardiol 31:220, 1973 18. WU, D, AMAT-Y-LEON,F, DENES, P, DHINGRA, R C, PIETRAS, R J AND ROSEN, K M: Demonstration of sustained sinus and atrial re-entry as a mechanism of paroxysmal supraventricular tachycardia. Circulation 51:234, 1975 19. RYTAND, D A: The circus m o v e m e n t (entrapped circuit wave) hypothesis and atrial flutter. Ann Intern Med 65:125, 1966 20. SVENSON, R H, GALLAGHER,J J, SEALY, W C AND WALLACE, A G: An electrophysiologic approach to the surgical treatment of the WolffP a r k i n s o n - W h i t e syndrome. Report of two cases utilizing catheter recording and epicardial mapping techniques. Circulation 49:799, 1974 21. WELLENS, H J AND DURRER, D: Pathway of tachycardia in WPW syndrome. Circulation 50 (Suppl III): III-58, 1974 22. ZIPES, D P, DEJOSEPH, R L AND ROTHBAUM, D A: Unusual properties of accessory pathways. Circulation 49:1200, 1974 23. WELLENS, H J J: Contribution of cardiac pacing to o u r u n d e r s t a n d i n g of t h e WolffP a r k i n s o n - W h i t e s y n d r o m e . Br H e a r t J 37:231, 1975 24. WELLENS, H J J, SCHUILENBURG, R M AND DURRER, D: Electrical stimulation of the heart

J. ELECTROCARDIOLOGY, VOL. 9, NO. 4, 1976

25.

26.

27.

28.

29.

30.

31.

32.

33. 34.

35.

36.

37.

38.

363

in patients with Wolff-Parkinson-White syndrome, type A. Circulation 43:99, 1971 NEUSS, H, SCHLEPPER, M AND THORMANN, J: Analysis of re-entry mechanisms in three patients with concealed Wolff-Parkinson-White syndrome. Circulation 51:75, 1975 SPURRELL,R A J, KRIKLER, D M AND SOWTON, E: Problems concerning assessment of anatomical site of accessory p a t h w a y in WolffP a r k i n s o n - W h i t e s y n d r o m e . Br H e a r t J 37:127, 1975 GALLAGHER,J J, GILBERT, M, SVENSON, R H, SEALY, W C, KASELL, J AND WALLACE, A G: Wolff-Parkinson-White syndrome. The problem, evaluation, and surgical correction. Circulation 51:767, 1975 TOUBOUL, P, TESSIER, Y, MAGRINA, J, CLEMENT, C AND DELAHAYE, J P: His bundle recording and electrical stimulation of atria in p a t i e n t s with Wolff-Parkinson-White syndrome type A. Br Heart J 34:623, 1972 DENES, P, Wu, D, DHINGRA, R, PIETRAS, R J AND ROSEN, K M: The effects of cycle length on cardiac refractory periods in man. Circulation 49:32, 1974 SLAMA, P R, COUMEL, P AND BOUVRAIN, Y: Les syndromes de Wolff-Parkinson-White de type A inapparents ou latents en rythme sinusal. Arch Mal Coeur 66:639, 1973 WELLENS, J AND DURRER, D: Patterns of vent r i c u l o - a t r i a l c o n d u c t i o n in t h e WolffParkinson-White syndrome. Circulation 49: 22, 1974 DE LA FUENTE D, SASYNIUK, B AND MOE, G K: Conduction through a narrow isthmus in isolated canine atrial tissue. A model of the W-P-W syndrome. Circulation 44:803, 1971 NARULA, O S: Retrograde preexcitation. Circulation 50:1129, 1974 SPURRELL, R A J, KRIKLER, D M AND SOWTON, E : Concealed bypass of the atrioventricular node in patients with paroxysmal supraventricular tachycardia revealed by intracardiac electrical stimulation and verapmil. Am J Cardiol 33:590, 1974 WELLENS, H J AND 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, 1975 COBB, F R, BLUMENSCHEIN, S D, SEALY, W C, BOINEAU, J P, WAGNER, G S AND WALLACE, A G: Successful surgical interruption of the bundle of K e n t in a p a t i e n t w i t h W o l f f Parkinson-White syndrome. Circulation 38:1018, 1968 WALLACE, A G, SEALY, W C, GALLAGHER,J J, SVENSON, R H, STRAUSS, H C AND KASELL, J: Surgical correction of anomalous left ventricular pre-excitation: W o l f f - P a r k i n s o n - W h i t e (type A). Circulation 49: 206, 1974 COUMEL, P AND ATTUEL, P: Reciprocating tachycardia in overt and latent preexcitation. Influence of functional bundle branch block on the rate of the tachycardia. E u r J Cardiol 1:423, 1974