Characteristics and coexistence of two forms of ventricular echo phenomena

Characteristics and coexistence of two forms of ventricular echo phenomena

Masood Akhtar, M.D. Anthony N. Damato, M.D. Jeremy N. Ruskin, M.D. J. Bimbola Ogunkelu, M.D. C. Pratap Reddy, M.D. Carol J. Leeds, R.N. Staten Island, N. Y.

The phenomenon of re-entry has been demonstrated both experimentally and clinically to occur in most cardiac tissues including the sinus and A-V nodes and the His-Purkinje system.:-:: Those conditions which are considered requisite for the occurrence of re-entry include (1) delayed or asynchronous conduction, (2) unidirectional block, and (3) recovery of excitability. Re-entry may result in one or more echo beats or a sustained tachycardia. Ventricular echo beats resulting from delayed retrograde A-V nodal conduction of premature ventricular beats has been previously described. :~-1~ More recently, it was demonstrated in the human heart that closely coupled premature ventricular beats could also result in ventricular echo beats due to intraventricular re-entry involving the His- Purkinje system. TM It is the purpose of this report to describe a group of patients in whom single premature ventricular beats resulted in two types of ventricular echo beats. In addition, a closely coupled premature ventricular beat produced consecutive ventricular echo beats resulting sequentially from intraventricular and A-V nodal re-entry. Both types of re-entrant phenomena

From the Cardiopulmonary Laboratory, United States Public Health Service Hospital, Staten Island, N. Y.

This work was supported in part by the Bureau of Medical Services, National Heart and Lung Institute Project HL 12536-05.

Received for publication July 1, 1975.

Reprint requests: Masood Akhtar, M.D., Cardiopulmonary Labora- tory, United States Public Health Service Hospital, Staten Island, N. Y. 10304.

will be individually characterized and their occurrence and coexistence as a function of delayed retrograde conduction within the A-V node and His-Purkinje systems will be discussed.

Materials and methods

Right heart catheterization was performed in 45 patients with the use of local anesthesia in a nonsedated, postabsorptive state. The experi- mental nature of the procedure was explained to all patients and signed consents were obtained. Electrode catheters were percutaneously intro- duced into the antecubital and femoral veins and fluoroscopically positioned in the region of the high right atrium, tricuspid valve area, and right ventricular apex for local intracardiac electrogram recordings and/or electrical stimulation: 1: Intracardiac electrograms, standard elec- trocardiogram (ECG) Leads I, II, III, and V: and time lines generated at 10 and 100 msec. were displayed on a multichannel oscilloscope and recorded onto a magnetic tape. The records were subsequently reproduced and recorded on a photographic paper at a speed of 150 mm. per second. Retrograde refractory periods were performed at a basic ventricular cycle length ($1 $1 or V: V:) with the ventricular extrastimulus method ($2 or V~). :8 The ventricular coupling interval ($1 $2 or V1 V2) was gradually decreased by 5 to 20 msec. to the point of ventricular muscle refractoriness. For electrical stimulation of the ventricles, rectangular impulses of 1.5 msec. duration were delivered through an isolation unit at a minimum milliamperage (< 1 ma. ) which allowed

174 August, 1976, VoL 92, No. 2, pp. 174-182

Two forms of ventricular echo phenomen a

reliable ventricular Capture. All equipment was carefully grounded. No incidence of untoward effects occurred.

None of the pat ients had prior evidence of tachyarrhythmias, Wolff-Parkinson-White syn- drome, or spontaneous atrial or ventricular extra beats. Patients with acute myocardial ischemia or electrolyte imbalance were excluded from the study.

Definition of terms TM

The A-H interval was measured from the onset of low atrial electrogram (on the His bundle electrogram recording) to the onset of His bundle potential and was taken as an approximation of antegrade A-V nodal conduction time. Similarly the H-V interval which represented antegrade conduction time in the His-Purkinje system was measured from the onset of His bundle potential to the earliest recordable ventricular activity on the His bundle electrogram recording or the surface ECG.

During retrograde conduction, the V-A interval representing retrograde His-Purkinje and A-V nodal conduction time was measured from the corresponding stimulus artifact (S) to the begin- ning of the low atrial electrogram. When retrograde His bundle potential could be recognized during the basic ventricular drive beat (H~) or when the His bundle deflection emerged from the

ven t r i cu la r electrogram with the premature ventricular beats (H~), the retrograde His- Purkinje conduction time was measured from the corresponding stimulus artifact to the end of the His bundle potential. Likewise, H-A interval representing retrograde A-V nodal conduction time was measured from the end of the His

�9 bundle potential to the onset of low atrial electrogram.

Results

In a group of 45 patients with intact A-V conduction both antegrade and retrograde conduction and refractory period studies were performed, but only the results obtained during retrograde refractory period studies will be pre- sented in this report. Forty of the 45 patients (group A) demonstrated intact ventricutoatrial (V-A) conduction during basic ventricular drive and five of 45 patients (group B) demonstrated no evidence of V-A conduction at all ventricular

paced rates. In the latter group, the A-V node was the site of unidirectional block.

Ventricular echo beats (Ve) resulting from re- entry within the A-V node. This form of ventricular echo phenomenon occurred in 12 of 40 patients in group A and in none of the five patients (group B) who had no V-A conduction. At predetermined basic ventricular cycle lengths (range, 500 to 1,000 msec.) the sequence of premature ventricular stimulation was initiated with a relatively late premature beat ($1 $2 50 to 100 msec. shorter than $1 $1). Progressive decreases in $1 $2 interval resulted in progressive increases in $2 A~ intervals in group A patients. Within a certain range of $1 $2 intervals (range, 600 to 330 msec.) and $2 A2 intervals (range, 220 to 550 msec.) another ventricular beat (Ve) appeared in 12 of the group A patients (Fig. 1). In most patients the retrograde His bundle potential (H2) for these relatively late premature beats was obscured within the ventricular etectrogram and for the reasons listed below it can be reasonably inferred that the Ve resulted from A-V nodal re- entry and henceforth will be referred to as Ve- AVN.

1. Ve-AVN was preceded by retrograde activation of the atria, i.e., a low-to-high atrial activation sequence in contrast to the sequence of atrial activation during the sinus beats which was from the high-to-low atrium.

2. Ve-AVN was always preceded by an H-V interval equal to that of sinus beats.

3. The QRS morphology of Ve-AVN was the same as that of sinus beats.

4. The occurrence of Ve-AVN was dependent upon achievement of critical $2 A~ or H~ A2 delays (see below),

5. Ve-AVN did not occur when $2 retrogradely blocked in the A-V node, but reappeared when V2 A2 conduction resumed at closer $1 $2 coupling intervals (phenomenon of retrograde gaps)2 ~

6. Ve-AVN was never observed in the five patients who had no V-A conduction (group B).

7. Ve-AVN disappeared at closer V V~ intervals because the latter resulted in longer S~ H2 delays which permitted recovery of A-V node and pre- vented at tainment of the requisite H~ As delay.

It is important to note that Ve-AVN occurred at relatively long $1 $2 intervals and prior to the emergence of H~ from the V o electrogram. There- fore, direct measurements of the degree of retro-

American Heart Journal 175

A k h t a r e t a l .

A CL800 1_

B

c 1 . . . .

I I I I - - I I I I I I ~ I l f l l l l l - - ~ .

Fig. 1. Ventricular echo (re-entry A-V node). Tracings in each panel are ECG Leads I, It, V, high right atrial electrogram (HRA), His bundle electrogram (HBE), and time lines (T) at 10 and 100 msec. S denotes stimulus artifact. The same abbreviations are used in subsequent tracings. The basic ventricular cycle length (S 1 $1) is 800 msec. in all panels and S I A 1 measures 300 msec. In panel A, a premature ventricular beat (V2) coupled at an S t S 2 interval of 550 msec. conducts retrogradely with a n S 2 A 2 interval of 340 m s e c . A 2 is followed by another ventricular beat (Ve A VN) having the same QRS morphology and H-V interval as the sinus beat which follows. Note the low- to-high atrial activation sequence during ventricular pacing whereas a high-to-low sequence is recorded during sinus beats. At a closer coupling interval (panel B) S 2 retrogradely blocks prior to emergence of H 2 from the V 2 electrogram. Panel C shows emergence of H 2 from the V 2 electrogram at closer S t S 2 intervals and H 2 is not followed by atrial activation (retrograde A-V nodal block). Retrograde block o f S 2 in the A-V node is not associated with Ve-A VN. The amplitude of QRS complexes has been deliberately reduced to avoid excessive levels during ventricular pacing on the tape recorder.

grade A-V nodal (Hs A~ interval) delays were not always available. However, following the emergence of H2 from V2 at closer coupling intervals it could be documented tha t this form of ventricular echo beat was dependent upon H~ A2 delays ra ther than Ss Hs delays. Furthermore, in nine of 40 patients the retrograde His bundle potent ial was identifiable during the basic ventr icular drive and it could be directly determined tha t with late premature beats (i.e., with $1 S~ of 450 msec. or longer) increases in S~ As intervals were entirely the result of increases in Hs A~ intervals and not due to delays below the bundle of His (i.e., $2 Hi interval).

The degree of retrograde A-V nodal delay was, up to a point, inversely related to the V~ Vs interval. At very short V1 Vs intervals premature

ventr icular beats (Vs) encountered retrograde conduct ion delay within the His-Purkinje system, causing an increase in the $1 Hs intervals. The relatively later arrival of the Vs impulse into the A-V node resulted in a decrease in t h e H2 A2 interval. Therefore, for a given $1 Ss interval the resulting $1 H2 interval was lesser or greater compared to the S1 Hs interval resulting from longer or shorter S~ Ss intervals.

In the remaining 28 patients with intact V-A conduct ion Ve-AVN did not occur despite premature ventricular s t imulat ion at comparable V1 V2 intervals and the a t t a inmen t of comparable V2 As interval delays. Thus, the frequency of Ve-AVN was found to be 30 per cent (12 of 40) in patients with in tac t V-A conduction.

Ventr icular echo beats resulting from re-entry

176 A u g u s t , 1976, Vol. 92, No. 2

T w o f o r m s o f v e n t r i c u l a r echo p h e n o m e n a

Fig. 2. Ventricular echo (re-entry HPS). This figure demonstrates further continuation of the sequence of ventricular premature stimulation at progressively decreasing coupling intervals in the same patient and at the same basic ventricular cycle length as Fig. 1. In Panel D S 2 conducts to the His bundle with an S 2 H 2 interval of 210 msec. but is blocked in the A - V node (no A2). V 2 is followed by another ventricular beat (Ve-HPS) which has similar QRS morphology and axis orientation as V2, and is preceded by H-V interval of 115 msec. In panel E, at a closer S l S 2 interval of 280 msec. S 2 blocks below the bundle of His and Ve-HPS does not occur. Panel F simply shows the S 1 S 2 interval at which S 2 fails to evoke a ventricular response.

within the His-Purkinje system.Within a given range of short V1 V~ intervals, all 45 patients demons t ra ted retrograde conduct ion delay within the HPS, which was reflected in emergence of H2 from the V2 electrogram.

In 20 of 45 patients, retrograde conduct ion delay within the HPS was associated with ano ther type of ventr icular echo beat, hereafter referred to as Ve-HPS (Fig. 2) and having the following characteristics.

1. Ve-HPS, when present, always occurred after H2 emerged from the V~ electrogram.

2. Ve-HPS occurred within a narrow range of close V1 V~ intervals (210 to 350 msec.).

3. The occurrence of Ve-HPS was dependent upon Sz H2 delays (range, 120 to 350 msec.) and was independent of H~ A delays.

4. Ve-HPS did not occur when S~ retrogradely blocked below the bundle of His and reappeared

when $2 H2 conduct ion resumed at closer ventricular coupling intervals (the phenomenon of retrograde gaps). TM

5. Ve-HPS persisted when $2 blocked above the bundle of His (A-V node) and was also seen in two of five patients w h o had no V-A conduction across the A-V node.

6. When the right ventricular apex was site of s t imulat ion the QRS morphology and axis orienta t ion of Ve-HPS was similar to V2 (left bundle branch block pattern).

7. Ve-HPS did not occur in pat ients having a pre-existing right bundle branch block p a t t e r n (see below).

The aforementioned characteristics of Ve-HPS strongly suggest tha t re-entry of V2 was via a macro re-entrant circuit utilizing the bundle branches and bundle of His. TM I t is postulated tha t within the critical range of coupling intervals $2,

A m e r i c a n H e a r t J o u r n a l 177

A k h t a r et al .

A : :CL 500 :: :: v,=AVN

.~...,...~.,.....~!.~ ~ B Ve HPS Ve AVN

IT 270 ' "

Fig. 3. Dual re-entry (A-V node and HPS). The basic ventricular CL is 500 msec. in all panels. The retrograde His bundle potential is recognizable during the basic drive (H 1). At an S l S 2 interval of 280 msec. (Panel A ) S 2 conducts to the atria with an S 2 H 2 interval of 190 (H 2 follows V 2) and an H2A 2 interval of 255 msec., and a Ve-A V N follows. Compare the atrial activation sequence preceding Ve-A V N with sinus beats. Panel B shows that at closer S 1 S 2

interval and longer S 2 H 2 interval (compared to panel A) V 2 is followed by another ventricular beat labeled Ve- HPS. Ve-HPS precedes A 2 and is preceded by an H-V interval of 115 msec. The QRS morphology of Ve-HPS (RBBB) is compatible with activation from the left ventricular (see text for details). The Ve-HPS is followed by another ventricular beat (Ve-A VN) which is. preceded by similar H 2 A 2 and A-H intervals as in panel A, but a longer H-V interval (140 msec.). The QRS morphology of V e - A V N (LBBB pattern) suggests that the Ve-HPS after activating the ventricles failed to engage the right bundle branch retrogradely and the latter was utilized by the A-V nodal re-entrant impulse. Panel C shows essentially the same events as panel B except that the A-V nodal re-entrant impulse antegradely blocks below the bundle of His. This is not unexpected if one considers that the H- V interval in panel B represents markedly prolonged conduction time in the HPS.

wh ich is de l ivered to the r igh t ven t r ic le , is re t ro- g rade ly b locked w i t h i n the r ight b u n d l e b r a n c h . T h e l a t e r a r r iva l of $2 w i t h i n the lef t b u n d l e b r a n c h p e r m i t t e d r e t rog rade c o n d u c t i o n back to the b u n d l e of His, a f ter which, if t he r igh t b u n d l e b r a n c h a n d / o r v e n t r i c u l a r musc le recovered suffi- c ien t ly , a n t e g r a d e c o n d u c t i o n a n d r e - exc i t a t i on

of the r igh t ven t r i c l e was possible. Th i s r o u t e of r e - e n t r y also exp la ins the s imi lar i t ies b e t w e e n t he Q R S m o r p h o l o g y a n d axis o r i e n t a t i o n of V e - H P S

a n d t h a t of Vs. T h e fac t t h a t V e - H P S were preceded by H-V i n t e r v a l s cons ide rab ly longer t h a n those of s inus be a t s ~ndicates t h a t the re- e n t r a n t impu l se was a n t e g r a d e l y c o n d u c t e d d u r i n g t he i n c o m p l e t e recovery phase of the r ight b u n d l e b r a n c h - P u r k i n j e sys t em a n d / o r vent r ic - u l a r musc le . These obse rva t i ons also stiggest t h a t local r e - e n t r y occur r ing n e a r the site of s t i m u l a - t ion is a n u n l i k e l y m e c h a n i s m of V e - H P S in th is

group of pa t i en t s .

1 78 A u g u s t , 1976, Vol. 92, No. 2

T w o f o r m s o f v e n t r i c u l a r echo p h e n o m e n a

Fig. 4. Dual re-entry (A-V node and HPS). The basic ventricular drive rate is 700 msec. Panel A shows a Ve-A VN resulting from an S 2 A 2 of 270 msec. at a ventricular coupling interval of 350 msec. In panel B S 2 blocks retrogradely in the A-V node and Ve-AVN does not occur. At a closer coupling interval of 270 msec. (panel C) S 2 still blocks retrogradely in the A-V node but is associated with longer S 2 H 2 interval (175 msec.) which results in Ve-HPS. Note the similarity between the QRS complexes of V 2 and Ve-HPS. Panel D shows a Ve-HPS occurring at an S t S 2 interval of 260 msec. and an S 2 H 2 interval of 190 msec. The longer Sl H2 interval in panel D of 450 msec. (not labeled) compared to panels B and C (445 msec.) results in resumption of retrograde A-V nodal conduction and Ve-A VN (a retrograde gap phenomenon). The Ve-A V N in panel D has a left bundle branch block pattern and longer H-V interval compared to panel A (see text for details).

I n two p a t i e n t s V e - H P S had a Q R S m o r p h o - logy of r igh t b u n d l e b r a n c h b lock p a t t e r n ind ica t - ing exc i t a t i on s t a r t i n g f rom the left ven t r i c l e (Fig. 3). Th i s is cons i s t en t w i th r e - en t ry by reciproca- t ion w i t h i n the left b u n d l e b r a n c h sys t em or

pe rhaps V2 was r e t rog rade ly c o n d u c t e d by the r igh t b u n d l e b r a n c h a n d t h e n a n t e g r a d e l y acti-

v a t e d the ven t r i c les by the left b u n d l e b r anc h .

T h e foregoing hypo thes i s is based u p o n t he a s s u m p t i o n t h a t in some p a t i e n t s r e t rog rade re f rac to r iness of the left b u n d l e b r a n c h exceeds t h a t of the r igh t b u n d l e b r a n c h . I n two p a t i e n t s V e - H P S was preceded by H-V i n t e r v a l s t h a t were

shor t e r t h a n H - V in t e rva l s of s inus beats . U n d e r these se t t ings d e p e n d i n g u p o n the Q R S m o r p h o - logy of V e - H P S one m a y p o s t u l a t e r ec ip roca t ion

A m e r i c a n H e a r t J o u r n a l 1 79

Akhtar et al.

700

600

5O0

Imsec ) 4O0

3O0

200,

100,

VCL 700 (m sec)

Jo I"-'1 I'~--'-I ~ ~ 0 ~

: rl I ~ 1 7 6 ERP I ~ I VENT U ~ ~ . .

~_~o , V2H 2 Reentry j HPS

i I 250 300

O

O

o A1A2

]][]ZONE OF NO V-A COND.

�9 V2A 2

O Reentry A-Vnode

I II I I ' I 60o

VlV2 (rnsec) Fig, 5. Dual re-entry (A-V node and HPS). The figure is a graphic display of the sequence of events during premature ventricular stimulation and depicts some of the typical aspects of dual re-entry (same patient and cycle length as Fig. 4). The coupling intervals (abscissa) are plotted against V 2 H2, V2A2, and A 1 A2 intervals (ordinate). Note progressive increase in V 2 A 2 intervals as V~ V; intervals are decreased. A-V nodal re-entrant echo beats, Ve

{larger circles), appeared at V t V 2 intervals of 400 msec. or less and V 2 A 2 of 230 msec. or greater prior to the emergence of H 2 from V 2. At V~ V 2 of 340 msec. V 2 blocks retrogradely (zone of no V-A conduction) and Ve-A V N is abolished. The H e emerges from V 2 (larger dots) at a V 1 V z of around 320 msee. which localizes the site of retrograde block to the A-V node. At closer V z V 2 interval of 270 msee. when V z H 2 interval is of sufficient magnitude Ve- I IPS appears (bracketed) while the retrograde A-V nodal block persists {see also Fig. 4). At closer coupling intervals V-A conduction resumes and V 2 results in dual re-entry up to the point of ventricular muscle refractoriness.

within the right or left bundle branch. Dual re-entry (Ve-AVN and Ve-HPS). In nine

patients from group A both Ve-AVN and Ve-HPS were observed during t he sequence of premature ventricular st imulation. In all nine patients Ve- AVN was initiated at longer ventricular coupling intervals ($1 $2 range, 330 to 5 8 0 msee.; Figs. 1, 3, 4, and 5) and Ve-HPS was initiated at shorter coupling intervals (S~ S~ range, 270-340; Figs. 2 to 5}. In five of these nine patients bo th forms of re- en t ran t ventricular echo beats resulted from a single premature ventricu]ar impulse (Figs. 3 to 5).

The zone of $1 S~intervals at which both forms of ventricular echo beats resulted fi'om a single $2 impulse were quite narrow (30 to 90 msec.; range of S~ $2, 200 to 300 msec.).

The QRS morphology of Ve-AVN was always aberrant when a Ve-HPS preceded it. The aber- ran t QRS morphology of the Ve-AVN was either of a left or right bundle b ranch block type (Figs. 3 and 4).

Discussion

The results of this s tudy demonst ra te tha t at least two different types of ventricular echo beats may result from premature s t imulat ion of the right ventricle. Relat ively late premature ventric- Mar beats produce only Ve-AVN, whereas closer p remature beats may produce either Ve-AVN or Ve-HPS or both. The occurrence of one or the other type of ventr icular echo beat was directly related to the degree of retrograde conduct ion delay achieved in either the A-V node or the HPS. Manifestat ion of reent ry in the form of echo beats depend upon the interplay of many factors. The precise role of the various factors involved in the re-ent rant process is far from clear. However, some of the more accepted concepts may be briefly mentioned in relation to the observations made during the present study.

1. C o n d u c t i o n de lay . TM ,9 The association of c o n d u c t i o n delays and re-entrant phenomena, a frequently observed relationship, was consistent- ly seen during the present study. The Ve-AVN

1 8 0 A u g u s t , 1976, Vol. 92, No . 2

Two forms of ventricular echo phenomena

appeared to be dependent upon retrograde conduction delay in the A-V node and Ve-HPS upon conduction delay within the HPS.

2. Unid i rec t iona l block. 1, 10, 20, 21 The comple- tion of a re-entrant phenomenon is difficult to envision without accepting the concept of unidirectional block. On the assumption ttlat the proposed mechanism of Ve-HPS is most likely, it would appear that a retrograde block in the right bundle branch system was required for manifesta- tion of Ve-HPS. In all probability similar mechanism was operative during Ve-AVN; however, documentation of unidirectional block during A-V nodal re-entrant process is more difficult to obtain.

3. Recovery of excitability. It is obvious that recovery of excitability must occur before a tissue can be re-excited, which is the case during manifest form of any re-entry. The concealed form of re-entry probably occurs more frequently than is generally realized and may be the case in some patients in this series in whom significant degrees of conduction delays were achieved but Ve-AVN and/or Ve-HPS did not occur.

4. Further considerations. Finally it must be pointed out that even if all the above conditions are met a critical balance between conduction and refractoriness must exist within the various limbs of a re-entrant circuit for effective propaga- tion of a re-entrant impulse.

In the present series Ve-AVN occurred only in those patients in whom the requisite Vz A2 delays were the result of conduction delay in the A-V node (i.e., H~ A~ delay).

In 12 of 40 patients in group A, requisite V~ A~ delays were achieved but Ve-AVN did not occur. It became apparent in these patients that at close S1 $2 intervals, when H2 emerged from the V2 electrogram, the long V2 A2 intervals resulted primarily from $2 H~ delays. The H2 Az delays were of relatively short duration, i.e., < 50 msec. Consequently, requisite retrograde A-V nodal delay for re-entry was never achieved. It is also interesting to note that in these 12 patients $2 never retrogradely blocked in the A-V node. Likewise, in the five patients who had no V-A conduction Ve-AVN did not occur. These observations suggest that lack of sufficient conduction delay and absence of conduction across the A-V node will not favor the occurrence of manifest A- V nodal re-entrant phenomenon. In the remain-

ing 16 patients who had no Ve-AVN the magnitude of Hi A2 delays was the same as in those patients who did have re-entry. For these patients one may postulate that factors other than conduction delay as mentioned above were not operative.

The Ve-HPS was seen relatively more frequently in this series of patients i.e., 20 of 45. This is particularly striking if one considers that 10 of 45 patients in this series had pre-existing complete right bundle branch block pattern, a condition which does not favor Ve-HPS (one 9f ten patients). This means that in the absence of complete right bundle branch block Ve-HPS occurred in 19 of 35 patients or 54 per cent, whereas Ve-AVN occurred in 12 of 45 patients (27 per cent). If the mechanism and route of re-entry of Ve-HPS is t h e one suggested above (see results), then one will not expect to see Ve-HPS in patients with antegrade right bundle branch block or retrograde left bundle branch block when the premature ventricular beat originates from the right ventricle. Three patients in this series had pre-existing left bundle branch block pattern, two of which were rate related. The Ve- HPS was seen in the two patients with rate- related left bundle branch block pattern.

Both Ve-AVN and Ve-HPS in this study were seen generally as one and occasionally as two consecutive beats and the process terminated spontaneously. The lack of sustained re-entry may relate to the fact that the critical balance of conduction and refractoriness between the various limbs of the re-entrant circuit, which is necessary to sustain any form of re-entry, was not attained in these patients.

The coexistence of dual re-entry, i.e., A-V nodal and His-Purkinje at the same time, can produce complex ECG patterns, and may mimic multiple multifocal ventricular beats. Results of this study indicate that some of these ventricular beats may be of A-V nodal re-entrant origin. This of course will be difficult to determine from the surface ECG. The QRS morphology and the axis orientation of Ve-AVN depend upon the influence and the degree of penetration of the HPS by the preceding Ve-HPS.

For example, if the Ve-HPS after activating the ventricular muscle fails to retrogradely penetrate the left bundle branch, the oncoming A-V nodal re-entrant impulse will find the right bundle

American Heart Journal 1 8 1

Ak htar et al.

b r a n c h m o r e r e f r a c t o r y s ince i t was t h e l a s t one to be a c t i v a t e d a n d d e s c e n d a l o n g t h e le f t b u n d l e b r a n c h w i t h r e s u l t a n t Q R S c o m p l e x d i s p l a y i n g r i g h t b u n d l e b r a n c h b l o c k p a t t e r n . On t h e o t h e r h a n d , if V e - H P S does p e n e t r a t e t h e l e f t b u n d l e b r a n c h r e t r o g r a d e l y , t h e n t h e o n c o m i n g A-V n o d a l r e - e n t r a n t i m p u l s e m a y p r o p a g a t e a l o n g t h e r i g h t b u n d l e b r a n c h a n d the r e s u l t i n g Q R S c o m p l e x wil l h a v e a le f t b u n d l e b r a n c h b l o c k p a t t e r n (Fig. 4). R e g a r d l e s s of t h e or ig in of Ve- H P S , a t t i m e s b o t h b u n d l e b r a n c h e s a n d / o r t h e P u r k i n j e n e t w o r k m a y be e f fec t ive ly r e f r a c t o r y to t h e A - V n o d a l r e - e n t r a n t i m p u l s e w h i c h m a y t h e n d i s p l a y a b l o c k w i t h i n t he H P S (Fig. 3).

Summary

D u r i n g t h e s c a n n i n g of p a c e d bas i c v e n t r i c u l a r cyc le l e n g t h s (V~ V1) w i t h e x t r a s t i m u l u s m e t h o d (V~) two f o r m s of v e n t r i c u l a r echo p h e n o m e n a (Ve) were r ecogn ized . T h e Ve r e s u l t i n g f r o m A-V n o d a l r e - e n t r y ( V e A V N ) o c c u r r e d in 12 of 45 p a t i e n t s , f r om r e - e n t r y in t h e H i s - P u r k i n j e s y s t e m ( V e - H P S ) in 20 of 45 p a t i e n t s , a n d s imu l - t a n e o u s d u a l r e - e n t r y ( V e - A V N a n d V e - H P S ) o c c u r r e d in five of 45 p a t i e n t s . T h e V e - A V N (1) a p p e a r e d a t l onge r V1 V~ in t e rva l s , (2) was depen - d e n t on r e t r o g r a d e A - V n o d a l c o n d u c t i o n de lay , (3) h a d n o r m a l Q R S c o m p l e x e s a n d H - V in t e r - vals , a n d (4) d id n o t o c c u r when V2 b l o c k e d in t h e A - V node . (5) V e - A V N h a d a b e r r a n t Q R S c o m p l e x e s w h e n p r e c e d e d b y V e - H P S . T h e Ve- H P S (1) a p p e a r e d a t s h o r t e r V1 V2 i n t e r v a l s , (2) was d e p e n d e n t u p o n r e t r o g r a d e c o n d u c t i o n d e l a y in t h e H P S , (3) i t s Q R S m o r p h o l o g y a n d axis o r i e n t a t i o n r e s e m b l e d V:, i.e., lef t b u n d l e b r a n c h b l o c k p a t t e r n , w h e n r i g h t v e n t r i c u l a r apex was t h e s i t e of s t i m u l a t i o n , (4) pe r s i s t ed w h e n V: b l o c k e d in t h e A - V n o d e a n d was a b o l i s h e d w h e n V2 b l o c k e d b e l o w t h e b u n d l e of His , a n d (5) r a r e l y o c c u r r e d in p a t i e n t s w i t h p r e - e x i s t i n g r i g h t b u n d l e b r a n c h b lock . I t is c o n c l u d e d t h a t (1) a t l e a s t two f o r m s of Ve can r e su l t f r o m i n d u c e d p r e m a t u r e v e n t r i c u l a r bea t s , (2) V e - H P S is m o r e c o m m o n t h a n V e - A V N in t h e p re sence of n o r m a l Q R S complexes , a n d (3) coex i s t ence of V e - A V N a n d V e - H P S c a n give r ise to c o m p l e x E C G p a t t e r n m i m i c k i n g m u l t i p l e m u l t i f o c a l p r e m a t u r e v e n t r i c u l a r bea t s .

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Characteristics and coexistence of two forms of ventricular echo phenomena

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