Nature of the Gap Phenomenon in Man

Transcription

1 Nature of the Gap Phenomenon in Man By Delon Wu, Pablo Denes, Ramesh Dhingra, and Kenneth M. Rosen BSTRCT The atrioventricular (V) gap phenomenon occurs when the effective refractory period of a distal site is longer than the functional refractory period of a proximal site and when closely coupled stimuli are delayed enough at the proximal site to allow distal site recovery. ccording to previous studies, in type 1 gap, the distal site of block is distal to the His bundle (ventricular specialized conduction system) and the proximal site of block is in the V node. In type 2 gap, both the proximal and the distal sites of conduction block are within the ventricular specialized conduction system. Using His bundle recordings and atrial extra-stimulus techniques in man, we observed three previously undescribed types of gaps between (1) the V node (distal) and the atrium (proximal), (2) the His bundle (distal) and the V node (proximal), and (3) the ventricular specialized conduction system or a bundle branch (distal) and the His bundle (proximal). The delays at the His bundle in the second and third types of gaps seen in this study were demonstrated as splitting of His bundle potentials. Gaps between the V node or the His bundle and the ventricular specialized conduction system were more easily demonstrated at long cycle lengths, but gaps between the atrium and the V node were more easily demonstrated at short cycle lengths. Therefore, the previous subdivision of gaps into two types is an oversimplification, because gaps can occur between multiple sites in the conduction system. The gap phenomenon may be potentiated by both long and short cycle lengths; long cycle lengths increase the effective refractory period of a distal site, e.g., the His bundle and the ventricular specialized conduction system, and the short cycle lengths decrease the functional refractory period of a proximal site, e.g., the atrium and the V node. KEY WORDS atrial extra stimuli functional block cycle length His bundle electrogram supernormal conduction refractory period split His bundle potentials intra-atrial conduction delay One type of supernormal conduction, i.e., the paradoxical propagation of closely coupled stimuli when stimuli at longer coupling intervals are blocked, reflects a gap phenomenon (1-6). This phenomenon occurs when the refractory period of a distal conduction site limits conduction. With closely coupled stimuli, enough proximal delay occurs so that the impulse arrives at the distal conducting site late enough to be conducted. Gallagher and co-workers (5) have defined two types of gaps. In type 1 gap, the initial distal site of block is distal to the His bundle recording site, and the proximal site of delay is in the atrioventricular (V) node. In type 2 gap, both the distal and the proximal site of conduction delay are distal to the His bundle recording site (5). third kind of gap has recently been From the Section of Cardiology, Department of Medicine, braham Lincoln School of Medicine of the University of Illinois College of Medicine, and the West Side Veterans dministration Hospital, Chicago, Illinois This work was supported in part by the Myocardial Infarction Program Contract from the National Heart and Lung Institute and by Basic Institutional Support, West Side Veterans dministration Hospital. Received September 17, ccepted for publication February 20, described by gha and co-workers (6) in a patient with V block; however, this kind of gap appears to reflect supernormal conduction, and proximal and distal sites of delay have not been defined (6). In the present study, previously undescribed types of gaps between (1) a bundle branch or ventricular specialized conduction system (distal) and the His bundle (proximal), (2) the V node (distal) and the atrium (proximal), and (3) the His bundle (distal) and the V node (proximal) were demonstrated. These findings suggest that classification of gap phenomena into types 1 and 2 is an oversimplification. Gap phenomena can occur between any two portions of the V conducting system from the atrium to the distal Purkinje system. The two conditions necessary for development of a gap are (1) a distal site with an effective refractory period that is longer than the functional refractory period of proximal conducting tissues and (2) a proximal site with a relative refractory period that allows enough delay between impulses to ensure that the effective refractory period of the distal site is exceeded. The effects of cycle length on the gap phenomenon were also investigated in this study. 682

2 GP PHENOMENON 683 Methods Electrophysiological studies were performed in three patients during diagnostic cardiac catheterization in the supine, postabsorptive, nonsedated state. Informed consent was obtained from all patients. His bundle electrograms were recorded using previously described techniques (7). bipolar electrode catheter was percutaneously introduced into the right femoral vein and passed to the tricuspid valve for His bundle recording. second quadripolar electrode catheter was introduced into an antecubital vein and positioned fluoroscopically against the lateral wall of the high right atrium. The distal two electrodes were used for atrial stimulation and the proximal two were used for recording high right atrial electrograms. Lead I, II, and III electrocardiograms (ECG) and ventricular, high right atrial, and His bundle electrograms were recorded on a multichannel oscilloscopic photographic recorder (Electronics for Medicine DR-16) at paper speeds of 100 mm/sec and 200 mm/sec. The stimulus was a 2-msec square wave that was approximately twice diastolic threshold; it was provided by a digital programmable pulse generator. The basic intervals were recorded during sinus rhythm or with atrial pacing at varied rates. Refractory periods were measured with the atrial extra-stimulus technique. The test stimulus (S 2 ) was introduced after every eighth driving (Si) or spontaneous sinus beat. The coupling interval was decreased in increments of 5-10 msec. DEFINITIONS i, Hi, and Vi are the low right atrial, the His bundle, and the ventricular electrograms, respectively, of driven or spontaneous sinus beats recorded from the His bundle catheter, and 2, H 2, and V2 are the low right atrial, the His bundle, and the ventricular responses, respectively, to the test stimuli (S2). HRi and HR 2 are the high right atrial electrograms of driven or spontaneous beats and of test stimuli, respectively. -H, H-V, Hi-H 2, and Vi-V 2 intervals were measured as described by Wit et al. (8). H is the initial portion and H' is the delayed portion of split His bundle potentials. H 2 -H' 2 is the interval between the initial (H 2 ) and the delayed split His bundle potential (H' 2 ) of the test cycle; Hi-H' 2 is the interval between the His bundle potential of the driven or spontaneous beat (Hi) and the delayed portion of the split His bundle potential of the test beat (H' 2 ). The relative refractory period of the ventricular specialized conduction system was defined as the longest H!-H 2 interval at which H 2 was conducted to the ventricles with an increase in the H 2 -V 2 interval relative to the H-V (H1-V1) interval of driven beats. The effective refractory period of the ventricular specialized conduction system was defined as the longest H]-H 2 interval at which H 2 failed to propagate to the ventricles. The relative refractory period of the His bundle was defined as the longest H1-H2 interval at which H 2 duration relative to Hi duration was prolonged or at which splitting of the H 2 potential occurred. The refractory period of the left or right bundle was defined as the longest Hi-H 2 interval at which H 2 was conducted to the ventricles with electrocardiographic aberrancy of the left or right bundle branch block pattern. If splitting of H 2 was observed, the Hi-H' 2 interval was used to measure the refractory period of the bundle branch. The functional refractory period of the V node was the shortest attainable Hi-H 2 interval conducted from the atrium. The effective refractory period of the V node was the longest ^j. interval that failed to propagate to the His bundle. The functional refractory period of the atrium was the shortest attainable i- 2 interval. The effective refractory period of the atrium was the longest Si-S 2 (or HR!-S 2 ) interval at which S 2 failed to capture the atrium. Results Case 1 was a 48-year-old woman evaluated because of chest pain. Her electrocardiogram was within normal limits; electrophysiological studies during sinus rhythm revealed a rate ol 73 beats/min, an -H interval of 90 msec, and an H-V interval of 34 msec. trial premature stimuli were introduced at a cycle length of 650 msec (Figs. 1 and 2). The refractory period of the right bundle branch was 480 msec (H!-H 2 ). The effective refractory period of the V node was 300 msec (Fig. 1 and B). t S1-S2 intervals between 300 and 250 msec, the corresponding HR1-HR2 and i- 2 intervals were also between 300 and 250 msec; 2 was not conducted to the His bundle (Fig. IB and C). s the S1-S2 interval was decreased from 240 msec to 200 msec, the HR1-HR2 interval decreased similarly. However, the i- 2 interval increased to 310 msec, which allowed conduction through the V node (Fig. 2 and B). The effective refractory period of the atrium was 190 msec (Fig. 2C). In this patient, the initial distal site of block was in the V node, and the effective refractory period of the V node was longer than the functional refractory period of the atrium. Proximal delays in the atrium at shorter coupling intervals between the high and the low right atrium allowed the V node to recover. Thus, the gap was between the atrium and the V node. Case 2 was a 23-year-old male with coarctation of the aorta. His electrocardiogram showed sinus rhythm at 86 beats/min with a P-R interval of 160 msec and left ventricular hypertrophy. Electrophysiological studies during sinus rhythm revealed an -H interval of 103 msec

3 684 WU, DENES, DHINGR, ROSEN CL=650 S, V3I0 HR,,-HR 2 =3l0., 2 =3l0 H, H 2 = 375 HBE FIGURE 1 E.!S B E n V, S.Si=3OO HR r HR; 2 =3OO, /300 S.^250 HR,-HR2=250, 2 =250 I Demonstration of the gap phenomenon between the V node (distal) and the atrium (proximal) in case 1. Records of the lead II ECG (II) and ventricular (V,), His bundle (HBE), and high right atrial (E) electrograms are shown. See text for definitions of other abbreviations. Paper speed is 100 mm/sec and time lines represent 1 second on this and all subsequent illustrations. The basic driving cycle length was 650 msec. rrows indicate the first high-frequency atrial spikes of both driven and test beats recorded from the His bundle electrogram. : t an S,-S 2 interval of 310 msec, S 2 was conducted to the ventricles with an,- 2 interval of 310 msec. B and C: t an S,-S 2 interval between 300 and 250 msec, S 2 was blocked in the V node because the,- 2 interval was less than the effective refractory period of the V node (300 msec). The HR 2-2 interval was equal to the HR,-, interval. HBE E Circulation Research, Vol. XXXIV, May 197-4

4 GP PHENOMENON 685 =240 HR,-HR=i40., /310 H,H 2 =375 HBE E L4U Hi' HBE! HBE FIGURE 2 Demonstration of the gap phenomenon between the V node (distal) and the atrium (proximal) in case 1. and B: t an Si-S 2 interval between 240 and 200 msec, S 2 was again conducted to the ventricles because of sufficient intraatrial conduction delay; the HR 2-2 interval was longer than the HR,-, interval, which allowed the V node to recover. The fourth beat in B was a premature atrial contraction (PC). C: t an S,-S 2 interval of 190 msec, the effective refractory period of the atrium was achieved.

5 686 WU, DENES, DHINGR, ROSEN and an H-V interval of 40 msec. The His bundle potential duration was 30 msec and prolonged (9). Extra stimuli were introduced during sinus rhythm (cycle length 755 msec) (Fig. 3). t an i- 2 interval of 385 msec, H 2 was conducted to the ventricles with an Hi-H 2 interval of 425 msec (Fig. 3). t an i- 2 interval of 375 msec, the Hi-H 2 interval was 420 msec, and the H 2 potential duration increased. Thus, the relative refractory period of the His bundle was 420 msec (Fig. 3B). The QRS complex was essentially unchanged. s the i- 2 interval was further decreased to 370 msec, the H1-H2 interval decreased to 400 msec and splitting of H 2 potentials occurred. H 2 was conducted to the ventricles with a QRS complex characteristic of left bundle branch block (QRS 145 msec) during an H,- H' 2 interval of 425 msec (Fig. 3C). The refractory period of the left bundle was 425 msec. t an i- 2 interval of 330 msec, the Hi-H 2 interval was 390 msec and the Hi-H' 2 interval increased to 440 msec, which allowed recovery of the left bundle branch. s the : - 2 interval decreased from 330 msec to 230 msec, the H t -H 2 interval decreased from 390 msec to 315 msec, the H 2 -H' 2 interval increased, and therefore the Hi-H' 2 interval was lengthened. The configuration of the QRS complex was partially normalized at all Hi-H' 2 intervals equal to or greater than 425 msec (Fig. 3D and E). The effective refractory period of the atrium of 170 msec limited V conduction. When the atrium was driven at a cycle length of 520 msec, splitting of the His bundle potentials and left bundle branch block were not observed even at the shortest attainable H s -H 2 interval of 360 msec. In this patient, the initial distal site of block was in the left bundle branch, and the refractory period of the left bundle was shorter than the functional refractory period of the His bundle. Conduction delay in the common His bundle (proximal) allowed the left bundle branch (distal) time to recover. Therefore, this gap was between the His bundle and the left bundle branch. Shortening of the cycle length eliminated both the proximal and the distal sites of delay. Case 3 was a 65-year-old male with angina pectoris. His electrocardiogram revealed sinus rhythm of 68 beats/min, a P-R interval of 160 msec, and a QRS complex of 170 msec; the characteristics of the QRS complex revealed left bundle branch block. Electrophysiological studies during sinus rhythm revealed an -H interval of 90 msec and an H-V interval of 65 msec. trial test stimuli were coupled to spontaneous sinus rhythm (cycle length 879 ± 40 msec) (Figs. 4 and 5). With an i- 2 interval of 505 msec, the Hi-H 2 and Vi-V 2 intervals were 525 msec (Fig. 4). With i- 2 intervals between 500 and 450 msec, Hi-H 2 intervals were between 520 and 475 msec, and H 2 failed to propagate to the ventricles. Thus, the effective refractory period of the ventricular specialized conduction system was 520 msec (Fig. 4B). With an i- 2 interval between 445 and 400 msec, the Hi-H 2 interval decreased from 470 msec to 435 msec. With this decrease in the Hi-H 2 interval, splitting of H 2 was observed, and the H:-H' 2 interval increased from 495 msec to 520 msec. The Hi- H' 2 interval was equal to or less than the effective refractory period of the ventricular specialized conduction system and no conduction to the ventricles was observed (Fig. 4C). t an i- 2 interval between 395 and 370 msec, the Hi-H 2 interval decreased from 430 msec to 420 msec; splitting of H 2 increased with an Hi-H' 2 interval of msec, which allowed conduction to the ventricles, because the Hi-H' 2 interval was greater than the effective refractory period of the ventricular specialized conduction system (Fig. 4D). t an i- 2 interval between 365 and 355 msec, the Hi-H 2 interval increased because of V nodal refractoriness; this increase allowed the His bundle to recover partially a decrease in splitting and a decrease in the Hi-H' 2 interval to msec occurred. Thus, conduction to the ventricles again failed, because the Hi-H' 2 interval was shorter than the effective recovery period of the ventricular specialized conduction system (Fig. 4E). t the closest,- 2 interval ( msec), the H^H-. interval became longer than both the relative refractory period of the His bundle and the effective refractory period of the ventricular specialized conduction system; therefore, splitting of H 2 disappeared and conduction to the ventricles was resumed (Fig. 4F). When the atria were driven at a cycle length of 770 msec, j- 2 intervals of 420 msec or more produced corresponding Hi-H 2 intervals of 465 msec or more. s the i- 2 interval was decreased to 410 msec, the Hi-H 2 interval decreased to 460 msec, and H 2 was not propagated to the ventricles (Fig. 5B). Thus, the effective refractory period of the ventricular specialized

6 GP PHENOMENON 687 CL=755 It- FIGURE 3 Left: Records from case 2 showing prolongation of His bundle duration, splitting of His bundle potentials, and the gap phenomenon between the left bundle branch (distal) and the His bundle (proximal). The atrial extra stimuli were coupled to normal sinus rhythm at a cycle length of 755 msec. Right: Magnified His bundle potentials of the test beats. : t an,- 2 interval of 385 msec, 2 was conducted to the ventricles with an H,-H t interval of 425 msec. Both H, and H 2 duration were 30 msec. B: t an,-i interval of 375 msec, 2 was conducted to the ventricles with prolongation of H 2 duration (40 msec). C: t an,- : interval of 370 msec, the H,-H 2 interval was 400 msec, splitting of the H 2 potentials occurred, and H 2 was conducted to the ventricles with functional left bundle branch block. D: t an t - 2 interval of 330 msec, the H,-H 2 interval was 390 msec; H 2 was conducted to the ventricles with less left bundle branch block, because the delay in the His bundle allowed the left bundle branch to recover partially. E: t an,- 2 interval of 255 msec, H 2 was conducted to the ventricles with even less left bundle branch block, because of increased delays in the His bundle. Circulation Raearch, Vol. XXXIV, May 1974

7 688 WU, DENES, DHINGR, ROSEN conduction system was 460 msec. t i- 2 intervals between 390 and 360 msec, H,-H 2 intervals ranged from 430 to 415 msec, and splitting of the H 2 potential (H,-H' 2 interval msec, and H2-H' 2 interval msec) occurred; H' 2 was still not conducted to the ventricles. s the i- 2 interval was decreased from 350 msec to 340 msec, the Hi-H 2 interval increased from 450 msec to 460 msec, and splitting of the His bundle potential disappeared. t ]- 2 intervals between 340 and 320 msec, H r -H 2 intervals were greater than 465 msec, which was less than the effective refractory period of the ventricular specialized conduction system, and V conduction was resumed. s the Si-S 2 interval was decreased to 310 msec, the effective refractory period of the V node was achieved at an i- 2 interval of 310 msec (Fig. 6 and B). Further decreases in the coupling intervals resulted in a slight increase in latency CL=879 HBE FIGURE 4 Records from case 3 showing the V gap phenomena. The atrial extra stimuli were coupled to sinus rhythm at a cycle length of 879 msec. : t an,- 2 interval of 505 msec, H 2 was conducted to the ventricles with an H,-H 2 interval of 525 msec. B: t an,- 2 interval of 500 msec, H 2 was blocked in the ventricular specialized conduction system, because the effective refractory period of the ventricular specialized conduction system was achieved (520 msec). C:t an,- 2 interval of 400 msec, splitting of H 2 potentials occurred because the H,-H 2 interval (435 msec) was less than the relative refractory period of the His bundle (470 msec). H' 2 was still blocked in the ventricular specialized conduction system, since theh,-h' 2 interval (520 msec) was equal to the effective refractory period of the ventricular specialized conduction system. D: t an,- 2 interval of 395 msec, V conduction resumed because the H,-H' 2 interval (545 msec) was now longer than the effective refractory period of the ventricular specialized conduction system. E: t an,- 2 interval of 360 msec, the degree of splitting of H 2 decreased because of the increasing delay in the V node, which allowed the His bundle to recover partially. However, H' 2 was blocked in the ventricular specialized conduction system, because the H,-H' 2 interval was equal to the effective refractory period of the ventricular specialized conduction system. F: t an,- 2 interval of 340 msec, V conduction resumed because the H,-H 2 interval (525 msec) was longer than both the relative refractory period of the His bundle and the effective refractory period of the ventricular specialized conduction system.

8 GP PHENOMENON 689 msec H,H, v*v, B. msec H,H, H,H; GL=879 V,V, o o 1 1 CL=770 V, V, o rf> oo ' 1 I ,, FIGURE 5 < msec trioventricular conduction curves in case 3 showing multiple gap phenomena and their relations to the changes in cycle length. bscissa:,- 2 intervals. Ordinate: H,-H 2 intervals (open circles), H,-H' 2 intervals (solid circles), and V ; -V 2 intervals (triangles). : Cycle length = 879 msec. The effective refractory period of the ventricular specialized conduction system was 520 msec; the relative refractory period of the His bundle was 470 msec. The first gap between the ventricular specialized conduction system (distal) and the His bundle (proximal) occurred at an,- z interval between 500 and 400 msec; the second gap between the His bundle (distal) and the V node (proximal) occurred at an,- 2 interval between 445 and 340 msec; the third gap between the ventricular specialized conduction system (distal) and the V node occurred at an,- 2 interval between 365 and 355 msec. B: Cycle length = 770 msec. The effective refractory period of the ventricular specialized conduction system was 460 msec; the relative refractory period of the His bundle was 430 msec. The first gap between the ventricular specialized conduction system (distal) and the V node (proximal) occurred at an,- 2 interval between 410 and 345 msec; the second gap between the His bundle (distal) and the V node (proximal) occurred at an,- 2 interval between 390 and 360 msec. s the cycle length shortened, both the relative refractory period of the His bundle and the effective refractory period of the ventricular specialized conduction system decreased, and the pattern of the gaps changed. and a progressive increase in the,- 2 intervals due to intra-atrial conduction delays (prolongation of HR 2-2 interval). s the Si-S 2 interval was decreased to 265 msec or less, the i- 2 interval was increased to 320 msec and 2 again conducted to the ventricles (Fig. 6C and D). The effective refractory period of the atrium was 250 msec. These relationships are graphically demonstrated in Figure 5. Figure 5 shows the V conduction curve at a cycle length of 879 msec. The Hi-H 2 interval of 520 msec was the effective refractory period of the ventricular specialized conduction system, the H!-H 2 interval of 470 msec was the relative refractory period of the His bundle. The first gap between the His bundle and the ventricular specialized conduction system occurred at an i- 2 interval between 500 and 400 msec; the second gap between the V node and the His bundle occurred at an i- 2 interval between 445 and 340 msec; the third gap between the V node and the ventricular specialized conduction system occurred at an!- 2 interval between 365 and 355 msec. Figure 5B shows the V conduction curve at a cycle length of 770 msec. The H,-H 2 interval of 460 msec was the effective refractory period of the ventricular specialized conduction system; the Hi-H 2 interval of 430 msec was the relative refractory period of the His bundle. The first gap between the V node and the ventricular specialized conduction system occurred at an i- 2 or Sj-S 2 interval between 410 and 345 msec; the second gap between the V node and the His bundle was concealed on the surface electrogram and occurred at an,- 2 or Si S 2 interval between 390 and 360 msec. The third gap between the atrium and the V node occurred at an S,-S 2 interval between 310 and 270 msec and is not shown in Figure 5B. In this patient the left bundle branch block was probably complete. Thus, block distal to the His bundle (ventricular specialized conduction system) could reflect the effective refractory period of the right bundle. During sinus rhythm, three gaps were demonstrated. The first gap was between the ventricular specialized conduction system (distal) and the His bundle (proximal); splitting of the His bundle potential allowed the ventricular specialized conduction system to recover. The second gap was between the His bundle (distal) and the V. node (proximal). Relative refractoriness in the V node allowed Circulation Research, Vol. XXXIV, Slay 1974

9 690 WU, DENES, DHINGR, ROSEN CL=77O S,S 2 =3I5 HR,-HR=3I5, 2 =320 H, H/470 HBE B. S, S 2 =3IO HR.-HR/3IO, 2 =3IO HBE S,S 2 =270 HR,-HR 2 =3O5, 2 =3IO S,S 2 =265 HR,- HR 2 =300, 2 =320 H, H/465 V FIGURE 6 Records from case 3 showing gap phenomenon between the V node (distal) and the atrium (proximal). The arrows in and B indicate S 2. : t an S,-Sg interval of 315 msec, S 2 was conducted to the ventricles with an,- 2 interval of 320 msec. B: t an S,-S 2 interval of 310 msec, S 2 was blocked in the V node because the effective refractory period of the V node was achieved (310 msec). C: t an S,-S 2 interval of 270 msec, the latency of S 2 increased; S 2 was still blocked in the V node because the,- 2 interval (310 msec) was equal to the effective refractory period of the V node. D: t an S,-S 2 interval of 265 msec, the,- 2 interval increased because of an increase in both latency (S 2-2 ) and intra-atrial conduction delay (HR 2-2 ). S 2 was conducted to the ventricles because the,- 2 interval (320 msec) was longer than the effective refractory period Of the V node-

10 GP PHENOMENON 691 recovery of the His bundle and disappearance of splitting. The third gap was between the ventricular specialized conduction system (distal) and the V node (proximal) and was identical to type 1 gap previously described by Gallagher and co-workers (5). Discussion Microelectrode studies have shown that action potential durations and refractory periods in the canine His-Purkinje system increase progressively from the His bundle toward the peripheral Purkinje tissue. The area of maximum action potential duration and refractoriness, the "gate," is located 2-3 mm proximal to the termination of the His-Purkinje system in the myocardium (10, 11). Studies in intact dogs and humans that used His bundle and proximal bundle branch recordings have revealed functional blocks between the His bundle and the bundle branches with coupled stimulation (12, 13). In the present study, functional block in the His bundle was demonstrated by prolongation of the His bundle potentials, splitting of His bundle potentials, or both. The exact site of the delay that resulted in splitting of the His bundle potential could not be delineated, because the origin of catheter-recorded His bundle electrograms is controversial. Sano et al. (14), using isolated rabbit and dog hearts, have suggested that the His bundle electrogram is a composite resulting from depolarization of the entire His bundle. In contrast, Kupersmith et al. (15), using direct recordings of His bundle activity during open heart surgery, have suggested that the catheter-recorded His bundle electrogram is generated from the proximal His bundle. We propose that the site of splitting is somewhere in the His bundle. Therefore, the possible potential sites of delay or block with coupled atrial extra stimuli are (1) the distal gate of the His-Purkinje system, (2) the more proximal bundle branches, (3) the His bundle, (4) the V node, and (5) the atrium. It is also possible that several sites of block could occur in the His bundle or in the V node. Occurrence of the gap phenomenon depends on two conditions. The first condition requires that the effective refractory period of a distal tissue must be longer than the functional refractory period of proximal tissues, so that during a critical coupling interval there is block in a distal site. The second condition requires that the relative refractory period of a proximal tissue at close coupling intervals permits enough proximal delay so that the initially blocked distal tissue can recover. Gallagher et al. (5) classified gaps into two types. In type 1 gap the distal site of block was in either a bundle branch or the ventricular specialized conduction system (both distal to the His bundle), and the proximal site of delay was in the V node. In type 2 gap both the distal and the proximal site of delay were within the ventricular specialized conduction system. In the present study, we described three new types of gaps between the V node (distal) and the atrium (proximal), between the His bundle (distal) and the V node (proximal), and between the ventricular specialized conduction system or a bundle branch (distal) and the His bundle (proximal). Gallagher et al. (5) have described the occurrence of type 1 and 2 gaps in the same heart. In the present study (case 3), three gaps were observed in one patient. We also observed that gaps could be concealed on the surface electrocardiogram; for example, splitting of His bundle potentials was not apparent on the surface electrocardiogram and it was reversed as proximal delays in the V node increased the interval between impulses entering the His bundle. The previous classification of gaps into types 1 and 2 is thus an oversimplification because of the multiple sites of occurrence of the gap phenomenon. We recommend that this classification be eliminated and that gaps be described by noting both the distal and the proximal site of delays. The effect of cycle length on the gap phenomenon is predictable. Refractory periods of both the atrium and the His-Purkinje system decrease as the cycle length shortens (1, 16). Gaps with a distal site of block in the His-Purkinje system are less likely to occur at faster heart rates. t long cycle lengths, the atrium may limit V conduction. Decreasing the cycle length results in shortening of the effective refractory period of the atrium and reveals a gap phenomenon not seen when the atrium limits V conduction. The V nodal responses to changes in cycle length vary; however, the effective refractory period of the V node tends to lengthen and the functional refractory period tends to shorten with a decrease in cycle length (16). The effect of changes in cycle length on gaps involving' the V node depends on whether the V node is Circulation Research, Vol. XXXIV. May 1974

11 692 WU, DENES, DHINGR, ROSEN serving as the distal or the proximal site of delay and on relative changes in the effective refractory period and the functional refractory period of the V node compared with those of other conducting tissue. cknowledgment We wish to acknowledge the secretarial help of Ms. Mary Jo Moore in the preparation of this manuscript. References 1. MOE, G.K., MENDEZ, C, ND HN, J.: berrant -V impulse propagation in the dog heart: Study of functional bundle branch block. Circ Res 16: , DURRER, D.: Electrical aspects of human cardiac activity: Clinical physiological approach to excitation and stimulation. Cardiovasc Res 2:1-18, GOLDREYER, B.N., ND BIGGER, J.T., JR.: Spontaneous and induced reentrant tachycardia. nn Intern Med 70:87-98, WIT,.L., DMTO,.N., WEISS, M.B., ND STEINER, C: Phenomenon of gap in atrioventricular conduction in the human heart. Circ Res 27: , GLLGHER, J.J., DMTO,.N., CRCT,-.R., VRGHESE, P.J., JOSEPHSON, M.E., ND LU, S.H.: Gap in -V conduction in man: Type I and II. m Heart J 85:78-82, GH,.S., CSTELLNOS,., JR., WELLS, D., ROSS, M.D., BEFELER, B., ND MYERBURG, R.J.: Type I, type II and type III gaps in bundle branch conduction. Circulation 47: , SCHERLG, B.J., LU, S.H., HELFNT, R.H., BERKO- WITZ, W.D., STEIN, C, ND DMTO,.N.: Catheter technique for recording His bundle activity in man. Circulation 39:13-18, WIT,.L., WEISS, M.B., BERKOWITZ, W.D., ROSEN, K.M., STEINER, C, ND DMTO,.N.: Patterns of atrioventricular conduction in the human heart. Circ Res 27: , NRUL, O.S., SCHERLG, B.J., SMET, P., ND JVIER, R.P.: trioventricular block: Localization and classification by His bundle recordings. m J Med 50: , MYERBURG, R.J., STEWRT, J.W., ND HOFFMN, B.F.: Electrophysiological properties of the canine peripheral V conducting system. Circ Res 26: , MYERBURG, R.J., GELBND, H., ND HOFFMN, B.F.: Functional characteristics of the gating mechanism in the canine V conducting system. Circ Res 28: , LU, S.H., BOBB, G.., ND DMTO,.N.: Catheter recording and validation of left bundle branch potentials in intact dogs. Circulation 42: , ROSEN, K.M., RHIMTOOL, S.H., SrNO, M.Z., ND GUN- NR, R.M.: Bundle branch and ventricular activation in man. Circulation 43: , SNO, T., NKI, M., ND SUZUKI, F.: Nature of His potential in His electrogram. Jap Heart J 13: , KUPERSMITH, J., KRONGRD, E., ND WLDO,.L.: Conduction intervals and conduction velocity in human cardiac conduction systems: Studies during open heart surgery. Circulation 47: , DENES, P., Wu, D., DHINGR, R., PIETRS, R.J., ND ROSEN, K.: Effects of cycle length on cardiac refractory periods in man. Circulation 49:32-41, 1974.