Supraventricular nonreentrant tachycardia due to simultaneous conduction through dual atrioventricular nodal pathways

BRIEF REPORTS

Supraventricular Nonreentrant Tachycardia Due to Simultaneous Conduction Through Dual Atrioventricular Nodal Pathways

Patient l: A 33-year-old man was hospitalized for palpitations. A 24-hour Holter tape had previously revealed irregular paroxysmal supraventricular tachycardia which was interpreted as atrial fibrillation (Fig. 1). He received propranolol, 20 mg orally 4 times daily, which aggravated the palpitations. Administration of 50 mg of bethanecol chloride, orally, prolonged the episodes of supraventricular tachyeardia, which were terminated by 0.5 mg of atropine sulfate administered intravenously. During tachycardia an intraatrial electrogram showed that most of the P waves were followed by 2 QRS complexes (Fig. 2). When the P wave was followed by a single QRS complex, the P-R interval was markedly prolonged. Administration of procainamide and disopyramide also aggravated the arrhythmia. Pacing techniques included incremental atrial pacing until the development of second degree A V nodal block, programmed atrial extrastimuli scanning diastole during atrial pacing at a cycle length of 700 ms, and programmed single ventricular extrastimulus scanning diastole during sinus rhythm. No discontinuity of A ~-A2, A 2-H2 could be demonstrated, and no arrhythmia was induced by atrial pacing. During sinus rhythm an interpolated ventricular extrastimulus produced 2 distinct patterns (Fig. 3). When the coupling interval was <330 ms, no tachycardia was induced, and there was minimal prolongation of the A-H interval of ~he first sinus beat which followed the ventricular extrastimuli (Fig. 3 and 4). At longer coupling intervals, most extrastimulus beats had a prolonged A-H interval ranging from 400 to 550 ms (Fig. 3) and were followed by short runs of nonreentrant tachycardia (Fig. 5). The induced tachycardia was similar to the spontaneous tachycardia. A His potential was recorded preceding each QRS complex with the H-V interval constant at 45 ms. No ventriculoatrial conduction was present during ventricular pacing.

FREDERICK J. SUTTON, MD and YU-CHEN LEE, MD

Simultaneous conduction of atrial paced beats through dual atrioventricular (AV) nodal pathways was first described by Wu et al ~ in 1975. Subsequently, Csapo 2 reported on a patient with paroxysmal nonreentrant tachycardia due to this mechanism. Recently, Gomes et al3 performed electrophysiologic studies in 3 patients with supraventricular tachycardia and stated that procainamide altered conduction and refractoriness of the anterograde fast and slow pathways of the AV node so that simultaneous conduction could occur during atrial pacing. The present report describes 2 patients with sustained nonreentrant tachycardia due to simultaneous conduction through dual AV nodal pathways, and discusses various precipitating factors of this unusual arrhythmia. From the Division of Cardiology, Department of Medicine, University of Maryland Hospital, Baltimore, Maryland. Manuscript received June 7, 1982; revised manuscript received November 25, 1982, accepted November 27, 1982.

FIGURE 1. Patient 1. Holter tracing. After 2 sinus beats a rapid irregular rhythm is seen which was initially interpreted a s atrial fibrillation.

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FIGURE 2. Patient 1. Intraatrial electrogram after administration of bethanocal chloride. After 2 sinus beats a supraventricular tachycardia is seen. P waves are regular, and each P wave is followed by 2 QRS complexes.

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BRIEF REPORTS

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Patient 2: A 68-year-old man was referred for evaluation of supraventricular tachycardia, which developed after quinidine treatment for ventricular premature contractions. Procainamide and disopyramide also induced similar supraventricular tachycardia characterized by I P wave followed by 2 QRS complexes (Fig. 6).

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The supraventricular tachycardia in these 2 patients is extremely unusual in that the arrhythmia was aggravated by increased vagal tone, propranolol, and type I antiarrhythmic drugs. This tachyarrhythmia is most likely due to simultaneous conduction through dual AV nodal pathways. In the first patient, the spontaneous paroxysmal nonreentrant supraventricular tachycardia was repeatedly reproduced by appropriately timed ventricular stimuli during sinus rhythm. The interpolated ventricular beats partly penetrated the distal AV node, which remained refractory for the oncoming sinus impulse traveling through the fast pathway. However, the same sinus impulse traveling down the slow pathway was sufficiently delayed to allow recovery of the distal AV nodal tissue, making ventricular capture possible. The subsequent sinus impulse was conducted simultaneously through both fast and slow AV nodal tracts, resulting in 2 QRS complexes after each P wave (Fig. 7

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COUPLING INTERNAL (msec) FIGURE 3. Patient 1. The relation of the coupling interval of the programmed ventricular extrasystole and the A-H interval of the first sinus beat after the extrasystole, Prolonged A-H interval of the first sinus beat was seen only when the coupling interval was more than 330 ms. The supraventricular tachycardia was induced only when the A-H interval was prolonged.

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FIGURE 4. Patient 1. During sinus rhythm an interpolated ventricular extrastimuius (coupling interval of 320 ms) failed to induce a supraventricular tachycardia and the A-H interval of the following sinus beat prolonged minimally. I, aVF, V = surface electrocardiographic leads; RA = right atrial electrocardiogram; HBE1 and HBE2 = proximal and distal His bundle electrograms, respectively; V2 = programmed ventricular extrasystole.

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FIGURE 5. Patient 1. During sinus rhythm an interpolated ventricular extrastimulus (coupling interval of 460 ms) induced a nonreentrant supraventricular tachycardia. A-H interval of the first sinus beat after the ventricular extrastimulus was markedly prolonged (440 ms).

March 1, 1983

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FIGURE 6. Patient 2. Lead II surface electrocardiogram. The QR$ complexes occur in groups of 5. The first 2 P waves in each group are followed by 2 QRS complexes and the third P wave is followed by a single QRS complex.

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FIGURE 7. Patient 1. Laddergram of the proposed mechanism of tachycardia. Presence of retrograde conduction block of both pathways enabled simultaneous anterograde conduction of the sinus P waves. The fourth P wave is conducted through only the slow pathway (dotted line) due to deeper retrograde penetration of the fast pathway (solid line) which prevented anterograde conduction•

and 8). This rhythm was maintained because the refractory period of the distal common pathway was shorter than the shortest cardiac cycle, and the distal AV nodal pathway of either side was refractory to the retrograde stimuli from the opposite tract (Fig. 8). Shortening of the coupling interval of the ventricular extrastimulus to <330 ms allowed sufficient recovery time for the following sinus beat to conduct normally through the fast pathway, and this impulse could then penetrate the slow pathway retrogradely and abort the

tachycardia. The presence of 2 distinct patterns of A-H conduction in Figure 3 suggests dual nodal tracts which are not excluded by the failure to document a discontinuous A1-A2, A2-H2 curve in an anterograde fashion. 4 The supraventricular tachycardia of the first patient was aggravated by increased vagal tone and improved by atropine sulfate. Such paradoxical response has not been reported previously. One possible explanation is that increased vagal tone potentiated the unidirectional

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ATRIUM FIGURE 8. Mechanism of the programmed ventricular extrastimulus inducing supraventricular tachycardia. The ventricular extrasystole penetrated both pathways retrogradely, and was deep enough to prevent anterograde conduction of the first pathway. However, the slow pathway recovered soon enough to allow anterograde Conduction. Presence of retrograde conduction block of both pathways enabled subsequent simultaneous anterograde conduction of the sinus P waves. SN = sinus node; V = QRS conducted through fast pathway; V 1 = QRS conducted through slow pathway.

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BRIEF REPORTS

retrograde block that is present in the AV nodal pathway in the basal state. The increased vagal tone insulates both AV nodal pathways and makes anterograde conduction through both AV nodal pathways possible. The supraventricular tachycardia in the second patient probably had the same mechanism as that in the first patient, although electrophysiologic study could not be performed. The episodes manifested by QRS complexes in groups of 5 are explained by the presence of 3 to 2 anterograde AV block through the slow pathway. Procainamide has been reported to facilitate simultaneous conduction through dual AV nodal pathways by altering conduction and refractoriness of the anterograde fast and slow pathways of the AV node during atrial pacing. 3 However, we believe that the type 1 antiarrhythmic drug in our patients potentiated simultaneous conduction through dual AV nodal pathways by blocking retrograde conduction. Impairment

of retrograde conduction of the AV node by these drugs has been reported previously.5-7

Acknowledgment: We thank Leonard Scherlis, MD, for review of the manuscript, Debbie Trust for secretarial assistance, and Frank Morris, MD, for referring the second case. References 1. Wu D, Denes P, Dhlngra R, Pietras RJ, Rosen KM. New manifestations of dual A-V nodal pathways. Eur d Cardio11975;2:456-466. 2. Csapo G. Paroxysmal non-reentrant tachycardia due to simultaneous Conduction in dual atrioventricular nodal pathways. Am J Cardiol 1979;43: 1033-1045, 3. Gomes JAC, Kang PS, Kelen G, Khan R, El-Sherif N, Simultaneous anterograde fast slow atrioventricular nodal pathway conduction after procainamide. Am J Cardio11980;46:677-684. 4. Wu D. Dual atrioventricular nodal pathways: a reappraisal. PACE 1982;5: 72-69. 5. Shenasa M, Gilbert CJ, Schmidt DH, Akhtar M. Procainamideand retrograde atrioventricular nodal conduction in man. Circulation 1982;65:355-362. 6. Wu D, Hung J, Kuo C, Hsu K, Shleh W. Effects of quinidineon atTioventricular nodal reentrant paroxysmal tachycardia, Circulation 1961;64:823-831. 7. Swiryn S, Bauernfelnd RA, Wyndham CRC,Dhingra RC, Palileo E, Strasber9 B, Rosen KM. Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia. Circulation 1981;64:169-175.

Survival After Sudden Obstruction of The Left Main Coronary Artery MOSHE Y. FLUGELMAN, MD, MEIR SHALITI MD, ARIE SHEFER, MD, YONATHAN HASIN, MD, and MERVYN S. GOTSMAN, MD, FRCP

Left main coronary artery (LMCA) stenosis occurs in 10% of patients undergoing coronary arteriography, but total occlusion is rare. 1 Goldberg et al2 reported 6 cases of complete obstruction of the LMCA among 2,200 patients studied arteriographically. Sudden obstruction of the LMCA should be lethal,3 and we found no report describing survival with sudden obstruction of the LMCA. The present report describes such a patient. A 55-year-old man, a heavy smoker with no history of ischemic heart disease, had ventricular fibrillation 30 rainutes after the onset of severe retrosternal chest pain. Sinus rhythm was restored after 6 direct-current cardioversions combined with lidocaine infusion. After resuscitation, pulmonary edema developed; the patient had a systolic blood pressure of 60 mm Fig, a pulse rate of 120 beats~rain and frequent premature ventricular contractions. Electrocardiograms showed sinus tachycardia with frequent ventricular premature contractions and an acute extensive anterior myocardial infarction. The cardiac index, measured with a thermodilution Swan-Ganz catheter, was I liter/minim 2. An intraaortic counterpulsation balloon was inserted through the right femoral artery during resuscitation; the blood pressure increased to 110/70 mm Hg and the cardiac index

From the Department of Cardiology, Hadassah University Hospital, Jerusalem, Israel. Manuscript received June8, 1982;revised manuscript received September 10, 1982, accepted September 17, 1982.

FIGURE 1. Left coronary arteriogram (right anterior oblique view) showing complete obstruction of the left main coronary artery.

to 1.9 liters/min/m 2. Mechanical assistance was combined with intravenous treatment of glucose-potassium-insulin solutions and oral isorbide-dinitrate, digoxin, and diuretic agents. Cardiac catheterization and angiography, performed 15 days later, revealed a left ventricular end-diastolic pressure of 35 mm Hg, a large aneurysm of the anterior and apical regions, and normal contraction of the inferior wall. Coronary arteriography demonstrated complete obstruction of the LMCA (Fig. 1) while the right coronary artery was normal; there was no collateral filling of the left coronary system. The left ventricular ejection fraction was 16% with mechanical assistance and 5% without assistance. After 26 days, the patient developed a shaking chill and the intraaortic counterpulsation balloon was removed. The patient was discharged after 40 days. By this time he had signs of moderate congestive heart failure but no angina pectoris and was in New York Heart Association functional class III. On discharge, the cardiac index was 1.8 liters/