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Atrioventricular nodal gap conduction as a manifestation of dual nodal pathways
CASE REPORTS
Atrioventricular Nodal Gap Conduction as a Manifestation of Dual Nodal Pathways
DAVID JACK
M P
MIRVIS, BANDURA,
MD PHD,
MD
Memphis, Tennessee
Electrophysiologic studies were performed in a 76 year old patient for evaluation of sihus bradycardia. Atrial extrastimuli were induced duiing sinus rhythm at progressively decreasing coupling (AI-A*) Intervals. At an AI-AZ interval of 420 msec, right bundle branch block developed, and at 370 msec conduction failed below the His bundle. When the interval was reduced to 320 msec, conduction resumed wfth a normal QRS battern with an abrupt increase in A-H Intervals from 165 to 305 msec. These findings are interpreted as type I or atrioventricular (A-V) nodal gap conduction physiologically related to conversion from a rapfd to a slow A-V nodal conduction mode.
Intracardiac recording of electrocardiograms has permitted a more tailed understanding of many electrophysiologic events than was viously possible. Two phenomena defined using these techniques “dual atrioventricular (A-V) nodal pathways”1-4 and “gaps” in
depreare
A-V conduction.1,5-g In the former, functional longitudinal dissociation of A-V junctional fibers results in a rapidly conducting path and a second slower tract. Which one conducts an incoming impulse relates to the differences in their refractory periods. In the second phenomenon, a lapse or “gap” in conduction occurs when impulses are presented within a narrow range of prematurity; conduction is intact with either longer or shorter coupling intervals. In the case to be described, both of these relatively uncommon features coexisted. A mechanism whereby the former leads to the latter is suggested. Case Report
From the Section of Medical Physics, Divrsion of Circulatory Diseases, University of Tennessee, Center for the Health Sciences, Memphis, Tennessee This work was supported by Grant DRG613 from the Deborah Heart and Lung Center, Browns Mills, New Jersey and by Public Health Service Grant HL-20597 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Manuscript received August 25, 1977; revised manuscript received October 13. 1977, accepted October 19, 1977. Address for reprints. David M. Mirvis, MD, Section of Medical Physics, University of Tennessee Center for the Health Sciences, 95 1 Court Avenue, Room 339M, Memphis, Tennessee 38163
A 76 year old black man was referred for electrophysiologic evaluation because of persistent sinus bradycardia. The patient noted intermittent regular palpitations but was otherwise asymptomatm He was not receiving any cardioactive medication. Physical examination was normal. Standard electrocardiograms demonstrated sinus bradycardia (rate 40 to 58/min) with a normal P-R interval, QRS duration and frontal plane axis. There was no evidence of ventricular preexcitation. A 24 hour electrocardiographic tape recording revealed only sinus bradycardia. Informed consent was given for electrophysiologic study. Intracardiac recordmgs using two multipolar electrode catheters were obtained with the patient in a postabsorptive, unpremeditated state. Electrocardiograms were recorded after 40 to 500 hertz bandpass filtering. Atria1 extrastimuli were coupled to normal sinus QRS complexes using a previously described microprocessor-controlled stimulator with software program logic.lO Extrastimuli were introduced at coupling intervals of 555 to 100 msec at 25 msec decrements. Prematurity was quantitated by measuring the Al-A2 interval, that is, the interval from the last spontaneous atria1 deflection (Al) to the atria1 deflection of the premature beat (AZ). Results are presented in Figures 1 and 2. During normal sinus rhythm, the P-P, P-A, A-H and H-V intervals were 760,30, 125 and 40 msec, respectively. The sinus rate remained stable to within 40 msec of the mean cycle length during the period of study. With Al-A2 intervals of 720 to 445 msec, A-V conduction remained normal with A-H times of 125 to 160 msec (Fig. 1A). At an Al-A2 interval of 420 msec, right bundle branch block occurred with an increase in H-V
May 22, 1978
The American Journal of CARDfOLOGY
Volume 41
1115
DUAL PATHWAYS AND GAP CONDUCTION-MIRVIS AND BANDURA
FIGURE 1. Representabve cardiac cycles demonstrating the phenomena of dual atrioventricular (A-V) nodal pathways and A-V nodal gap His bundle electrograms (HBE) are recorded simultaneously with standard leads II and VI. A, at an atrial cycle length of 445 msec, A-V conduction is normal A,, HI and VI refer, respectively, to the atrial, His bundle and ventricular depolarization complexes induced by the sinus node. AZ. H2 and V2 identify atrial, His bundle and ventricular depolarization complexes, respectively, induced by a premature atrial stimulus, Sp. 6. right bundle branch block with prolonged H-V conduction occurs at a coupling interval of 420 msec. C, the atrial extrastimulus is blocked below the His bundle recording sate at an AI-A2 interval of 370 msec. The open arrow identifies the blocked His bundle response. D. at a coupling interval of 320 msec, A-H time increases to 305 msec from 165 msec (C) with resumption of conduction of the extrastimulus to the ventricles
Plots of AI-AZ intervals versus A- Vnodal conduction time and His bundle cycle lengths in the extrastimulus cycles (Fig.
time of 60 msec (Fig. 1B). Further reduction in coupling resulted in block of conduction distal to the His bundle recording site (AI-AZ = 370, Fig. 1C). When coupling was still closer (Al-A2 = 320 msec, Fig. lD), two phenomena were observed. First, the A-H interval abruptly increased to 305 msec. Second, conduction to the ventricles resumed with a normal QRS pattern and with a normal H-V time of 40 msec.
2) revealed discontinuous curves. At a critical Al-AZ interval of 320 msec, A-V nodal conduction time increased abruptly, as did His bundle cycle length. No echo beats were recorded. Sinoatrial conduction time and corrected sinus nodal recovery time were normal.
B.
A.
800
400
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+-+-
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500
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(msec)
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600
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700
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600
(msec)
FIGURE 2. Plot of atrial cycle length (AI-A2) versus A-V nodal conduction times (AZ-Hz) (A) and versus His bundle cycle lengths (HI-H*)(B) during atrial exlrastimulus testing. Beats conducted normally are identified by closed cfrdes. beats conducted with a right bundle branch pattern are identified by a plus sign and nonconducted atrial beats are identified by a cross. RBBB = right bundle branch block.
1116
May 22,1976
The American Journal of CARDIOLOGY
Volume 41
DUAL PATHWAYS AND GAP CONDUCTION-MIRVIS AND BANDURA
Discussion Dual A-V nodal pathways: The electrophysiologic data in this case support two diagnoses. First, the abrupt increase in A-V nodal conduction times at a critical coupling interval and the discontinuous coupling interval-conduction time plots (Fig. 2) suggest physiologic, and possibly anatomic, dual A-V nodal pathways.1-4 Conduction time and His bundle cycle length increase suddenly with transfer of conduction from the relatively fast to the slower mode. Previously described manifestations of this pattern include echo beats, supraventricular tachycardias, atypical A-V nodal Wenckebach periods and a specific form of “supernormal” conduction.” Other interpretations for the observed discontinuous curves may be proposed. For example, delay may be induced by arrival of a premature impulse during the relative refractory period of a portion of a single pathway.” The abrupt slowing of conduction, and hence the discontinuity in A-V conduction curves, may possibly represent conversion of propagation from a rapid, active mode to a slower, passive or electrotonici2 mechanism within a single path. Another hypothesis is that the prematurity of the impulse causes it to engage only part of the A-V node, resulting in loss of the summation effects observed with total nodal activation; propagation velocity would then also decrease.13 A-V nodal gap phenomenon: A second diagnosis is that of type I, or A-V nodal, gap phenomenon.1y5-g In this pattern of conduction, impulses are blocked within the His-Purkinje system when their prematurity encroaches upon the effective refractory periods of these structures. As the coupling or Al-As interval is further decreased, the increased delay in propagation through the A-V node permits greater recovery times for the distal tissues, and conduction resumes. Thus, the cycle length observed by the His-Purkinje system increases despite a reduction in coupling intervals and atria1 cycle lengths. A-V nodal gap patterns are uncommon; for example, they were noted in only 6 of 45 subjects studied by Wit et al6 The necessity for the simultaneous occurrence of two unusual electrophysiologic phenomena may explain this infrequency. First, the effective refractory period of the His-Purkinje system must exceed the functional refractory period of the A-V node. Second, the A-V nodal conduction time must increase substantially without being totally blocked with relatively small increases in prematurity. This permits recovery of the distal tissues, thereby allowing conduction to continue.
In our case, block occurred sequentially in multiple areas of the His-Purkinje system. At an Al-As interval of 420 msec, right bundle branch conduction was significantly retarded14 so as to produce an electrocardiographic pattern of right bundle branch block. The concurrent prolongation of the H-V time at this cycle length further suggests delay within the distal His bundle or left branch system.15 When the coupling interval further decreased to 370 msec, corresponding to a His bundle cycle length of 430 msec, conduction below the His bundle recording site ceased. Finally, at a shorter Al-A2 interval of 320 msec but at a longer Hi-Hz interval of 510 msec, A-V conduction resumed with a normal H-V time and QRS pattern.8 This occurred as the As-H2 interval abruptly increased from 165 to 305 msec, thought to result from transfer of A-V nodal conduction from a rapid to a slow transmission mode. Thus, the second requirement for gap conduction was provided by the coexistence of functionally dual A-V nodal pathways. Type I or A-V nodal gap may thus be considered an electrophysiologic consequence of dual A-V nodal pathways. Mechanism: Durrer5 proposed a mechanism whereby these two phenomena may be physiologically correlated. During normal conduction at long coupling intervals, conduction through high or junctional pathways occurs by way of the more rapidly conducting fibers. When prematurity increases and a gap in conduction is observed, the fast path is still used but the impulse reaches refractory tissue in the lower “final common” paths. Finally, conduction resumes as the effective refractory period of the fast system is reached and the impulse propagates through a slow path. The delay in reaching the final common pathway permits its recovery. This model is applicable to our case if one assumes the refractory site of the common path to be distal to the His bundle recording site. Several other reported cases may be similarly interpreted. Wit et a1.6 demonstrated an abrupt increase in A-H times of premature atria1 stimuli coincident with resumption of A-V conduction in a patient with a short P-R interval. This was attributed to conversion from a fast extranodal to a slower intranodal pathway at a critical coupling interval. In our case, an extranodal path was unlikely because the A-H times were normal at rest. Additionally, Damato et a1.7,g reported cases of A-V nodal gap in which seemingly disproportionate increases in A-H times with small increases in extrastimulus prematurity led to resumption of A-V conduction. Thus, the occurrence of dual A-V conduction modes may not be an uncommon substrate for the recording of A-V nodal gap conduction patterns.
References 1. Moe GK, Preston JB, Burlington H: Physiologic evidence for dual A-V transmission system. Circ Res 4.357-375. 1956 2 Wft AL, Weiss MB, Berkowitz WD, ef al: Patterns of atrioventncular conduchon rn the human heart Circ Res 27:345-359, 1970 3. Rosen KM, Mehta A, Miller RA: Demonstration of dual atrioventrtcular nodal pathways in man Am J Cardtol 33:291-294, 1974
May 22,1978
4
Rosen KM, Denes P, Wu D, et al: Electrophystological dtagnoses and manifestations of dual A-V nodal pathways. In. The Conduction System of the Heart (Wellens HJJ, Lie KI, Janse MJ, ed) Philadelphia, Lea & Febiger, 1976. p 453-466 5 Durrer D: Electrical aspects of human cardiac acttvity: a clinicalphystological approach to excitation and stimulation Cardiovasc
The American Journal of CARDIOLOGY
Volume 41
1117
DUAL PATHWAYS AND GAP CONDUCTION-MIRVIS AND BANDURA
Res 2.1-18, 1968 6. Wit AL, Damato AN, Weiss MB, et al: Phenomenon of the gap in atrioventricular conductron in the human heart Circ Res 27: 679-689, 1970 7 Damato AN, Akhtar M, Ruskin J, et al: Gap phenomena: antegrade and retrograde, Chap 28 In Reference 4, p 503-528 8 Agha AS, Castellanos A Jr, Wells D, et al: Type I, type II and type Ill gaps in bundle branch conduction Crrculation 47:325-330, 1973 9 Damato AN, Wit AL, Lau SH: Observations on the mechanism of one type of so-called supernormal A-V conduction Am Heart J 82:725-730, 1971 10. Keller FW, Mirvis DY, Laughter JS, et al: A microprocessor controlled timing device for cardiac electrical stimulation. Sub-
1118
May 22,197s
The American Journal of CARDIOLOGY
mitted for publication 11 Moore EN: Microelectrode studies n concealment of multiple atnal premature responses. Circ Res 18:660-672, 1966 12 Wennemark JR, Bandura JP: Microelectrcds study of Wenckebach periodicity in canine Purkinje fibers Am J Cardiol 33:390-398, 1974 13 Zlpes DP: Dual A-V nodal pathways and pre-excitation Circulation 50:861-862, 1974 14 Wu D, Denes P, Dhlngra R, et al: Bundle branch block: demonstration of the incomplete nature of some “complete” bundle branch and fascicular blocks by the extrastimulus technique. Am J Cardiol 33:583-589, 1974 15. Rosen KM, Rahimtoola SH, Sinno MZ et al: Bundle branch and ventricular activation in man. Circulation 43:193-203. 1971
Atrioventricular Nodal Gap Conduction as a Manifestation of Dual Nodal Pathways
DAVID JACK
M P
MIRVIS, BANDURA,
MD PHD,
MD
Memphis, Tennessee
Electrophysiologic studies were performed in a 76 year old patient for evaluation of sihus bradycardia. Atrial extrastimuli were induced duiing sinus rhythm at progressively decreasing coupling (AI-A*) Intervals. At an AI-AZ interval of 420 msec, right bundle branch block developed, and at 370 msec conduction failed below the His bundle. When the interval was reduced to 320 msec, conduction resumed wfth a normal QRS battern with an abrupt increase in A-H Intervals from 165 to 305 msec. These findings are interpreted as type I or atrioventricular (A-V) nodal gap conduction physiologically related to conversion from a rapfd to a slow A-V nodal conduction mode.
Intracardiac recording of electrocardiograms has permitted a more tailed understanding of many electrophysiologic events than was viously possible. Two phenomena defined using these techniques “dual atrioventricular (A-V) nodal pathways”1-4 and “gaps” in
depreare
A-V conduction.1,5-g In the former, functional longitudinal dissociation of A-V junctional fibers results in a rapidly conducting path and a second slower tract. Which one conducts an incoming impulse relates to the differences in their refractory periods. In the second phenomenon, a lapse or “gap” in conduction occurs when impulses are presented within a narrow range of prematurity; conduction is intact with either longer or shorter coupling intervals. In the case to be described, both of these relatively uncommon features coexisted. A mechanism whereby the former leads to the latter is suggested. Case Report
From the Section of Medical Physics, Divrsion of Circulatory Diseases, University of Tennessee, Center for the Health Sciences, Memphis, Tennessee This work was supported by Grant DRG613 from the Deborah Heart and Lung Center, Browns Mills, New Jersey and by Public Health Service Grant HL-20597 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Manuscript received August 25, 1977; revised manuscript received October 13. 1977, accepted October 19, 1977. Address for reprints. David M. Mirvis, MD, Section of Medical Physics, University of Tennessee Center for the Health Sciences, 95 1 Court Avenue, Room 339M, Memphis, Tennessee 38163
A 76 year old black man was referred for electrophysiologic evaluation because of persistent sinus bradycardia. The patient noted intermittent regular palpitations but was otherwise asymptomatm He was not receiving any cardioactive medication. Physical examination was normal. Standard electrocardiograms demonstrated sinus bradycardia (rate 40 to 58/min) with a normal P-R interval, QRS duration and frontal plane axis. There was no evidence of ventricular preexcitation. A 24 hour electrocardiographic tape recording revealed only sinus bradycardia. Informed consent was given for electrophysiologic study. Intracardiac recordmgs using two multipolar electrode catheters were obtained with the patient in a postabsorptive, unpremeditated state. Electrocardiograms were recorded after 40 to 500 hertz bandpass filtering. Atria1 extrastimuli were coupled to normal sinus QRS complexes using a previously described microprocessor-controlled stimulator with software program logic.lO Extrastimuli were introduced at coupling intervals of 555 to 100 msec at 25 msec decrements. Prematurity was quantitated by measuring the Al-A2 interval, that is, the interval from the last spontaneous atria1 deflection (Al) to the atria1 deflection of the premature beat (AZ). Results are presented in Figures 1 and 2. During normal sinus rhythm, the P-P, P-A, A-H and H-V intervals were 760,30, 125 and 40 msec, respectively. The sinus rate remained stable to within 40 msec of the mean cycle length during the period of study. With Al-A2 intervals of 720 to 445 msec, A-V conduction remained normal with A-H times of 125 to 160 msec (Fig. 1A). At an Al-A2 interval of 420 msec, right bundle branch block occurred with an increase in H-V
May 22, 1978
The American Journal of CARDfOLOGY
Volume 41
1115
DUAL PATHWAYS AND GAP CONDUCTION-MIRVIS AND BANDURA
FIGURE 1. Representabve cardiac cycles demonstrating the phenomena of dual atrioventricular (A-V) nodal pathways and A-V nodal gap His bundle electrograms (HBE) are recorded simultaneously with standard leads II and VI. A, at an atrial cycle length of 445 msec, A-V conduction is normal A,, HI and VI refer, respectively, to the atrial, His bundle and ventricular depolarization complexes induced by the sinus node. AZ. H2 and V2 identify atrial, His bundle and ventricular depolarization complexes, respectively, induced by a premature atrial stimulus, Sp. 6. right bundle branch block with prolonged H-V conduction occurs at a coupling interval of 420 msec. C, the atrial extrastimulus is blocked below the His bundle recording sate at an AI-A2 interval of 370 msec. The open arrow identifies the blocked His bundle response. D. at a coupling interval of 320 msec, A-H time increases to 305 msec from 165 msec (C) with resumption of conduction of the extrastimulus to the ventricles
Plots of AI-AZ intervals versus A- Vnodal conduction time and His bundle cycle lengths in the extrastimulus cycles (Fig.
time of 60 msec (Fig. 1B). Further reduction in coupling resulted in block of conduction distal to the His bundle recording site (AI-AZ = 370, Fig. 1C). When coupling was still closer (Al-A2 = 320 msec, Fig. lD), two phenomena were observed. First, the A-H interval abruptly increased to 305 msec. Second, conduction to the ventricles resumed with a normal QRS pattern and with a normal H-V time of 40 msec.
2) revealed discontinuous curves. At a critical Al-AZ interval of 320 msec, A-V nodal conduction time increased abruptly, as did His bundle cycle length. No echo beats were recorded. Sinoatrial conduction time and corrected sinus nodal recovery time were normal.
B.
A.
800
400
. _
.
300
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. .
: ?
. .
I” 1 200 u
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.
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.+
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100
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660
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+-+-
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500
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(msec)
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700
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600
(msec)
FIGURE 2. Plot of atrial cycle length (AI-A2) versus A-V nodal conduction times (AZ-Hz) (A) and versus His bundle cycle lengths (HI-H*)(B) during atrial exlrastimulus testing. Beats conducted normally are identified by closed cfrdes. beats conducted with a right bundle branch pattern are identified by a plus sign and nonconducted atrial beats are identified by a cross. RBBB = right bundle branch block.
1116
May 22,1976
The American Journal of CARDIOLOGY
Volume 41
DUAL PATHWAYS AND GAP CONDUCTION-MIRVIS AND BANDURA
Discussion Dual A-V nodal pathways: The electrophysiologic data in this case support two diagnoses. First, the abrupt increase in A-V nodal conduction times at a critical coupling interval and the discontinuous coupling interval-conduction time plots (Fig. 2) suggest physiologic, and possibly anatomic, dual A-V nodal pathways.1-4 Conduction time and His bundle cycle length increase suddenly with transfer of conduction from the relatively fast to the slower mode. Previously described manifestations of this pattern include echo beats, supraventricular tachycardias, atypical A-V nodal Wenckebach periods and a specific form of “supernormal” conduction.” Other interpretations for the observed discontinuous curves may be proposed. For example, delay may be induced by arrival of a premature impulse during the relative refractory period of a portion of a single pathway.” The abrupt slowing of conduction, and hence the discontinuity in A-V conduction curves, may possibly represent conversion of propagation from a rapid, active mode to a slower, passive or electrotonici2 mechanism within a single path. Another hypothesis is that the prematurity of the impulse causes it to engage only part of the A-V node, resulting in loss of the summation effects observed with total nodal activation; propagation velocity would then also decrease.13 A-V nodal gap phenomenon: A second diagnosis is that of type I, or A-V nodal, gap phenomenon.1y5-g In this pattern of conduction, impulses are blocked within the His-Purkinje system when their prematurity encroaches upon the effective refractory periods of these structures. As the coupling or Al-As interval is further decreased, the increased delay in propagation through the A-V node permits greater recovery times for the distal tissues, and conduction resumes. Thus, the cycle length observed by the His-Purkinje system increases despite a reduction in coupling intervals and atria1 cycle lengths. A-V nodal gap patterns are uncommon; for example, they were noted in only 6 of 45 subjects studied by Wit et al6 The necessity for the simultaneous occurrence of two unusual electrophysiologic phenomena may explain this infrequency. First, the effective refractory period of the His-Purkinje system must exceed the functional refractory period of the A-V node. Second, the A-V nodal conduction time must increase substantially without being totally blocked with relatively small increases in prematurity. This permits recovery of the distal tissues, thereby allowing conduction to continue.
In our case, block occurred sequentially in multiple areas of the His-Purkinje system. At an Al-As interval of 420 msec, right bundle branch conduction was significantly retarded14 so as to produce an electrocardiographic pattern of right bundle branch block. The concurrent prolongation of the H-V time at this cycle length further suggests delay within the distal His bundle or left branch system.15 When the coupling interval further decreased to 370 msec, corresponding to a His bundle cycle length of 430 msec, conduction below the His bundle recording site ceased. Finally, at a shorter Al-A2 interval of 320 msec but at a longer Hi-Hz interval of 510 msec, A-V conduction resumed with a normal H-V time and QRS pattern.8 This occurred as the As-H2 interval abruptly increased from 165 to 305 msec, thought to result from transfer of A-V nodal conduction from a rapid to a slow transmission mode. Thus, the second requirement for gap conduction was provided by the coexistence of functionally dual A-V nodal pathways. Type I or A-V nodal gap may thus be considered an electrophysiologic consequence of dual A-V nodal pathways. Mechanism: Durrer5 proposed a mechanism whereby these two phenomena may be physiologically correlated. During normal conduction at long coupling intervals, conduction through high or junctional pathways occurs by way of the more rapidly conducting fibers. When prematurity increases and a gap in conduction is observed, the fast path is still used but the impulse reaches refractory tissue in the lower “final common” paths. Finally, conduction resumes as the effective refractory period of the fast system is reached and the impulse propagates through a slow path. The delay in reaching the final common pathway permits its recovery. This model is applicable to our case if one assumes the refractory site of the common path to be distal to the His bundle recording site. Several other reported cases may be similarly interpreted. Wit et a1.6 demonstrated an abrupt increase in A-H times of premature atria1 stimuli coincident with resumption of A-V conduction in a patient with a short P-R interval. This was attributed to conversion from a fast extranodal to a slower intranodal pathway at a critical coupling interval. In our case, an extranodal path was unlikely because the A-H times were normal at rest. Additionally, Damato et a1.7,g reported cases of A-V nodal gap in which seemingly disproportionate increases in A-H times with small increases in extrastimulus prematurity led to resumption of A-V conduction. Thus, the occurrence of dual A-V conduction modes may not be an uncommon substrate for the recording of A-V nodal gap conduction patterns.
References 1. Moe GK, Preston JB, Burlington H: Physiologic evidence for dual A-V transmission system. Circ Res 4.357-375. 1956 2 Wft AL, Weiss MB, Berkowitz WD, ef al: Patterns of atrioventncular conduchon rn the human heart Circ Res 27:345-359, 1970 3. Rosen KM, Mehta A, Miller RA: Demonstration of dual atrioventrtcular nodal pathways in man Am J Cardtol 33:291-294, 1974
May 22,1978
4
Rosen KM, Denes P, Wu D, et al: Electrophystological dtagnoses and manifestations of dual A-V nodal pathways. In. The Conduction System of the Heart (Wellens HJJ, Lie KI, Janse MJ, ed) Philadelphia, Lea & Febiger, 1976. p 453-466 5 Durrer D: Electrical aspects of human cardiac acttvity: a clinicalphystological approach to excitation and stimulation Cardiovasc
The American Journal of CARDIOLOGY
Volume 41
1117
DUAL PATHWAYS AND GAP CONDUCTION-MIRVIS AND BANDURA
Res 2.1-18, 1968 6. Wit AL, Damato AN, Weiss MB, et al: Phenomenon of the gap in atrioventricular conductron in the human heart Circ Res 27: 679-689, 1970 7 Damato AN, Akhtar M, Ruskin J, et al: Gap phenomena: antegrade and retrograde, Chap 28 In Reference 4, p 503-528 8 Agha AS, Castellanos A Jr, Wells D, et al: Type I, type II and type Ill gaps in bundle branch conduction Crrculation 47:325-330, 1973 9 Damato AN, Wit AL, Lau SH: Observations on the mechanism of one type of so-called supernormal A-V conduction Am Heart J 82:725-730, 1971 10. Keller FW, Mirvis DY, Laughter JS, et al: A microprocessor controlled timing device for cardiac electrical stimulation. Sub-
1118
May 22,197s
The American Journal of CARDIOLOGY
mitted for publication 11 Moore EN: Microelectrode studies n concealment of multiple atnal premature responses. Circ Res 18:660-672, 1966 12 Wennemark JR, Bandura JP: Microelectrcds study of Wenckebach periodicity in canine Purkinje fibers Am J Cardiol 33:390-398, 1974 13 Zlpes DP: Dual A-V nodal pathways and pre-excitation Circulation 50:861-862, 1974 14 Wu D, Denes P, Dhlngra R, et al: Bundle branch block: demonstration of the incomplete nature of some “complete” bundle branch and fascicular blocks by the extrastimulus technique. Am J Cardiol 33:583-589, 1974 15. Rosen KM, Rahimtoola SH, Sinno MZ et al: Bundle branch and ventricular activation in man. Circulation 43:193-203. 1971