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A nonreentrant arrhythmia due to a dual atrioventricular nodal pathway
International Elsevier
CARD10
Journal of Cardtology,
217
26 (1990) 217-219
10141
Brief Reports
A nonreentrant arrhythmia due to a dual atrioventricular nodal pathway A. Middle Department of Medicine I, Faculty Hosprtal, Plxit.
(Received 21 April 1989; revision accepted
Czechoskxwkia
21 June 1989)
A 33-year-old woman presented with an atypical arrhythmia. The electrophysiologic study revealed dual atrioventricular nodal pathways. The difference in conductivity of these tracts enabled simultaneous atrioventricular conduction with a double ventricular response to a single atrial impulse. This disturbance is uncommon. Lack of awareness of the existence of dual nodal pathway can cause diagnostic difficulties and therapeutic errors. Key words: arrhythmia
Dual atrioventricular
nodal pathway;
Simultaneous
Introduction The functional dissociation of atrioventricular nodal pathways is recognized and is favourable for reentrant paroxysmal supraventricular tachycardias [l]. Under the condition of sufficient conduction delay in the slow pathway enabling the distal tissue to respond for the second time, however, and a retrograde unidirectional block in the slow pathway preventing the impulse in the fast pathway entering and colliding with the oncoming slow pathway impulse [2], it can give rise to a nonreentrant arrhythmia [3,4]. Case Report A 33-year-old woman was admitted for electrophysiologic study. For the past 9 years she had suffered from recurrent episodes of palpitation. The standard 12-lead electrocardiogram had shown bizarre arrhythmias (Fig. l), mainly evaluated as multiple extrasystoles, both supraventricular and ventricular. There was no evidence of paroxysmal supraventricular tachycardias. The pa-
Correspondence to: Alois Medicine I. Faculty Hospital, Czechoslovakia.
0167-5273/90/$03.50
MBdle, M.D., Department of Sverdlovskh 80, 323 18 Plreii,
0 1990 Elsevier Science
Publishers
dual atrioventricular
nodal conduction;
Nonreentrant
tient had been consecutively treated with metipranolol, digoxin. detajmium bitartarate, amiodarone and. finally, with quinidine and verapamil. The treatment was not successful except for the period of administration of amiodarone. This drug, however, had to be discontinued due to intolerable skin photosensitivity. The last drug combination containing verapamil made the arrhythmias even more frequent. Invasive electrophysiologic study, with recordings from the high right atrium and proximal His bundle and stimulation in the high right atrium, was performed after withdrawal of these drugs. The discontinuation of therapy caused the disappearance of a previously almost incessant arrhythmia. Atria1 extrastimulation did not induce reentrant tachycardia, but one of the premature atria1 activations led to double ventricular response with aberrant morphology of the latter QRS. Extrastimulation with greater prematurity caused only single atria1 echoes. On atria1 pacing with a rate of 80 per minute, abrupt changes in the duration of the A-H interval from 110 msec to 360 msec and vice versa were observed. These findings are indicative of dual atrioventricular nodal pathway [5]. After administration of verapamil 10 mg intravenously, an arrhythmia resembling the original one recurred. The intracardiac recording (Fig. 2) revealed undisturbed atria1 rhythm with atria1 impulses being
B.V. (Biomedical
Division)
218
I
II .
Fig. 1. The original
arrhythmia
Fig. 2. Intracardial electrogram showing the atrioventricular conduction pattern after administration of verapamil. Top panel: II and III = standard extremity leads; HRA = high right atria1 bipolar lead; HBE = proximal His bundle recording (both traces); A = low via the slow via the fast pathway; H,, at impulse conducted atria1 electrogram; H = His bundle potential (Hs, at impulse conducted pathway); V = ventricular activation. Bottom panel: A = atrium; AVN = atrioventricular node; HPS = His-Purkinje system: p = conduction via the fast pathway; a = conduction via the slow pathway.
219
conducted irregularly to the ventricles. Some traversed only the fast beta-pathway, some travelled via both beta- and alpha-pathways, while some were completely blocked. The average A-HB interval was 90 msec and the A-H, interval was 495 msec. These observations clarified the original arrhythmia (Fig. 1) which could be retrospectively interpreted as predominantly simultaneous anterograde conduction through both fast and slow pathways. Since the antiarrhythmic drug therapy was mostly ineffective, or even proarrhythmic, the patient has been left without medication. Discussion
Dual nodal pathways were detected in our patient. When treated with verapamil, there was exacerbation of intermittent simultaneous anterograde conduction through both the fast and slow pathways. Verapamil probably potentiated the delay in the slow pathway to such an extent that the H,-H, interval (Fig. 2) was longer than the effective refractoriness of the HisPurkinje system and, thus, enabled the ventricles to respond twice to a single atria1 impulse. The drug could also influence a retrograde unidirectional block in the slow pathway. Various degrees of the second QRS aberration, both during the study and in the original electrocardiogram, were the consequence of the relative refractoriness of His-Purkinje system. Such conduction, with a changing relationship between atria and ventricles, may have been influenced randomly by variation in refractoriness of nodal tracts. The regular sequence of conduction through both pathways, block in both tracts, and conduction solely through the fast pathway following intravenous verapamil (Fig. 2) represents type 3 : 2
block in the beta- and type 3 : 1 in the alpha-tract. We could speculate on absolute refractoriness of the fast and concealed conduction in the slow pathway next to double ventricular response and block in slow tract owing to the previous concealed conduction and spread via the fast pathway at the next atria1 impulse. Other mechanisms with intermittent retrograde penetration into the nodal tracts could also be proposed. Dual atrioventricular nodal pathways in the absence of invasive electrophysiologic study can be deduced from the occurrence of paroxysmal supraventricular tachycardias. If these tachycardias do not occur, like in our patient, the dual pathway remains concealed. Possible arrhythmias due to simultaneous conduction could then be interpreted incorrectly and could lead to erroneous drug treatment.
References
KM, Bauemfeind R4, Swiryn S, Strasberg B, Palileo EV. Dual AV nodal pathways and AV nodal reentrant paroxysmal tachycardia. Am Heart J 1981;101:691-695. Rosen
Lin FC, Yeh SJ, Wu D. Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways. Am Heart J 1985;109:963-970. Wu D, Denes P, Dhingra R, Pietras RJ. Rosen KM. New manifestations of dual AV nodal pathways. Em J Cardiol I975;2:456-466. Csapo G. Paroxysmal nonreentrant tachycardias due to simultaneous conduction in dual atrioventricular nodal pathways. Am J Cardiol 1979;43:1033-1045. Akhtar M. Paroxysmal atrioventricular nodal reentrant tachycardia. In: Narula OS, ed. Cardiac arrhythmias: electrophysiology, diagnosis and management. Baltimore/ London: Williams and Wilkins, 1979;294-317.
CARD10
Journal of Cardtology,
217
26 (1990) 217-219
10141
Brief Reports
A nonreentrant arrhythmia due to a dual atrioventricular nodal pathway A. Middle Department of Medicine I, Faculty Hosprtal, Plxit.
(Received 21 April 1989; revision accepted
Czechoskxwkia
21 June 1989)
A 33-year-old woman presented with an atypical arrhythmia. The electrophysiologic study revealed dual atrioventricular nodal pathways. The difference in conductivity of these tracts enabled simultaneous atrioventricular conduction with a double ventricular response to a single atrial impulse. This disturbance is uncommon. Lack of awareness of the existence of dual nodal pathway can cause diagnostic difficulties and therapeutic errors. Key words: arrhythmia
Dual atrioventricular
nodal pathway;
Simultaneous
Introduction The functional dissociation of atrioventricular nodal pathways is recognized and is favourable for reentrant paroxysmal supraventricular tachycardias [l]. Under the condition of sufficient conduction delay in the slow pathway enabling the distal tissue to respond for the second time, however, and a retrograde unidirectional block in the slow pathway preventing the impulse in the fast pathway entering and colliding with the oncoming slow pathway impulse [2], it can give rise to a nonreentrant arrhythmia [3,4]. Case Report A 33-year-old woman was admitted for electrophysiologic study. For the past 9 years she had suffered from recurrent episodes of palpitation. The standard 12-lead electrocardiogram had shown bizarre arrhythmias (Fig. l), mainly evaluated as multiple extrasystoles, both supraventricular and ventricular. There was no evidence of paroxysmal supraventricular tachycardias. The pa-
Correspondence to: Alois Medicine I. Faculty Hospital, Czechoslovakia.
0167-5273/90/$03.50
MBdle, M.D., Department of Sverdlovskh 80, 323 18 Plreii,
0 1990 Elsevier Science
Publishers
dual atrioventricular
nodal conduction;
Nonreentrant
tient had been consecutively treated with metipranolol, digoxin. detajmium bitartarate, amiodarone and. finally, with quinidine and verapamil. The treatment was not successful except for the period of administration of amiodarone. This drug, however, had to be discontinued due to intolerable skin photosensitivity. The last drug combination containing verapamil made the arrhythmias even more frequent. Invasive electrophysiologic study, with recordings from the high right atrium and proximal His bundle and stimulation in the high right atrium, was performed after withdrawal of these drugs. The discontinuation of therapy caused the disappearance of a previously almost incessant arrhythmia. Atria1 extrastimulation did not induce reentrant tachycardia, but one of the premature atria1 activations led to double ventricular response with aberrant morphology of the latter QRS. Extrastimulation with greater prematurity caused only single atria1 echoes. On atria1 pacing with a rate of 80 per minute, abrupt changes in the duration of the A-H interval from 110 msec to 360 msec and vice versa were observed. These findings are indicative of dual atrioventricular nodal pathway [5]. After administration of verapamil 10 mg intravenously, an arrhythmia resembling the original one recurred. The intracardiac recording (Fig. 2) revealed undisturbed atria1 rhythm with atria1 impulses being
B.V. (Biomedical
Division)
218
I
II .
Fig. 1. The original
arrhythmia
Fig. 2. Intracardial electrogram showing the atrioventricular conduction pattern after administration of verapamil. Top panel: II and III = standard extremity leads; HRA = high right atria1 bipolar lead; HBE = proximal His bundle recording (both traces); A = low via the slow via the fast pathway; H,, at impulse conducted atria1 electrogram; H = His bundle potential (Hs, at impulse conducted pathway); V = ventricular activation. Bottom panel: A = atrium; AVN = atrioventricular node; HPS = His-Purkinje system: p = conduction via the fast pathway; a = conduction via the slow pathway.
219
conducted irregularly to the ventricles. Some traversed only the fast beta-pathway, some travelled via both beta- and alpha-pathways, while some were completely blocked. The average A-HB interval was 90 msec and the A-H, interval was 495 msec. These observations clarified the original arrhythmia (Fig. 1) which could be retrospectively interpreted as predominantly simultaneous anterograde conduction through both fast and slow pathways. Since the antiarrhythmic drug therapy was mostly ineffective, or even proarrhythmic, the patient has been left without medication. Discussion
Dual nodal pathways were detected in our patient. When treated with verapamil, there was exacerbation of intermittent simultaneous anterograde conduction through both the fast and slow pathways. Verapamil probably potentiated the delay in the slow pathway to such an extent that the H,-H, interval (Fig. 2) was longer than the effective refractoriness of the HisPurkinje system and, thus, enabled the ventricles to respond twice to a single atria1 impulse. The drug could also influence a retrograde unidirectional block in the slow pathway. Various degrees of the second QRS aberration, both during the study and in the original electrocardiogram, were the consequence of the relative refractoriness of His-Purkinje system. Such conduction, with a changing relationship between atria and ventricles, may have been influenced randomly by variation in refractoriness of nodal tracts. The regular sequence of conduction through both pathways, block in both tracts, and conduction solely through the fast pathway following intravenous verapamil (Fig. 2) represents type 3 : 2
block in the beta- and type 3 : 1 in the alpha-tract. We could speculate on absolute refractoriness of the fast and concealed conduction in the slow pathway next to double ventricular response and block in slow tract owing to the previous concealed conduction and spread via the fast pathway at the next atria1 impulse. Other mechanisms with intermittent retrograde penetration into the nodal tracts could also be proposed. Dual atrioventricular nodal pathways in the absence of invasive electrophysiologic study can be deduced from the occurrence of paroxysmal supraventricular tachycardias. If these tachycardias do not occur, like in our patient, the dual pathway remains concealed. Possible arrhythmias due to simultaneous conduction could then be interpreted incorrectly and could lead to erroneous drug treatment.
References
KM, Bauemfeind R4, Swiryn S, Strasberg B, Palileo EV. Dual AV nodal pathways and AV nodal reentrant paroxysmal tachycardia. Am Heart J 1981;101:691-695. Rosen
Lin FC, Yeh SJ, Wu D. Determinants of simultaneous fast and slow pathway conduction in patients with dual atrioventricular nodal pathways. Am Heart J 1985;109:963-970. Wu D, Denes P, Dhingra R, Pietras RJ. Rosen KM. New manifestations of dual AV nodal pathways. Em J Cardiol I975;2:456-466. Csapo G. Paroxysmal nonreentrant tachycardias due to simultaneous conduction in dual atrioventricular nodal pathways. Am J Cardiol 1979;43:1033-1045. Akhtar M. Paroxysmal atrioventricular nodal reentrant tachycardia. In: Narula OS, ed. Cardiac arrhythmias: electrophysiology, diagnosis and management. Baltimore/ London: Williams and Wilkins, 1979;294-317.