his bundle recordings in atypical a-v nodal wenckebach block during cardiac pacing

Diagnostic Shelf

His Bundle Recordings in Atypical A-V Nodal Wenckebach Block

During Cardiac Pacing

CESAR CASTILLO, MD ORLANDO MAYTIN, MD AGUSTIN CASTELLANOS, Jr., MD, FACC

Miami, Florida

From the Department of Medicine, Uni- versity of Miami School of Medicine and the Cardiopulmonary Laboratory, Veterans Administration Hospital, Miami, Fla. Manu- script received February 17, 1970, ac- cepted May 8, 1970.

Address for reprints: Agustin Castel- lanes, Jr., MD, University of Miami School of Medicine, Section of Cardiology, Depart- ment of Medicine, P.O. Box 875, Biscayne Annex, Miami, Fla. 33152.

570

The features of the classic atrioventricular (A-V) nodal Wenckebach phenomenon are attributed to a conduction delay in the A-V nodal region. Changes in the P-R intervals merely represent the variations of the H-H intervals. The characteristic abnormalities of the latter consist of: (1) a gradual increase in P-H intervals; (2) a progressive decrease of the P-H increments; (3) a progressive diminution of the H-H intervals; (4) the long H-H interval produced by the nonconducted P wave is equal to the sum of the increments subtracted from twice the P-P intervals; and (5) the H-H interval after the intermission is longer than the H-H interval preceding the pause.

Tracings from 4 patients with atypical characteristics are presented. Case 1 showed an increase of the H-H intervals. In addition, the pause was terminated by an atrial echo. In Case 2 there was premature (retrograde) excitation of the His bundle. The last 2 patients had an A-V nodal Wenckebach phenomenon co-existing with a block below the His bundle (type II Mobitz block). In one, this double conduction disturbance occurred during forward propagation, whereas in the other it appeared during retrograde conduction.

Knowledge of human electrophysiology has been enhanced by the information obtained from His bundle recordings. The catheter technique has been most helpful in localizing the areas of conduction delay within the specialized atrioventricular (A-V) and intraventricular conducting tissues. Damato and co- workers1-4 have studied the different types of natural and iatro- genie A-V block. These authors, as well as Watanabe and Drei- fus,5 and Katz and Pick,0 have stressed that the Wenckebach phenomenon can show significant variations from the classic pat- tern. The purpose of this report is to present His bundle recordings from patients with second degree block not displaying the characteristic structure of the Wenckebach phenomenon at the nodal level.

Material and Methods

The technique used in our laboratory is similar to the one introduced by Scherlag et al.1 After obtaining proper consent from t,he patient, a tripolar catheter electrode was introduced through the femoral vein and positioned across the septal leaflet of the tricuspid valve. Three different sets of filtered (40 to 2,000 cycles/set) bipolar leads of the His bundle (HBE) were obtained. Two additional bipolar catheters were introduced through an antecubital vein. One was advanced into the right atrium and placed in close proximity to the sinus node. This lead, which was also filtered, registered the bipolar atria1 electrocardiogram (BAE)

The American Journal of CARDIOLOGY

HIS BUNDLE RECORDINGS IN WENCKEBACH BLOCK

Figure 1. Diagrammatic representation of a classic atrioventricular (A-V) nodal Wenckebach phenomenon. Time intervals are expressed in msec. A and V sig

P, PZ p3 p4 % ‘6 nal the onset of atrial and ventricular

A I 600 I 600

A-H \ 100, I_

600 depolarization, respectively. H repre- \ sents depolarization of the His bundle.

H ,100.350=

HI 800 Hz 700 H3 650 H4 850 Hs A-H and H-V indicate the areas of de-

H-V \60 \60 \60 \60 \60 lay above and below the His bundle.

V 1100 350=

800 700 650 850 H-V conduction time is represented by

RI R2 R3 R4 the numbers at the corresponding level.

K5 Numbers at A-H level indicate the value of successive P-H increments. Intrai- atrial conduction was ,considered to be constant.

high in the right atrium. In 1 patient (see Fig. 2) a unipolar atria1 lead was also recorded. The third catheter was used for atria1 or ventricular pacing as required. One or several standard leads were obtained simultaneously with the intracardiac leads using an Electronics for Medicine recorder. Electrocardiograms were also stored on magnetic tape for future playback. Paper speed was 50 or 100 mm/see.

The following measurements were made from lead II and the His bundle electrogram (HBE) : (1) P-R interval: from the onset of atria1 activation (emission of the spike during atria1 pacing) to the beginning of ventricular depolarization. (2) P-H interval: from the onset of atria1 activation (emission of the spike during atria1 pacing) to the onset of the His bundle (H) deflection. (3) H-R interval: from the beginning of the H deflection to the onset of ventricular depolarization. (4) R-P- interval: from the emission of the spike de- livered to the ventricles to the onset of atria1 activity, wherever it occurred in the bipolar atria1 or His bundle leads. The latter were used because the beginning of the retrograde P waves could not be identified clearly in lead II during retrograde conduction. (5) R-H- interval: from the emission of the spike to the onset of the (retrograde) His bundle deflection.

Four cases showing certain atypical characteristics of the nodal Wenckebach phenomenon were selected for presentation. Conventional ladder diagram@ were modified to incorporate the His bundle deflection and the corresponding A-H and H-V intervals.

Characteristics of the Classic A-V Nodal Wenckebach Phenomenon

The classic features of this conduction distur- banceas7 are shown in Figure 1 and Table I. The Wenckebach phenomenon is represented as occurring between the atria and His bundle.

TABLE I

1. The best known manifestation of the Wencke- bath phenomenon is progressive prolongation of the P-R intervals in each series (Table I). This is manifested in the His bundle electrogram as a gradual increase in P-H intervals (Table I). Since the varying block occurs exclusively above the His bundle, the H-R intervals were diagrammed as having a fixed value, which was selected arbitrarily (to facilitate other measurements) as 60 msec (Table I). (In actual recordings an H-R conduction time of 60 msec is abnormal.) The P-H intervals after P,, Pz, PB and Pq measured 140, 340,440 and 490 msec, respectively. The cycle is terminated by a blocked P wave ( P5).

2. The P-R increments show a gradual shorten- ing. This is manifested in the His bundle electrogram as a progressive diminution of the P-H increments (Table I, column 3). The term “increments” is used in reference to the increase of each P-H interval over the preceding one. The successive increments in Figure 1 measure ZOO, 100 and 50 msec, respectively.

3. The progressive diminution of the R-R intervals is due to a similar change in the H-H interval (Table I, column 4). For instance, HI-H2 measures 800 m&c, resulting from the addition of 200 msec (first increment) and 600 msec (PI-P, interval).

4. The pause the blocked (P,) wave produces equals the sum of the increments subtracted from twice the P-P intervals. The long H-H results from the sum of 2 P-P intervals (600 msec + 600 msec = 1,200 msec) modified by an encroach- ment represented by the difference between the first and the longest P-H intervals (490 msec -

Measurements in Classic A-V Nodal Wenckebach Block with P-P Intervals of 600 msec (Fig. 1)

P-R Intervals P-H Intervals (ms=) (ms@

Increments of Successive P-H Intervals

(msec) Resulting H-H Intervals

(msec) H-R Intervals

(msec)

PI-R, = 200 Pz-Re = 400 Pa-R* = 500 P,-R, = 550 Pg blocked

PI-HI = 140 HI-RI = 60 Pt-Ht = 340 1st increment = 340 - 140 = 200 HI-H* = 600 + 200 = 800 HrRz = 60 Pa-Ho = 440 2nd increment = 440 - 340 = 100 H~HJ = 600 + 100 = 700 HrRz = 60 PI-H, = 490 3rd increment = 490 - 440 = 50 Ha-H, = 600 + 50 = 650 H,-R, = 60

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CASTILLO ET AL.

A

A-H H

H-V

V

140 msec = 350 msec). A value of 350 msec is also obtained by adding all the increments : 200 msec + 100 msec + 50 msec = 350 msec. In consequence, the pause after the blocked P wave (P,) measures 1,200 msec - 350 msec = 850 msec. To facilitate understanding of this relationship, Schamroth’ represents the P-P intervals by the letter “M” and the successive increments by a, b, c and so on. Therefore, the long pause (that is, the one includ- ing the blocked P wave) is expressed by the for- mula: 2M - (a + b + c . . .)

5. The last H-H cycle preceding the pause is shorter than the first H-H interval after it. This occurs because the latter contains the longest P-H increment, whereas the former contains the short- est increment.

Atypical Cases Case 1. A-V nodal Wenckebach phenomenon (ter-

minated by an atria1 echo) showing an increase in H-H intervals : Continuous atria1 pacing usually produces a Wenckebach phenomenon above the His bundle (A-H region).2 Since the H-R intervals are constant, changes in the R-R intervals are a reflection of the H-H variations. Figure 2 was obtained during (low) right atria1 pacing at a rate of 120/min. There was a progressive increase in the P-H intervals from

P i p I I i

Figure 2. Case 1. Atypical A-V nodal Wenckebach phenomenon induced by low right atrial pacing. The middle lead is a unipolar recording from the atria. HBE = His bundle electrogram. Note that in contrast with the usual nodal Wenckebach phenomenon, the long pause is terminated by an atrial echo. In addition, the last R-R interval before the intermission is longer than the first R-R interval in the cycle. In this figure, numbers in both A-H and H-V regions represent absolute time intervals. The last P-H interval preceding the echo measured 400 msec. Paper speed = 50 mm/set. St = pacer stimulus artefact.

120 (first cycle) to 400 msec (last cycle). In contrast, the H-H intervals did not show the expected diminution. In fact, the last. interval before the pause measured 560 msec. This unusual finding occurred because the increments did not follow the classic law: They first decreased, but later increased (Table II). The reasons why this occurred are presented in the discussion.

The beat. labeled P-, following the longest P-H interval (400 msec), appeared slightly ahead of the oncom- ing stimulus artefact (second from the end of the tracing). In consequence, this spike was ineffective since it fell in the refractory period of the atria. This beat was an atria1 echo. The ninth P wave could have entered exclusively the intranodal alpha pathway and at a moment in which the beta pathway was refractory.8 However, if the latter had recovered by the time that the impulse reached the deflection point, propagation could have occurred: (1) through the beta pathway toward the atria producing an echo beat, and (2) via the intranodal final common pathway to the His bundle and thereafter to the ventricles (QRS complex labeled R,). The similar polarity of spontaneous and paced beats indicates that both propagated in a similar (inferosuperior) direction throughout the atria.

Case 2. A-V nodal Wenckebach phenomenon with retrograde excitation of the His bundle: In the classic A-V nodal Wenckebach phenomenon the non-

A I a25 I a25 I a25 1 . 285 370 A 310

H 1 \60 _.__L \60

V

Figure 3. Case 2. Atypical spontaneous A-V nodal Wenckebach phenomenon. Retrograde (premature) activation of the His bundle could have represented an automatic His bundle discharge, or a reexcitation of the His bundle by the second atrial impulse. Numbers at the A-V level represent. absolute time intervals. Paper speed = 100 mm/set.

572 The American Journal of CARDIOLOGY


TABLE II III aVR aVL CIVF Measurements in Atypical A-V Nodal Wenckebach Block (P-P interval of 500 set; Fig. 2)

increments (msec)

Resulting H-H Intervals

(mW

1st 40 H-H = 540 2nd 10 H-H = 510 3rd 10 H-H = 510 4th 30 H-H = 530 5th 20 H-H = 520 6th 60 H-H = 560 7th 50 H-H = 550 8th 60 H-H = 560 Total 280

conducted P waves are blocked above the His bundle (Fig. 1). By contrast, in Figure 3, the blocked P wave appeared (at first glance) to have failed below the bundle of His. The second P-H interval was longer th!an the first (3’70 msec > 285 msec). The third P, which did not activate the ventricles, was followed, after an interval of 220 msec, by a distorted His bundle deflection. This P-H interval was shorter than the preceding one-a departure from the classic Wenckebach sequence (Fig. 1). Such a premature and bizarre H deflection might have occurred if the impulse originated by the second P wave, after activating the His bundle, had reentered somewhere from within the H-V region (bundle branch-Purkinje system) finally reexciting the His bundle in a retrograde fashion. Spontaneous pacemaker discharge in the His bundle or in the H-V region seems more likely. Another possibility is that the long preceding P-H interval of 370 msec plus the time from the His deflection to the end of the (second) QRS complex was sufficiently long to allow the A-V node to be sufficiently recuperated. Hence, when the third P wave appeared, its conduction time through the A-V node (P-H interval) was normal. It appears that the third P-H interval was similar to the first P-H interval in the sequence. Since the R-P interval of the third atria1 impulse was short and preceded by a longer pause, it could have behaved like an atria1 paced beat4 when arriving at the bundle branch-Purkinje system during its refractory period. In consequence, the P wave would be blocked below the His bundle, Whatever its origin might have been, this premature H beat penetrated the nodal region, producing concealed conduction in the latter. Hence, the P-H interval after the blocked P wave measured 310 msec instead of the expected 285 msec, which was the duration of the first P-H interval in every cycle. This is another departure from the classic Wenckebach phenomenon in which the initial P-H interval in each series is usually the same or shorter (when the pause is terminated by an escape beat) .6

Case 3. A-V nodal Wenckebach phenomenon with second degree A-V block probably of the Mobitz II type below the His bundle: The tracings presented in Figures 4 to 6 were obtained from a patient with chronic complete right bundle branch block and con-

v2 v3 v4 V5 V6 Figure 4. Case 3. Complete right bundle branch block with right axis deviation due to block in the posteroinferior division of the left branch. The patient had symptomatic intermittent A-V block requiring pacemaker implantation.

P P P P

H ‘. H 1 I t

H m ! H

Figure 5. Case 3. His bundle recording obtained during 2:l A-V block. Nonconducted P waves (second and fourth) are blocked below the His bundle. BAE is a bipolar lead obtained from the high right atrium. During sinus rhythm the onset of atrial depolarization occurred in BAE before that in the HBE (bipolar lead recording from the low right atrium). This indicates superoinferior spread of activation throughout the atria. In this and in Figures 6 to 9, paper speed was 100 mm/set.

SI st st st St !

II -

I 1

Figure 6. Case 3. Classic A-V nodal Wenckebach coexisting with type II (Mobitz) block below the His bundle during continuous atrial pacing. Numbers at the A-H and H-V levels indicate absolute time intervals.

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CASTILLO ET AL.

II

III

,

BAE-+ . *d-----

! H t-l

HBE-++

Figure 7. Case 4. Complete right bundle branch block, block in the posteroinferior division of the left branch and first degree A-V block. The H-R interval is longer than normal (80 msec). During sinus rhythm the onset of atrial depolarization occurred in the BAE before that in HBE. This indicates superoinferior spread of activation throughout the atria.

comitant right axis deviation (Fig. 4). Since there was no evidence of chronic lung disease, right ventricular hypertrophy or extensive lateral wall infarction, right axis deviation was attributed to block in the posteroinferior division of the left branch.lOJi A pacemaker had to be implanted because of syncopal attacks due to intermittent advanced A-V block. The first blocked P wave was not preceded by previous (progressive) P-R prolongation (type II block). Figure 5 shows the con- trol tracing before the onset of atria1 pacing. At this moment there was 2 : 1 A-V block. The conducted beat had a P-R interval of 200 msec. The P-H and H-R intervals measured 140 and 60 msec, respectively. (The upper limits of the H-R interval in our department is 55 msec.) During sinus rhythm, nonconducted P waves were invariably blocked below the His bundle. In the presence of established complete block in the right branch and in the posteroinferior division of the left branch, block below the His bundle could have been due to interruption of conduction in the previously patent anterosuperior division of the left branch. Hence, this patient had evidence of trifascicular block: complete in 2 tracts and intermittent in another tractlo-l2

An interesting arrhythmia appeared during atria1 pacing at a rate of 138/min (P-P intervals of 435 msec) (Fig. 6.). The second P wave, which showed a greater delay through the A-V node, was completely blocked below the His bundle. The third P-H interval was even longer (260 msec) than the preceding one. The corresponding impulse was also blocked below the His bundle. Finally, the fourth P wave failed to reach the His bundle and, of course, did not activate the ventricles. The last P wave re-initiated a similar series of events.

This patient had second degree A-V block probably of the Mobitz II type below the His bundle and Wencke- bath (4:3) block in the nodal region. The classic features of this phenomenon were present, namely: (1) progressive prolongation of P-H intervals, 155, 210 and 260 msec, respectively; (2) gradual decrease in increments, 55 and 50 msec ; (3) decreasing H-H inter-

Figure 8. Case 4. 2:l retrograde (V-A) block above the His bundle during continuous ventricular pacing. In the presence of retrograde conduction the onset of atrial activation was first detected in the lead recording from the low right atrium (HBE). This indicates inferosuperior spread of activation throughout the atria.

vals, 490 and 485 msec; and (4) the pause produced by the blocked P wave (765 msec) was equal to the sum of the increments (105 msec) substracted from twice the P-P interval (870 msec) .

Case 4. Reversed nodal Wenckebach phenomenon with retrograde Mobitz II block below the His bundle: Tracings presented in Figures 7, 8 and 9 were obtained from a patient in whom complete right bundle branch block coexisted with block in the posteroinferior division of the left branch.lOsli During sinus rhythm the P-R interval measured 230 msec (Fig. 7). His bundle recordings showed an H-V conduction time of 80 msec, indicating additional delay through the anterosuperior division or low His bundle, or left bundle.

Various degrees .of retrograde (V-A) conduction were easily produced by ventricular pacing (Fig. 8 and 9). Retrograde activation of the His bundle occurred after almost all ectopic beats. When present, the R-H- interval had a fixed value of 170 msec. Retrograde P waves were inscribed first in the bipolar lead recording the electrical activity of the low right atrium (HBE), indicating inferosuperior spread of activation throughout the atria.

Figure 8 is an example of 2 :l V-A block occurring above the His bundle when the ventricles were paced at a rate of 125/min. Since the R-H- intervals remained constant, variations in R-P- intervals reflected the changes in the H-P-- intervals. The first H--P- interval measured 190 msec. The second stimulus was blocked above the His bundle since the H- was not followed by a negative P wave. Retrograde conduction occurred after the third QRS complex, the H--P- interval measur- ing 140 msec. Block of the fourth stimulus also occurred above the His bundle. However, it created concealed retrograde conduction in the A-V node so that the H----P- interval of the last beat was prolonged to 190 msec. A similar phenomenon must have occurred before the first QRS complex in the series. That the H- de- flections were due to retrograde activation of the His



Figure 9. Case 4. Two different types of retrograde (V-A) block during continuous ventricular pacing: Wenckebach in the A-V node and type II (Mobitz) below the His bundle.

bundle rather than the result of antegrade depolarization induced by the retrograde P waves is suggested by the fact that the third and fifth H- appeared even when not preceded by retrograde P waves. This validates the diagrammatic representation of the arrhythmia.

Pacing rate was reduced to lOO/min in Figure 9. The first 3 QRS complexes had fixed R--H- intervals (1’70 msec). However, they showed a progressive increase in the R-P- intervals. The varying retrograde block was due exclusively to a gradual prolongation of the H--P- intervals (180, 250 and 320 msec, respectively). Hence, the retrograde Wenckebach phenomenon occurred within the A-V node. In a typical reversed Wenckebach phenomenon the atria1 rate should ac- celerate, that is, the P--P- intervals should become shorter. This occurs because the atria are located distal to the area ‘of the block. In contrast, diagrammatic representation of this arrhythmia indicated that the P--P- intervals did not change because the 2 H--P- increments were equal (70 msec).

The fourth QRS complex was not followed by a retrograde P wave. Failure of transmission did not occur at the area where conduction was becoming pro- gressively impaired (A-V node). In fact, the impulse failed to reach the His bundle (block below the His bundle). The R-H- block was not preceded by previous progressive R-H prolongation. Therefore it can be classified as type II (Mobitz) .

The events in this case are similar to those presented in Figures 4 to 6. In both patients, a Wenckebach phenomenon in the A-V node coexisted with a type II (Mobitz) block below the His bundle. Yet in Figure 6, the conduction delays occurred during forward transmission, whereas in Figure 9 they were seen during retrograde conduction.

Discussion

The most frequent type of Wenckebach phenomenon, the typical one, can be diagrammed easily since it shows the classic features. However, atypical variants may be more difficult to inter-

pret.BJ3 In Figure 2 the longest H-H interval (ex- cluding that of the pause itself) appeared immedi- ately before the intermission. This occurred, in spite of P-H prolongation, because of the erratic behavior of the increments.

Atypical Wenckebach periods have been attributed to inhomogeneous conduction within the specialized tissues connecting the atria with the ordinary ventricular myocardium. According to Watanabe and Dreif us,l* once propagation through the A-V node is sufficiently slowed significant degrees of wavefront fractionation can produce more distal forms of conduction disturbances. Decre- ment thus induced can be implied in the genesis of the unusual characteristics of the Wenckebach phenomenon.

Intranodal conduction irregularities: The work of Moe and Mendezs is also significant in this re- spect. They emphasized that intranodal (that is, within the A-H region) conduction irregularities in the so-called alpha and beta pathways could produce unexpected changes in the P-R intervals. Since these pathways are located above the His bundle, it is obvious that the P-R changes will produce equivalent variations of the H-H intervals.

Rapid atria1 pacing stresses intranodal conduction producing unequal depression of the various routes.15 For instance, when the pacing rate ap- proaches the limit for 1: 1 conduction the range of P-P intervals within which the second P wave of each pair enters the node and fails to reach the ventricles (presumably because of block above the His bundle) may alternate from beat to beat.15 In an instance of 3:2 Wenckebach it is possible for the first P wave to be conducted through both alpha and beta pathways, whereas P, may transverse only one of them (alpha). If Pz reenters through the beta fiathway, it can travel toward the atria and be extinguished in its journey toward the latter. In consequence, Pa will be blocked. PZ can also depolarize the atria prematurely, thereby resulting in an atria1 echo (Fig. 2). On the other hand, if the second P wave does not enter the beta pathway (only the alpha), the third P wave can reach the ventricles through the former, and hence is conducted at a faster speed than the preceding atria1 impulse. An echo will not occur.

Mobitz (type II) block : Concealed reexcitation within the A-V node is a potential cause of type II (Mobitz) block as shown in the experimental studies of Watanabe and Dreifus.5 This was first reported by Langendorf and Mehlanle in 1947. These authors observed A-V nodal extrasystoles confined to the A-V junction, and which failed to reach the atria or the ventricles. They caused either a sudden P-R prolongation that could not be accounted for by any other conduction disturbance or a dropped beat not preceded by the usual, yro- gressive P-R prolongation. Recently, Myerburg

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et al.lT confirmed the presence of extrasystoles confined to the region between the A-V node and the ventricular muscle.

A type II (Mobitz) block is diagnosed from the conventional electrocardiogram whenever a blocked P wave is not preceded by previous progressive P-R prolongation.B His bundle recordings seem to indicate that this type of block is usually below the His bundle and associated with bilateral or trifascicular blocks.12J8 A type II (Mobitz) block is generally symptomatic and requires intracardiac pacing.lg

Block caused by atria1 pacing: The usual type of block produced by continuous atria1 pacing is located within the A-H region.1-4 This response occurred even in the presence of a probable Mobitz II block below the His bundle (Fig. 6). It is known that the induction of A-V block by continuous atria1 stimulation at rates over lOO/min need not indicate organic nodal disease.2J Moreover, Da- mato and co-workers4 have shown that coupled pacing can produce functional block, both below

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

and above the His bundle. Hence, the results of atria1 pacing have to be interpreted with caution when this procedure is used as a stress test to ex- pose latent (Iorganic) A-V nodal block, as well as block below the His bundle (bilateral or trifascicular block).

Clinical implications : The technique of His bundle recordings in the human heart has corroborated the usefulness of deductive reasoning in the analysis of clinical electrocardiograms.B It has narrowed the number of possibilities postulated in the absence of direct recordings from the specialized conducting tissues. For instance, the phenomenon shown in Figure 3 would have been difficult to suspect from the conventional leads only. Moreover, the location of the area (above or below the His bundle) where the impulses were totally blocked in Figures 5 to 9 could not have been de- fined by the use of conventional leads alone. The value of the catheter technique1-4 in understanding basic electrophysiologic phenomena has thus been corroborated.

References

Scherlag BJ, Lau SH, Helfant RH, et al: Catheter technique for recording His bundle activity in man. Circula- tion 39:13-18, 1969 Damato AN, Lau SH, Helfant. RH, et al: Study of atrioventricular conduction in man using electrode catheter recordings of His bundle activity. Circulation 39:287- 296, 1969 Damato AN, Lau SH, Helfant R, et al: A study of heart block in man using His bundle recordings. Circulation 39:297-305, 1969 Damato AN, Lau SH, Patton RD, et al: A study of atrioventricular conduction in man using premature atrial stimulation and His bundle recordings. Circulation 40: 61-69, 1969 Watanabe Y, Dreifus LS: Second degree atrioventricular block. Cardiovasc Res 1:150-158, 1967 Katz LN, Pick A: Clinical Electrocardiography. Part I. The Arrhythmias. Philadelphia, Lea & Febiger, 1956, p 551-552 Schamroth L: The theory and mechanism of the Wenckebach phenomenon. S Afr Med J 41:827-832, 1967 Moe GK, Mendez C: The physiologic basis of reciprocal rhythms. Progr Cardiovasc Dis 8:461-482, 1966 Langendorf R: Concealed A-V conduction. Amer Heart J 35:542-552, 1948 Rosenbaum MB, Elizari MV, Lazzari J: Los Hemibloques. Buenos Aires, Ed. Paidos, 1967

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Rosenbaum MB, Elizari MV, Lazzari JO, et al: Intra- ventricular trifascicular blocks. I. Four cases of right bundle branch block with intermittent left anterior and posterior hemiblocks. Amer Heart J 78:306-317, 1969 Castellanos A Jr, Maytin 0, Arcebal AG, et al: Alternat- ing and co-existing block in the divisions of the left branch. Dis Chest 56:103-109, 1969 Myerburg RJ, Goodman JS, Marriott HJL: Atypical forms of the Wenckebach phenomenon. Amer J Cardiol 11: 418-423, 1963 Watanabe Y, Dreifus LS: Inhomogeneous conduction in the A-V node. A model for reentry. Amer Heart J 70:505- 514, 1966 Moe GK, Childers RW, Meredith J: An appraisal of suoernormal conduction. Circulation 38:5-27. 1968 Langendorf R, Mehlan JS: Blocked (non-conducted) A-V nodal premature systoles imitating first and second degree heart block. Amer Heart J 34:500-506, 1947 Myerburg RJ, Gelband H, Hoffman BF: Confinement of premature impulses in functional compartments of the A-V conducting system. Circ Res (in press) Castellanos A Jr, Lemberg L, Arcebal AG, et al: Post- infarction conduction disturbances: a self-teaching pro- gram. Dis Chest 56:421-439, 1969 Langendorf R, Pick A: Atrioventricular block (Type II) Mobitz. Its nature and clinical significance. Circulation 38:819-822,1968


his bundle recordings in atypical a-v nodal wenckebach block during cardiac pacing

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