Sinus
node re-entry
Devkishin B. Pahlajani, Robert A. Miller, M.D. Maria Serratto, M.D.
and sinus
node tachycardia
M.D.
Chicago, Ill.
The occurrence of echo beats in human hearts is a well recognized phenomenon and has been demonstrated to be one of the mechanisms for supraventricular tachycardia.’ Bundle of His recordings in human hearts have clearly demonstrated that the site of re-entry can be within the A-V node’ or in the His-Purkinje system (HPS).’ Animal experiments have indicated that the reentry can also occur in the sinus node (SN) and can possibly be a mechanism for reciprocating tachycardia.“-5 Recently, Paulay, Varghese, and Damato6 reported their observations on the effect of early atria1 depolarization in man and found SN re-entry in some of their cases. Our present report deals with five cases in whom SN echoes could be demonstrated with the extrastimulus technique. In one of them such echoes were responsible for initiating reciprocating tachycardia. Such attacks were also noted to occur spontaneously in the laboratory. Materials
and methods
Four patients were subjected to cardiac catheterization primarily for hemodynamic studies. His bundle electrograms (HBE) were obtained after completing these studies. The fifth patient was catheterized primarily for conduction studies as he had bifascicular block following repair of a ventricular-septal defect. The clinical and electrocardiogram findings are listed in Table I. Technique. The recordings were performed in the postabsorptive state under demerol, phenerFrom the Division of Pediatric Cardiology, Cook Hospital, and the Hektoen Institute for Medical Ill. Supported Received
in part by for publication
the Children’s July 30, 1974.
Reprint requests: Dr. Maria Serratto, Cook County Children’s Hospital, 60612.
September,
Heart
County Research,
Research
Division of Pediatric 700 S. Wood St.,
1975, Vol. 90, No. 3, pp. 305-311
Children’s Chicago, Foundation. Cardiology, Chicago, 111.
gan, and sparine sedation. Informed consent was obtained from the parents. None of these patients were on cardioactive drugs at the time of study. The recordings were made on photographic paper using Electronics for Medicine multichannel recorder. HBE were obtained via a tripolar catheter placed near the tricuspid valve.’ A quadripolar catheter was positioned against the lateral wall of the right atrium (RA).The two distal poles were used to record high right atria1 electrograms (RAE) and the two proximal poles to deliver stimuli to the RA. Leads I, II, and III were recorded simultaneously. All stimuli were delivered to the RA through a Grass Stimulator Model DS88. The RA was paced by a basic pacing stimulus (S,) at the slowest possible rate producing stable capture without sinus escape beats. Extrastimulus (S,) technique was used to study SN function.8 The S, was delivered in late diastole and moved progressively earlier in 10 to 20 msec. decrements until the effective refractory period of the atrium was reached. In each test cycle the basic stimulus (S,) following the S? was omitted to recognize the occurrence of A-V junctional or SN echoes prior to sinus escapes. A, H, and V following S, will be referred to as A,, H,, and V,, respectively; and the A, H, and V following S, will be referred to as A,, HZ, and V,, respectively. The return cycle or sinus escape interval (SEI) is the time between AZ and the following sinus A-wave. The A, H, and V of the return cycle will be designated as A:,, H,, and V,, respectively. To evaluate the expected time of the appearance of A,, sinus node recovery time or SE1 at the basic pacing rate was measured at least three times in each patient. In none of the patients was the SE1 shorter than the basic S,S, interval. The following terms have been used in the text:” (1) reset: Resetting of SN is said to occur when the
American
Heart
Journal
305
Pahlajani,
Miller,
and
Serratto
I
I
Fig. 1. Patient No. 1. Leads I, II, and III are simultaneously recorded with two HBE HBE represent activation of low RA. S,S, interval represents the basic pacing rate. represent the cycle length of the basic pacing rate, the coupling interval, and the return Lead I represents the sum of the test cycle (A,A,) and the return cycle. (A,) is an SN waves in Leads II and III and the earlier appearance of the A-wave in RAE than in
Table
1 2 3 4 5
I. Summary of clinical and electrophysiologic
JT GN MC AK BD
M - male; F - female; defect; PDA - patent
11 yrs. 10 yrs. 2yrs. 14 yrs. 11 yrs.
M M F M M
PORBB+ LAD Normal heart ASD + PDA AI AI
PORBB + LAD - postoperative ductus atieriosus.
Results
All five patients demonstrated SN echoes following extrastimulation of RA. All had a definite echo zone (Table I). Fig. 1 is a representative tracing from patient No. 1. He was paced at 470 msec. cycle length and his SE1 ranged from 550 to 705 msec. Resetting of
306
data
RBBB Normal IRBBB LVH LVH
+ LAD
right bundle branch block with left axis deviation;
postectopic pause or return cycle (A,-A,) equals or exceeds SEI; (2) complete interpolation: The sinus escapebeat or A, appears as it would have in the absence of S,; (3) incomplete interpolation: appearance of A, is delayed but the return cycle (AZ-A,) is still shorter than the SEI; and (4) SN echoes: A, appears earlier than it would have in the absence of S,.
and RAE. The A-waves in The numbers in Lead III cycle. The number above echo. Note the upright PHBE.
125 100 115 95 110
515-960 655-900 555-705 750-650 600-720
AI - aortic insufficiency;
270-220 270-200 240-210 270-250 260-230 ASD - atrial-septal
SN occurred up to a coupling interval of 290 msec. At the coupling interval of 270 msec. the effective refractory period of the A-V node is reached as A, is not conducted to HB. A, is followed by a beat which is an SN echo because: (1) The A,A, interval is only 175 msec. and A,A, only 445 msec., which is shorter than the basic pacing cycle length S,S, (470 msec.) and also shorter than SE1 (550 to 705 msec.). (2) P-waves are upright in Leads II and III. (3) The sequence of atria1 activation is from high RA to low RA. (4) There is a definite echo zone ranging from 270 to 220 msec. The prolonged A,H, is due to antegrade concealed conduction of A,. The effective refractory period of atrium was reached at 200 msec. In Case No. 2, the SN echoes were responsible
September,
1975, Vol. 90, No. 3
Sinus node re-entry
Fig. 2,A.
Fig. 2.8.
Patient
Patient
No. 2. Panel
No. 2. Panel
B shows
SN echoes
for a reciprocating tachycardia. Basic atria1 pacing was performed at 600 msec. cycle length. The SE1 ranged from 655 to 900 msec. At A,A, interval of 590 msec. the SN is reset (Fig. 2, A). Reset occurred up to 290 msec. delay. At 270 msec. delay, the A,A, interval suddenly shortened to 290 msec. with an A,A, interval of 560 msec. This interval is shorter than the basic pacing interval and the SEI. The P-waves were not
American
Heart
Journal
A shows
which
resetting
and tachycardia
of SN
are blocked
proximal
to HB
clearly seen at this coupling interval. However, they are unquestionably upright in Leads II and III at subsequent test cycles (Figs. 2, B and C). The high RA is activated earlier than the low RA. There was a definite echo zone from 270 to 200 msec. At 250 msec. delay, the SN echo produced a presumably reciprocating tachycardia. There are three SN echoes seen in Fig. 2, C. The P-wave in A., appears to be biphasie and one Can argue that
307
Pahlajani,
Miller,
Fig. 2.C. represent
and
Serratto
Patient No. 2. Panel C shows a series of three SN echoes (A,,A,,A,). the cycle length between these echoes. See text for details.
it is an A-V junctional echo. However, the pattern of atria1 activation is from high to low RA and, therefore, it is more likely to be an SN echo. In the laboratory, this patient had several spontaneous attacks of presumably reciprocating tachycardia (rate of 160 per minute). The P-waves were upright in Leads II and III with high RA activated earlier than low RA which is highly suggestive of re-entry through SN. They could be easily terminated by a single atria1 premature depolarization (Fig. 3) or with multiple premature stimuli delivered at slower rate than the tachycardia. To demonstrate that the echoes were not related to the delay in A-V node, the AH intervals at fixed atria1 pacing producing Wenckebach block were compared with the A,H, intervals following S,, which produced the SN echoes. Fig. 4 is from patient No. 3. SN echoes were observed at coupling intervals of 240, 230, 220, and 210 msec. (panel A). The A,H, intervals at these coupling intervals were 225, 230, 240, and 260 msec. Atria1 pacing at 180 per minute produced 9:8 Wenckebach block (panel B). Though the AH lengthened from 105 to 270 msec., no echoes are observed. This confirms that the echoes in panel A are not A-V junctional echoes. None of the echoes were related to the specific delay in HPS,
308
as the H,V, cases.
The numbers
interval
in the lowest
remained
tracing
constant
in all
Discussion
The rarity of demonstrating SN echoes may be due to difficulties in studying sinus node function in the human heart. In 1962, Langendorf and coworkers? presented a case with atria1 parasystole in which they ascribed shortening of the return cycle to interpolation and postextrasystolic sinoatria1 conduction delay. Recently, the technique of extrastimulation of the atrium has been utilized to study the SN function in the human heart.“~8~10 Such work has enabled us to understand the mechanism of short and long returning cycles. When an atria1 premature depolarization (APD) falls in atria1 diastole, it usually penetrates, discharges, and resets the SN. In this situation, the return cycle equals or exceeds the SEI. Other factors which may influence the duration of the return cycle are postectopic depression of automaticity, sinoatrial conduction delay or block, or both.*.lO.ll In our studies, the SE1 was measured repeatedly in each case, since it varied from time to time. However, at no time was it shorter than the basic driving rate. We preferred
September,
1975, Vol. 90, No. 3
Sinus node re-entry and tachycardia
Fig. 3. It is a The P-waves between Lead captures the
tracing from patient No. 2 during a spontaneous attack on SN tachycardia (rate of 160 per mmute). are upright in Leads II and III and A-waves appear earlier in RAE than in HBE. The numbers III and HBE represent the cycle length between the subsequent A-waves. A properly timed APD atrium (A,) and terminates the tachycardia.
to pace the heart to insure a constant basic cycle length which otherwise may be variable due to sinus arrhythmia in children. A short return cycle may be caused by incomplete or complete interpolation” or by an SN echo.4 Incomplete interpolation occurs when the APD only partially enters the SN and fails to reset it. The next sinus impulse (A,) is generated at the expected time, but progresses slowly and though the return cycle is short, the A,A, interval is longer than the SEI. In complete interpolation, an APD does not gain access to SN, which is not reset.R.9.‘o.1Z Strauss and Bigger’” have assumed a zone of perinodal fibers which could possibly serve as a site of block of such early APD’s. The next ensuing sinus impulse occurs as if S, were absent. Thus, interpolation results in a short return cycle and the A,A, interval equals the SEI. With echoes, the return cycle is very short and the A,A, interval is shorter than SEI. The site of re-entry could be through the A-V node, HPS, or SN. The most important clues as to the site of reentry are: (1) the sequence of atria1 activation in RAE and HBE; (2) configuration of P-waves in Leads II, III, and aV,; (3) relation of echoes to critical delay in the A-V node or in the HPS. When re-entry occurs through the A-V node or HPS, the low RA is activated earlier than the high RA due to retrograde activation. As a result, the P-waves in Leads II, III, and aV, are inverted.
American Heart Journal
Moreover, re-entry through the A-V node or the HPS is related to the critical delay in these structures.‘,” In all our cases the sequence of atria1 activation is from high to low RA. P-waves could be clearly seen in two cases and were upright in Leads II and III in both. In the remaining three cases, the P-waves were submerged in QRS complexes. In none of these cases, however, was the re-entry related to a specific delay in the A-V node or HPS. In case No. 2, attacks of reciprocating tachycardia through the SN could be experimentally induced and also occurred spontaneously in the laboratory. The diagnosis of SN reciprocating tachycardia is confirmed by the following evidence: (1) it was initiated by an SN echo; (2) there was a definite echo zone and APD’s occurring in this zone produced either SN echoes or reciprocating tachycardia; (3) an appropriately timed APD terminated the attack. Han, Malozzi, and Moe,’ demonstrated SN reciprocation in the rabbit heart and concluded that “an APD may fail to engage one margin of the SN, enter another site, and travel through the SN so slowly that the atrium has recovered in time to respond again to the emerging stimulus.” For re-entry to occur, the premature stimulus must find part of the tissue refractory and part excitable. The conduction must be slow enough to allow the tissue that is to be re-excited to recover from its refractoriness. Evidence of dissociation in
309
Pahlajani,
Miller,
and
Fig. 4.A. interval.
Patient
Serratto
No. 3. SN echoes
are seen in panel
A (A,).
Numbers
between
A, and H, represent
the A,H,
Fig. 4,B. Patient No. 3. Panel B shows pacing at fixed rate of 180 per minute which produces 9:8 Wenckebach cycles. The numbers in the lower HBE represent the AH interval which has progressively prolonged from 105 to 270 msec. S, is blocked proximal to HB. See text for details.
A-V node has been demonstrated in the rabbit heart by Han, Malozzi, and Moe.3 In a recent review of atria1 tachyarrhythmias by Wellens,15 there was no case where SN re-entry could be a mechanism for atria1 tachycardia. However, it would appear that at least some of the atria1 tachycardias use the SN as a path for re-entry. If an impulse can re-enter the atrium through the SN once, there is no question that this re-entry can be self-sustaining. This has been clearly
310
shown in one of our cases.However, the incidence of such an arrhythmia in clinical practice is yet to be determined. Summary
Five patients are reported with SN echoes which could be produced by the technique of APD. The RA was paced at the basic rate and the SE1 was measured repeatedly. SN echoes were diagnosed on the basis of: (1) A,A, interval
September,
1975, Vol. 90, No. 3
Sinus nook re-entry and tachycardia
shorter than the SEI; (2) upright P-waves in Leads II and III; (3) activation of high RA preceding the activation of low RA; (4) lack of relation to critical delay in the A-V node or HPS; (5) definite echo zone. In one of the cases, attacks of reciprocating tachycardia through the SN occurred spontaneously and also could be initiated by an SN echo. These were terminated by a single APD or by atria1 pacing. We are grateful to Dr. Richard Langendorf suggestions in the preparation of this paper.
Bigger, J. T., Jr., and Goldreyer, B. N.: The mechanism of supraventricular tachycardia, Circulation 42:673, 1970. 2. Varghese, P. J., Damato, A. N., Caracta, A. R., Gallagher, J. J., Josephson, M. E., and Lau, S. H.: Intraventricular conduction delay as a determinant of atria1 echo beats, Circulation 49:805, 1974. 3. Han, J., Malozzi, A. M., and Moe, G. K.: Sinoatrial reciprocation in the isolated rabbit heart, Circ. Res. 22: 355, 1968. 4. Childers, R. W., Arnsdorf, M. F., De la Fuente, D. J., Gambetta, M., and Svenson, R.: Sinus node echoes, clinical case report, and canine studies, Am. J. Cardiol. 31:220, 1973. 5. Wallace, A. G., and Daggett, W. M.: Re-excitation of the atrium. The echo phenomenon, AM. HEART J. 66:661, 1964. 6. Paulay, K. L., Varghese, P. J., and Damato, A. N.: Atria1
American Heart Journal
9.
for his valuable
REFERENCES 1.
8.
10. 11.
12.
13.
14.
15.
rhythms in response to an early atrial premature depolarization in man, AM. HEART J. 653323. 1973. Scherlag, B. J., Lau, S. H., Helfant, R. II., Berkowitz, W. D., Stein, E., and Damato, A. N.: Catheter technique for recording His bundle activity in man, Circulation 39:13, 1969. Strauss, H. C., Saroff, A. L., Bigger. J. T., Jr., and Giardinae, G. V.: Premature atria1 stimulation as a key to the understanding of sinoatrial conduction in man. Presentation of data and critical review of the literature, Circulation 47:&X, 1973. Langendorf, R., Lesser, M. E., Plotkin. P., and Levin, B. D.: Atria1 parasystole with interpolation. Observations on prolonged sino-atria1 conductioll. AX HEART J. 633549, 1962. Goldreyer, B. N., and Damato, A. N.. Sinoatrial node entrance block, Circulation 44:789, 1971. Klein, H. O., Singer, D. H., and Hoffman, B. F.: Effects of atria1 premature systoles on sinus rhythm in the rabbii, Circ. Res. 32:480, 1973. Bonke, F. I. M., Bouman, L. N., and Schopman, F. J. G.: Effect of an early atria1 premature beat on activity of the sinoatrial node and atria1 rhythm in the rabbit, Circ. Res. 29:704, 1971. Strauss, H. C., and.Bigger, J. T., Jr.: Electrophysiological properties of the rabbit sinoatrial perinodal fibers, Circ. Res. 31:490, 1972. Goldreyer, B. N., and Damato, A. N.: The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular t,achycardia, Circulation 43:679, 1971. Wellens, H. J. J.: Electrical Stimulation of the Heart in the Study and Treatment of Tachycardias. Baltimore. 1971, University Park Press.
311
node re-entry
Devkishin B. Pahlajani, Robert A. Miller, M.D. Maria Serratto, M.D.
and sinus
node tachycardia
M.D.
Chicago, Ill.
The occurrence of echo beats in human hearts is a well recognized phenomenon and has been demonstrated to be one of the mechanisms for supraventricular tachycardia.’ Bundle of His recordings in human hearts have clearly demonstrated that the site of re-entry can be within the A-V node’ or in the His-Purkinje system (HPS).’ Animal experiments have indicated that the reentry can also occur in the sinus node (SN) and can possibly be a mechanism for reciprocating tachycardia.“-5 Recently, Paulay, Varghese, and Damato6 reported their observations on the effect of early atria1 depolarization in man and found SN re-entry in some of their cases. Our present report deals with five cases in whom SN echoes could be demonstrated with the extrastimulus technique. In one of them such echoes were responsible for initiating reciprocating tachycardia. Such attacks were also noted to occur spontaneously in the laboratory. Materials
and methods
Four patients were subjected to cardiac catheterization primarily for hemodynamic studies. His bundle electrograms (HBE) were obtained after completing these studies. The fifth patient was catheterized primarily for conduction studies as he had bifascicular block following repair of a ventricular-septal defect. The clinical and electrocardiogram findings are listed in Table I. Technique. The recordings were performed in the postabsorptive state under demerol, phenerFrom the Division of Pediatric Cardiology, Cook Hospital, and the Hektoen Institute for Medical Ill. Supported Received
in part by for publication
the Children’s July 30, 1974.
Reprint requests: Dr. Maria Serratto, Cook County Children’s Hospital, 60612.
September,
Heart
County Research,
Research
Division of Pediatric 700 S. Wood St.,
1975, Vol. 90, No. 3, pp. 305-311
Children’s Chicago, Foundation. Cardiology, Chicago, 111.
gan, and sparine sedation. Informed consent was obtained from the parents. None of these patients were on cardioactive drugs at the time of study. The recordings were made on photographic paper using Electronics for Medicine multichannel recorder. HBE were obtained via a tripolar catheter placed near the tricuspid valve.’ A quadripolar catheter was positioned against the lateral wall of the right atrium (RA).The two distal poles were used to record high right atria1 electrograms (RAE) and the two proximal poles to deliver stimuli to the RA. Leads I, II, and III were recorded simultaneously. All stimuli were delivered to the RA through a Grass Stimulator Model DS88. The RA was paced by a basic pacing stimulus (S,) at the slowest possible rate producing stable capture without sinus escape beats. Extrastimulus (S,) technique was used to study SN function.8 The S, was delivered in late diastole and moved progressively earlier in 10 to 20 msec. decrements until the effective refractory period of the atrium was reached. In each test cycle the basic stimulus (S,) following the S? was omitted to recognize the occurrence of A-V junctional or SN echoes prior to sinus escapes. A, H, and V following S, will be referred to as A,, H,, and V,, respectively; and the A, H, and V following S, will be referred to as A,, HZ, and V,, respectively. The return cycle or sinus escape interval (SEI) is the time between AZ and the following sinus A-wave. The A, H, and V of the return cycle will be designated as A:,, H,, and V,, respectively. To evaluate the expected time of the appearance of A,, sinus node recovery time or SE1 at the basic pacing rate was measured at least three times in each patient. In none of the patients was the SE1 shorter than the basic S,S, interval. The following terms have been used in the text:” (1) reset: Resetting of SN is said to occur when the
American
Heart
Journal
305
Pahlajani,
Miller,
and
Serratto
I
I
Fig. 1. Patient No. 1. Leads I, II, and III are simultaneously recorded with two HBE HBE represent activation of low RA. S,S, interval represents the basic pacing rate. represent the cycle length of the basic pacing rate, the coupling interval, and the return Lead I represents the sum of the test cycle (A,A,) and the return cycle. (A,) is an SN waves in Leads II and III and the earlier appearance of the A-wave in RAE than in
Table
1 2 3 4 5
I. Summary of clinical and electrophysiologic
JT GN MC AK BD
M - male; F - female; defect; PDA - patent
11 yrs. 10 yrs. 2yrs. 14 yrs. 11 yrs.
M M F M M
PORBB+ LAD Normal heart ASD + PDA AI AI
PORBB + LAD - postoperative ductus atieriosus.
Results
All five patients demonstrated SN echoes following extrastimulation of RA. All had a definite echo zone (Table I). Fig. 1 is a representative tracing from patient No. 1. He was paced at 470 msec. cycle length and his SE1 ranged from 550 to 705 msec. Resetting of
306
data
RBBB Normal IRBBB LVH LVH
+ LAD
right bundle branch block with left axis deviation;
postectopic pause or return cycle (A,-A,) equals or exceeds SEI; (2) complete interpolation: The sinus escapebeat or A, appears as it would have in the absence of S,; (3) incomplete interpolation: appearance of A, is delayed but the return cycle (AZ-A,) is still shorter than the SEI; and (4) SN echoes: A, appears earlier than it would have in the absence of S,.
and RAE. The A-waves in The numbers in Lead III cycle. The number above echo. Note the upright PHBE.
125 100 115 95 110
515-960 655-900 555-705 750-650 600-720
AI - aortic insufficiency;
270-220 270-200 240-210 270-250 260-230 ASD - atrial-septal
SN occurred up to a coupling interval of 290 msec. At the coupling interval of 270 msec. the effective refractory period of the A-V node is reached as A, is not conducted to HB. A, is followed by a beat which is an SN echo because: (1) The A,A, interval is only 175 msec. and A,A, only 445 msec., which is shorter than the basic pacing cycle length S,S, (470 msec.) and also shorter than SE1 (550 to 705 msec.). (2) P-waves are upright in Leads II and III. (3) The sequence of atria1 activation is from high RA to low RA. (4) There is a definite echo zone ranging from 270 to 220 msec. The prolonged A,H, is due to antegrade concealed conduction of A,. The effective refractory period of atrium was reached at 200 msec. In Case No. 2, the SN echoes were responsible
September,
1975, Vol. 90, No. 3
Sinus node re-entry
Fig. 2,A.
Fig. 2.8.
Patient
Patient
No. 2. Panel
No. 2. Panel
B shows
SN echoes
for a reciprocating tachycardia. Basic atria1 pacing was performed at 600 msec. cycle length. The SE1 ranged from 655 to 900 msec. At A,A, interval of 590 msec. the SN is reset (Fig. 2, A). Reset occurred up to 290 msec. delay. At 270 msec. delay, the A,A, interval suddenly shortened to 290 msec. with an A,A, interval of 560 msec. This interval is shorter than the basic pacing interval and the SEI. The P-waves were not
American
Heart
Journal
A shows
which
resetting
and tachycardia
of SN
are blocked
proximal
to HB
clearly seen at this coupling interval. However, they are unquestionably upright in Leads II and III at subsequent test cycles (Figs. 2, B and C). The high RA is activated earlier than the low RA. There was a definite echo zone from 270 to 200 msec. At 250 msec. delay, the SN echo produced a presumably reciprocating tachycardia. There are three SN echoes seen in Fig. 2, C. The P-wave in A., appears to be biphasie and one Can argue that
307
Pahlajani,
Miller,
Fig. 2.C. represent
and
Serratto
Patient No. 2. Panel C shows a series of three SN echoes (A,,A,,A,). the cycle length between these echoes. See text for details.
it is an A-V junctional echo. However, the pattern of atria1 activation is from high to low RA and, therefore, it is more likely to be an SN echo. In the laboratory, this patient had several spontaneous attacks of presumably reciprocating tachycardia (rate of 160 per minute). The P-waves were upright in Leads II and III with high RA activated earlier than low RA which is highly suggestive of re-entry through SN. They could be easily terminated by a single atria1 premature depolarization (Fig. 3) or with multiple premature stimuli delivered at slower rate than the tachycardia. To demonstrate that the echoes were not related to the delay in A-V node, the AH intervals at fixed atria1 pacing producing Wenckebach block were compared with the A,H, intervals following S,, which produced the SN echoes. Fig. 4 is from patient No. 3. SN echoes were observed at coupling intervals of 240, 230, 220, and 210 msec. (panel A). The A,H, intervals at these coupling intervals were 225, 230, 240, and 260 msec. Atria1 pacing at 180 per minute produced 9:8 Wenckebach block (panel B). Though the AH lengthened from 105 to 270 msec., no echoes are observed. This confirms that the echoes in panel A are not A-V junctional echoes. None of the echoes were related to the specific delay in HPS,
308
as the H,V, cases.
The numbers
interval
in the lowest
remained
tracing
constant
in all
Discussion
The rarity of demonstrating SN echoes may be due to difficulties in studying sinus node function in the human heart. In 1962, Langendorf and coworkers? presented a case with atria1 parasystole in which they ascribed shortening of the return cycle to interpolation and postextrasystolic sinoatria1 conduction delay. Recently, the technique of extrastimulation of the atrium has been utilized to study the SN function in the human heart.“~8~10 Such work has enabled us to understand the mechanism of short and long returning cycles. When an atria1 premature depolarization (APD) falls in atria1 diastole, it usually penetrates, discharges, and resets the SN. In this situation, the return cycle equals or exceeds the SEI. Other factors which may influence the duration of the return cycle are postectopic depression of automaticity, sinoatrial conduction delay or block, or both.*.lO.ll In our studies, the SE1 was measured repeatedly in each case, since it varied from time to time. However, at no time was it shorter than the basic driving rate. We preferred
September,
1975, Vol. 90, No. 3
Sinus node re-entry and tachycardia
Fig. 3. It is a The P-waves between Lead captures the
tracing from patient No. 2 during a spontaneous attack on SN tachycardia (rate of 160 per mmute). are upright in Leads II and III and A-waves appear earlier in RAE than in HBE. The numbers III and HBE represent the cycle length between the subsequent A-waves. A properly timed APD atrium (A,) and terminates the tachycardia.
to pace the heart to insure a constant basic cycle length which otherwise may be variable due to sinus arrhythmia in children. A short return cycle may be caused by incomplete or complete interpolation” or by an SN echo.4 Incomplete interpolation occurs when the APD only partially enters the SN and fails to reset it. The next sinus impulse (A,) is generated at the expected time, but progresses slowly and though the return cycle is short, the A,A, interval is longer than the SEI. In complete interpolation, an APD does not gain access to SN, which is not reset.R.9.‘o.1Z Strauss and Bigger’” have assumed a zone of perinodal fibers which could possibly serve as a site of block of such early APD’s. The next ensuing sinus impulse occurs as if S, were absent. Thus, interpolation results in a short return cycle and the A,A, interval equals the SEI. With echoes, the return cycle is very short and the A,A, interval is shorter than SEI. The site of re-entry could be through the A-V node, HPS, or SN. The most important clues as to the site of reentry are: (1) the sequence of atria1 activation in RAE and HBE; (2) configuration of P-waves in Leads II, III, and aV,; (3) relation of echoes to critical delay in the A-V node or in the HPS. When re-entry occurs through the A-V node or HPS, the low RA is activated earlier than the high RA due to retrograde activation. As a result, the P-waves in Leads II, III, and aV, are inverted.
American Heart Journal
Moreover, re-entry through the A-V node or the HPS is related to the critical delay in these structures.‘,” In all our cases the sequence of atria1 activation is from high to low RA. P-waves could be clearly seen in two cases and were upright in Leads II and III in both. In the remaining three cases, the P-waves were submerged in QRS complexes. In none of these cases, however, was the re-entry related to a specific delay in the A-V node or HPS. In case No. 2, attacks of reciprocating tachycardia through the SN could be experimentally induced and also occurred spontaneously in the laboratory. The diagnosis of SN reciprocating tachycardia is confirmed by the following evidence: (1) it was initiated by an SN echo; (2) there was a definite echo zone and APD’s occurring in this zone produced either SN echoes or reciprocating tachycardia; (3) an appropriately timed APD terminated the attack. Han, Malozzi, and Moe,’ demonstrated SN reciprocation in the rabbit heart and concluded that “an APD may fail to engage one margin of the SN, enter another site, and travel through the SN so slowly that the atrium has recovered in time to respond again to the emerging stimulus.” For re-entry to occur, the premature stimulus must find part of the tissue refractory and part excitable. The conduction must be slow enough to allow the tissue that is to be re-excited to recover from its refractoriness. Evidence of dissociation in
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Pahlajani,
Miller,
and
Fig. 4.A. interval.
Patient
Serratto
No. 3. SN echoes
are seen in panel
A (A,).
Numbers
between
A, and H, represent
the A,H,
Fig. 4,B. Patient No. 3. Panel B shows pacing at fixed rate of 180 per minute which produces 9:8 Wenckebach cycles. The numbers in the lower HBE represent the AH interval which has progressively prolonged from 105 to 270 msec. S, is blocked proximal to HB. See text for details.
A-V node has been demonstrated in the rabbit heart by Han, Malozzi, and Moe.3 In a recent review of atria1 tachyarrhythmias by Wellens,15 there was no case where SN re-entry could be a mechanism for atria1 tachycardia. However, it would appear that at least some of the atria1 tachycardias use the SN as a path for re-entry. If an impulse can re-enter the atrium through the SN once, there is no question that this re-entry can be self-sustaining. This has been clearly
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shown in one of our cases.However, the incidence of such an arrhythmia in clinical practice is yet to be determined. Summary
Five patients are reported with SN echoes which could be produced by the technique of APD. The RA was paced at the basic rate and the SE1 was measured repeatedly. SN echoes were diagnosed on the basis of: (1) A,A, interval
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1975, Vol. 90, No. 3
Sinus nook re-entry and tachycardia
shorter than the SEI; (2) upright P-waves in Leads II and III; (3) activation of high RA preceding the activation of low RA; (4) lack of relation to critical delay in the A-V node or HPS; (5) definite echo zone. In one of the cases, attacks of reciprocating tachycardia through the SN occurred spontaneously and also could be initiated by an SN echo. These were terminated by a single APD or by atria1 pacing. We are grateful to Dr. Richard Langendorf suggestions in the preparation of this paper.
Bigger, J. T., Jr., and Goldreyer, B. N.: The mechanism of supraventricular tachycardia, Circulation 42:673, 1970. 2. Varghese, P. J., Damato, A. N., Caracta, A. R., Gallagher, J. J., Josephson, M. E., and Lau, S. H.: Intraventricular conduction delay as a determinant of atria1 echo beats, Circulation 49:805, 1974. 3. Han, J., Malozzi, A. M., and Moe, G. K.: Sinoatrial reciprocation in the isolated rabbit heart, Circ. Res. 22: 355, 1968. 4. Childers, R. W., Arnsdorf, M. F., De la Fuente, D. J., Gambetta, M., and Svenson, R.: Sinus node echoes, clinical case report, and canine studies, Am. J. Cardiol. 31:220, 1973. 5. Wallace, A. G., and Daggett, W. M.: Re-excitation of the atrium. The echo phenomenon, AM. HEART J. 66:661, 1964. 6. Paulay, K. L., Varghese, P. J., and Damato, A. N.: Atria1
American Heart Journal
9.
for his valuable
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rhythms in response to an early atrial premature depolarization in man, AM. HEART J. 653323. 1973. Scherlag, B. J., Lau, S. H., Helfant, R. II., Berkowitz, W. D., Stein, E., and Damato, A. N.: Catheter technique for recording His bundle activity in man, Circulation 39:13, 1969. Strauss, H. C., Saroff, A. L., Bigger. J. T., Jr., and Giardinae, G. V.: Premature atria1 stimulation as a key to the understanding of sinoatrial conduction in man. Presentation of data and critical review of the literature, Circulation 47:&X, 1973. Langendorf, R., Lesser, M. E., Plotkin. P., and Levin, B. D.: Atria1 parasystole with interpolation. Observations on prolonged sino-atria1 conductioll. AX HEART J. 633549, 1962. Goldreyer, B. N., and Damato, A. N.. Sinoatrial node entrance block, Circulation 44:789, 1971. Klein, H. O., Singer, D. H., and Hoffman, B. F.: Effects of atria1 premature systoles on sinus rhythm in the rabbii, Circ. Res. 32:480, 1973. Bonke, F. I. M., Bouman, L. N., and Schopman, F. J. G.: Effect of an early atria1 premature beat on activity of the sinoatrial node and atria1 rhythm in the rabbit, Circ. Res. 29:704, 1971. Strauss, H. C., and.Bigger, J. T., Jr.: Electrophysiological properties of the rabbit sinoatrial perinodal fibers, Circ. Res. 31:490, 1972. Goldreyer, B. N., and Damato, A. N.: The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular t,achycardia, Circulation 43:679, 1971. Wellens, H. J. J.: Electrical Stimulation of the Heart in the Study and Treatment of Tachycardias. Baltimore. 1971, University Park Press.
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