- Email: [email protected]
Atrioventricular node reentry that utilizes triple nodal pathways
Volume Number
124 3
Brief communications
sis, several studies have shown that angioplasty for ostial disease is associated with decreased technical success, more complications, and an increased incidence of restenosis.5-6 These cases demonstrate that coronary ostial stenosis can occur in an isolated lesion in elderly patients and that directional coronary atherectomy should be considered as therapy for these patients. REFERENCES
1. Prichard CL, Mudd GJ, Barner HB. Coronary ostial stenosis. Circulation 1978;52:46-8. 2. Thompson R. Isolated coronary ostial stenosis in women. J Am Co11 Cardiol 1986;7:997-1003. 3. Rissanen V. Occurrence of coronary ostial stenosis in necropsy series of myocardial infarction, sudden death and violent death. Br Heart J 1975;37:182-91. 4. Tillman CH, Mukerji V, Alpert AM, Sanfillipo JF. Isolated coronary ostial stenosis in men. AM HEART J 1988,115:1127-8. 5. Mathias DN, Mooney FJ, Lange HW, et al. Frequency of success and complications of coronary angioplasty of stenosis at ostium of branch vessel. Am J Cardiol 1991:67:491-5. 6. Top01 EJ, Ellis SG. Fishman J, Leimgraber P, et al. Multicenter study of percutaneous transluminal angioplasty for right coronary ostial stenosis. J Am Co11 Cardiol 1987;9:121418.
Atrioventricular node reentry that utilizes triple nodal pathways Kevin L. Sublett, MD, and Osamu Fujimura, MD Lexington,
Ky.
Although discontinuous curves that suggesttriple atrioventricular (AV) nodal pathways have been described,lf2 few caseshave demonstrated the participation of all of thesepathways during AV node reentry. We describea case in which two distinct forms of AV nodal reentry that utilize three nodal pathways are clearly demonstrated. A 5%year-old man with interstitial lung diseasewasseen in electrophysiology consultation for evaluation of paroxysmal supraventricular tachycardia. A la-lead ECG, which was obtained during normal sinus rhythm, demonstrated evidence of previous inferior myocardial infarction, and during tachycardia showeda narrow QRS complex tachycardia at a rate of 140 beats/min. Electrophysiologic study was performed in the postabsorptive state while the patient was under mild sedation after informed consent was obtained. The study was performed in the absenceof antiarrhythmic therapy. The technique for electrophysiologic study for patients with
From the Arrhythmia Service, Division of Cardiology, University of Kentucky Medical Center. Reprint requests: Osamu Fujimura, MD, Division of Cardiology, Room MN 6’70. Iiniversity of Kentucky, 800 Rose St. Lexington, KY 40536-0084. 4/4/36716
777
supraventricular tachycardia has been described.3Briefly, quadripolar catheters were introduced percutaneously and were positioned in the high right atrium, coronary sinus, right ventricular apex, and acrossthe tricuspid valve to record the potential in the bundle of His. Bipolar electrogramswere recorded at frequency responsesof 50 to 500 Hz. The interelectrode distanceswere 5 mm, 5 mm, and 10 mm for the atrial, coronary sinus,and bundle of His electrograms, respectively. The width of the electrode for each catheter was1 mm. Intracardiac electrogram and multiple surface ECG leadswere recorded simultaneously at paper speedsof 100to 250 mm/set. The heart wasstimulated at twice the diastolic threshold current with a pulse width of 2 msec. Anterograde dual AV nodal pathway physiology wasdemonstratedduring incremental atria1pacing but not with atria1 extrastimuli at 3 pacing cycle lengths. No retrograde discontinuouscurve wasdemonstrated. The effective refractory period of the AV node was less than 280 msec.The shortest cycle length to maintain 1:l conduction over the “fast” nodal pathway was400 msecand that for the “slow” pathway was 340msec.Retrograde 1:l conduction occurred up to 400msec.There wasno evidence of anterograde conduction over an accessory pathway. Two types of sustainedtachycardia were reproducibly induced by ventricular but not by atria1 stimulation (Fig. 1). The QRS complex during tachycardia waseither normal or had right bundle branch block structure. Characteristics of the first episode of tachycardia were: (1) initiation of the arrhythmia only after a critical AV nodal conduction delay (AH interval prolongation) had been reached; (2) earliest retrograde atria1 activation occurrenceat the orifice of the coronary sinus(ventriculoatrial conduction time there was 80 msec) (Fig. 2, A); (3) failure to advance the atria1 electrogram by ventricular extrastimuli at a time when the bundle of His wasrefractory; (4) preexcitation index equal to 150 msec4;and (5) no effect of functional right bundle branch block on the ventriculoatrial conduction time. The secondtype of narrow QRS complex tachycardia had the following findings: (1) the arrhythmia was induced by single ventricular extrastimuli during the first episodeof tachycardia (Fig. 1); (2) the earliest retrograde atria1 activation occurred almost simultaneously in the bundle of His and posteroseptal regions (ventriculoatrial conduction times were 20 to 25 msec)(Fig. 2, B); (3) singleventricular extrastimuli during tachycardia could not preexcite the atria at a time when the bundle of His wasrefractory; (4) the preexcitation index was 130 msec;and (5) functional right bundle branch block did not affect the ventriculoatria1 interval. These findings were compatible with two types of AV node reentry that use triple AV nodal pathways. The first episodeof tachycardia utilized a slow pathway anterogradely and an intermediate pathway retrogradely. The secondarrhythmia utilized the slow pathway anterogradely and a fast pathway retrogradely. Although double AV nodal discontinuous curves that suggesttriple AV nodal pathways have been described,l,2 few data that detail participation of all these pathways during tachycardia exist. For example, Dopirak et a1.2reported a patient with clinical supraventricular tachycardia
September
770
Brief communications
American
Heart
1992 Journal
Fig. 1. Induction of two types of AV node reentry. A single ventricular extrastimulus introduced during a first type of AV node reentry induced a second type of AV node reentry, as evidenced by an abrupt decrease in ventriculoatrial conduction time. The first episode of tachycardia utilized a slow pathway anterogradely and a fast pathway retrogradely. Although two distinct AH intervals may indicate the participation of a fourth pathway, this may simply represent a phenomenon that results from the change in tachycardia rate. Retrograde atria1 activation sequence that occurred after the extrastimulus suggested that the stimulus created conduction block in the intermediate pathway with resultant propagation over the fast pathway. (See Fig. 2 for differences in retrograde atria1 activation sequence.) This in turn led to induction of the second arrhythmia. Recordings from top to bottom are: ECG leads are 3 and Vr; intracavitary bipolar recordings from the right ventricular (R V), right atrium (RA), proximal and distal bundle of His (HB), proximal coronary sinus (CS,), and distal coronary sinus (CSJ. A, Atria1 electrogram; H, His; V, ventricular electrogram.
in whom doubly discontinuous AV nodal conduction curves were provoked by means of atria1 extrastimulus testing. Neither echoes nor tachycardia could be induced in their patient. Swiryn et a1.2 described 10 patients with two distinct discontinuities in AV nodal conduction curves. In all five patients in whom tachycardia was inducible, the common type of AV node reentry with tachycardia was also inducible, and the common type of AV node reentry with anterograde slow and retrograde fast pathway conduction was the mechanism. In one of the patients, however, ventricular extrastimuli that were delivered during tachycardia initiated a second episode of tachycardia, which was associated with an abrupt increase in ventriculoatrial conduction time. Although this suggests the possibility of conduction over an intermediate nodal pathway, other mechanisms cannot be totally excluded because the tachycardia terminated after 5 beats.
Changes in the ventriculoatrial conduction time during AV nodal reentry may result from several mechanisms. First, an alternate conduction over an accessory AV pathway should always be considered. Without an eccentric atria1 activation sequence to indicate a left lateral accessory pathway, posteroseptal and right-sided accessory pathways must be ruled out. Failure to advance the atrial electrogram with ventricular extrastimuli that were delivered during refractoriness of the bundle of His and a large preexcitation index virtually exclude the possibility of participation of an accessory pathway in our case.4, ,5 Second, atria1 tachycardia may be difficult to diagnose when it originates in the vicinity of the AV node. Fixed HA intervals recorded in spite of spontaneous AA interval variation during episodes of tachycardia provide strong evidence against this mechanism.6 Consequently, these findings strongly indicate that AV node reentry underlies each
Volume
124
Number
3
Brief communications
f ._,. i _.,. i ,... I....i....i
.,.. i .,,. i .,., I . . . . I....:
..,. f .,.. i...,t..,
i....:
. . . . i....i
. . . . i . . . . i....;
779
*... i....:.*..:l.,.:..
Fig. 2. A, Spontaneouspremature ventricular contraction (PVC) during AV nodal reentrant tachycardia
utilizing the intermediate pathway for retrograde conduction. Two proximal electrode pairs (C’S,) were placed slightly outside the orifice of the coronary sinus,and the distal pairs (CSd) were placed slightly inside. Numbers shown on each electrogram were intervals between the atria1 electrogram of the CSdposition and the first rapid deflection of each atria1 electrogram. Earliest activation site wasnoted in the CS, position. An uncaptured ventricular stimulus (s) followed the premature ventricular contraction. B, Spontaneouspremature ventricular contraction during AV nodal reentrant tachycardia utilizing the fast pathway retrogradely. The coronary sinus catheter was in the sameposition. Earliest activation siteswere recorded in the bundle of His and C&j positions, followed by the CS, position.
episode of tachycardia.7 Additionally, the possibility of decremental conduction or longitudinal dissociation of a singleretrograde nodal pathway is rather unlikely because of two distinct ventriculoatrial conduction times and retrograde atria1 activation sequences.Finally, although two distinct anterograde nodal conduction times during episodesof tachycardia may indicate the participation of a fourth nodal pathway, this phenomenonmay simply be due to the change in tachycardia cycle length. In conclusion, this caseillustrates that all of theseAV nodal pathways are electrophysiologically different and can participate in AV node reentry. Furthermore, two distinct atria1 activation sequencesimply that atria1 insertion sites of the fast and intermediate pathways are located separately.
2. Swiryn S, Bauernfeind RA, Palileo EA, Strasberg B, Duffy CE, Rosen KM. Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia. AM HEART J 1982;103:168-76. 3. Fujimura 0, Kuo CS, Smith BA. Pre-excited RR intervals during atria1 fibrillation in the Wolff-Parkinson-White syndrome: influence of the atrioventricular node refractory period. J Am Co11 Cardiol 1991;18:1722-6. 4. Miles WM, Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways. Circulation 1986;74:496-500. 5. Prystowsky EN. Diagnosis and management of preexcitation syndromes. Curr Probl Cardiol 1988;13:230-310. 6. Fujimura 0, Kuo CS, Smith BA. Preexcited tachycardia due to atrioventricular node reentry with a bystander accessory pathway diagnosed after procainamide infusion. AM HEART J
REFERENCES
7. Sharma AD, Yee R, Guiraudon GM, Klein GJ. AV nodal reentry current concepts and surgical treatment. Prog Cardiol 1988;1:129-45.
1. Dopirak in man?
1990;120:1475-7. MR, Schaal SF, Leier CV. Triple J Electrocardiol 1980;13:185-8.
AV nodal
pathways
124 3
Brief communications
sis, several studies have shown that angioplasty for ostial disease is associated with decreased technical success, more complications, and an increased incidence of restenosis.5-6 These cases demonstrate that coronary ostial stenosis can occur in an isolated lesion in elderly patients and that directional coronary atherectomy should be considered as therapy for these patients. REFERENCES
1. Prichard CL, Mudd GJ, Barner HB. Coronary ostial stenosis. Circulation 1978;52:46-8. 2. Thompson R. Isolated coronary ostial stenosis in women. J Am Co11 Cardiol 1986;7:997-1003. 3. Rissanen V. Occurrence of coronary ostial stenosis in necropsy series of myocardial infarction, sudden death and violent death. Br Heart J 1975;37:182-91. 4. Tillman CH, Mukerji V, Alpert AM, Sanfillipo JF. Isolated coronary ostial stenosis in men. AM HEART J 1988,115:1127-8. 5. Mathias DN, Mooney FJ, Lange HW, et al. Frequency of success and complications of coronary angioplasty of stenosis at ostium of branch vessel. Am J Cardiol 1991:67:491-5. 6. Top01 EJ, Ellis SG. Fishman J, Leimgraber P, et al. Multicenter study of percutaneous transluminal angioplasty for right coronary ostial stenosis. J Am Co11 Cardiol 1987;9:121418.
Atrioventricular node reentry that utilizes triple nodal pathways Kevin L. Sublett, MD, and Osamu Fujimura, MD Lexington,
Ky.
Although discontinuous curves that suggesttriple atrioventricular (AV) nodal pathways have been described,lf2 few caseshave demonstrated the participation of all of thesepathways during AV node reentry. We describea case in which two distinct forms of AV nodal reentry that utilize three nodal pathways are clearly demonstrated. A 5%year-old man with interstitial lung diseasewasseen in electrophysiology consultation for evaluation of paroxysmal supraventricular tachycardia. A la-lead ECG, which was obtained during normal sinus rhythm, demonstrated evidence of previous inferior myocardial infarction, and during tachycardia showeda narrow QRS complex tachycardia at a rate of 140 beats/min. Electrophysiologic study was performed in the postabsorptive state while the patient was under mild sedation after informed consent was obtained. The study was performed in the absenceof antiarrhythmic therapy. The technique for electrophysiologic study for patients with
From the Arrhythmia Service, Division of Cardiology, University of Kentucky Medical Center. Reprint requests: Osamu Fujimura, MD, Division of Cardiology, Room MN 6’70. Iiniversity of Kentucky, 800 Rose St. Lexington, KY 40536-0084. 4/4/36716
777
supraventricular tachycardia has been described.3Briefly, quadripolar catheters were introduced percutaneously and were positioned in the high right atrium, coronary sinus, right ventricular apex, and acrossthe tricuspid valve to record the potential in the bundle of His. Bipolar electrogramswere recorded at frequency responsesof 50 to 500 Hz. The interelectrode distanceswere 5 mm, 5 mm, and 10 mm for the atrial, coronary sinus,and bundle of His electrograms, respectively. The width of the electrode for each catheter was1 mm. Intracardiac electrogram and multiple surface ECG leadswere recorded simultaneously at paper speedsof 100to 250 mm/set. The heart wasstimulated at twice the diastolic threshold current with a pulse width of 2 msec. Anterograde dual AV nodal pathway physiology wasdemonstratedduring incremental atria1pacing but not with atria1 extrastimuli at 3 pacing cycle lengths. No retrograde discontinuouscurve wasdemonstrated. The effective refractory period of the AV node was less than 280 msec.The shortest cycle length to maintain 1:l conduction over the “fast” nodal pathway was400 msecand that for the “slow” pathway was 340msec.Retrograde 1:l conduction occurred up to 400msec.There wasno evidence of anterograde conduction over an accessory pathway. Two types of sustainedtachycardia were reproducibly induced by ventricular but not by atria1 stimulation (Fig. 1). The QRS complex during tachycardia waseither normal or had right bundle branch block structure. Characteristics of the first episode of tachycardia were: (1) initiation of the arrhythmia only after a critical AV nodal conduction delay (AH interval prolongation) had been reached; (2) earliest retrograde atria1 activation occurrenceat the orifice of the coronary sinus(ventriculoatrial conduction time there was 80 msec) (Fig. 2, A); (3) failure to advance the atria1 electrogram by ventricular extrastimuli at a time when the bundle of His wasrefractory; (4) preexcitation index equal to 150 msec4;and (5) no effect of functional right bundle branch block on the ventriculoatrial conduction time. The secondtype of narrow QRS complex tachycardia had the following findings: (1) the arrhythmia was induced by single ventricular extrastimuli during the first episodeof tachycardia (Fig. 1); (2) the earliest retrograde atria1 activation occurred almost simultaneously in the bundle of His and posteroseptal regions (ventriculoatrial conduction times were 20 to 25 msec)(Fig. 2, B); (3) singleventricular extrastimuli during tachycardia could not preexcite the atria at a time when the bundle of His wasrefractory; (4) the preexcitation index was 130 msec;and (5) functional right bundle branch block did not affect the ventriculoatria1 interval. These findings were compatible with two types of AV node reentry that use triple AV nodal pathways. The first episodeof tachycardia utilized a slow pathway anterogradely and an intermediate pathway retrogradely. The secondarrhythmia utilized the slow pathway anterogradely and a fast pathway retrogradely. Although double AV nodal discontinuous curves that suggesttriple AV nodal pathways have been described,l,2 few data that detail participation of all these pathways during tachycardia exist. For example, Dopirak et a1.2reported a patient with clinical supraventricular tachycardia
September
770
Brief communications
American
Heart
1992 Journal
Fig. 1. Induction of two types of AV node reentry. A single ventricular extrastimulus introduced during a first type of AV node reentry induced a second type of AV node reentry, as evidenced by an abrupt decrease in ventriculoatrial conduction time. The first episode of tachycardia utilized a slow pathway anterogradely and a fast pathway retrogradely. Although two distinct AH intervals may indicate the participation of a fourth pathway, this may simply represent a phenomenon that results from the change in tachycardia rate. Retrograde atria1 activation sequence that occurred after the extrastimulus suggested that the stimulus created conduction block in the intermediate pathway with resultant propagation over the fast pathway. (See Fig. 2 for differences in retrograde atria1 activation sequence.) This in turn led to induction of the second arrhythmia. Recordings from top to bottom are: ECG leads are 3 and Vr; intracavitary bipolar recordings from the right ventricular (R V), right atrium (RA), proximal and distal bundle of His (HB), proximal coronary sinus (CS,), and distal coronary sinus (CSJ. A, Atria1 electrogram; H, His; V, ventricular electrogram.
in whom doubly discontinuous AV nodal conduction curves were provoked by means of atria1 extrastimulus testing. Neither echoes nor tachycardia could be induced in their patient. Swiryn et a1.2 described 10 patients with two distinct discontinuities in AV nodal conduction curves. In all five patients in whom tachycardia was inducible, the common type of AV node reentry with tachycardia was also inducible, and the common type of AV node reentry with anterograde slow and retrograde fast pathway conduction was the mechanism. In one of the patients, however, ventricular extrastimuli that were delivered during tachycardia initiated a second episode of tachycardia, which was associated with an abrupt increase in ventriculoatrial conduction time. Although this suggests the possibility of conduction over an intermediate nodal pathway, other mechanisms cannot be totally excluded because the tachycardia terminated after 5 beats.
Changes in the ventriculoatrial conduction time during AV nodal reentry may result from several mechanisms. First, an alternate conduction over an accessory AV pathway should always be considered. Without an eccentric atria1 activation sequence to indicate a left lateral accessory pathway, posteroseptal and right-sided accessory pathways must be ruled out. Failure to advance the atrial electrogram with ventricular extrastimuli that were delivered during refractoriness of the bundle of His and a large preexcitation index virtually exclude the possibility of participation of an accessory pathway in our case.4, ,5 Second, atria1 tachycardia may be difficult to diagnose when it originates in the vicinity of the AV node. Fixed HA intervals recorded in spite of spontaneous AA interval variation during episodes of tachycardia provide strong evidence against this mechanism.6 Consequently, these findings strongly indicate that AV node reentry underlies each
Volume
124
Number
3
Brief communications
f ._,. i _.,. i ,... I....i....i
.,.. i .,,. i .,., I . . . . I....:
..,. f .,.. i...,t..,
i....:
. . . . i....i
. . . . i . . . . i....;
779
*... i....:.*..:l.,.:..
Fig. 2. A, Spontaneouspremature ventricular contraction (PVC) during AV nodal reentrant tachycardia
utilizing the intermediate pathway for retrograde conduction. Two proximal electrode pairs (C’S,) were placed slightly outside the orifice of the coronary sinus,and the distal pairs (CSd) were placed slightly inside. Numbers shown on each electrogram were intervals between the atria1 electrogram of the CSdposition and the first rapid deflection of each atria1 electrogram. Earliest activation site wasnoted in the CS, position. An uncaptured ventricular stimulus (s) followed the premature ventricular contraction. B, Spontaneouspremature ventricular contraction during AV nodal reentrant tachycardia utilizing the fast pathway retrogradely. The coronary sinus catheter was in the sameposition. Earliest activation siteswere recorded in the bundle of His and C&j positions, followed by the CS, position.
episode of tachycardia.7 Additionally, the possibility of decremental conduction or longitudinal dissociation of a singleretrograde nodal pathway is rather unlikely because of two distinct ventriculoatrial conduction times and retrograde atria1 activation sequences.Finally, although two distinct anterograde nodal conduction times during episodesof tachycardia may indicate the participation of a fourth nodal pathway, this phenomenonmay simply be due to the change in tachycardia cycle length. In conclusion, this caseillustrates that all of theseAV nodal pathways are electrophysiologically different and can participate in AV node reentry. Furthermore, two distinct atria1 activation sequencesimply that atria1 insertion sites of the fast and intermediate pathways are located separately.
2. Swiryn S, Bauernfeind RA, Palileo EA, Strasberg B, Duffy CE, Rosen KM. Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia. AM HEART J 1982;103:168-76. 3. Fujimura 0, Kuo CS, Smith BA. Pre-excited RR intervals during atria1 fibrillation in the Wolff-Parkinson-White syndrome: influence of the atrioventricular node refractory period. J Am Co11 Cardiol 1991;18:1722-6. 4. Miles WM, Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways. Circulation 1986;74:496-500. 5. Prystowsky EN. Diagnosis and management of preexcitation syndromes. Curr Probl Cardiol 1988;13:230-310. 6. Fujimura 0, Kuo CS, Smith BA. Preexcited tachycardia due to atrioventricular node reentry with a bystander accessory pathway diagnosed after procainamide infusion. AM HEART J
REFERENCES
7. Sharma AD, Yee R, Guiraudon GM, Klein GJ. AV nodal reentry current concepts and surgical treatment. Prog Cardiol 1988;1:129-45.
1. Dopirak in man?
1990;120:1475-7. MR, Schaal SF, Leier CV. Triple J Electrocardiol 1980;13:185-8.
AV nodal
pathways