Enhancement of conduction in an accessory pathway by local noncaptured stimuli

lACC Vol. 9, No.2 February 1987:455-8

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Enhancement of Conduction in an Accessory Pathway by Local Noncaptured Stimuli RICHARD ROTHSCHILD, MD, WILLIAM G. STEVENSON, MD, THOMAS KLITZNER, MD, JAMES WEISS, MD, FACC Los Angeles, California

Subthreshold stimuli have been reported to prolong the refractory period of myocardial tissue. This report presents the first case of reproducible acceleration of a reentrant tachycardia by apparently subthreshold stimuli delivered to the os of the coronary sinus during the atrial refractory period in a child with incessant orthodromic

With the advent of catheter ablation for the treatment of tachyarrhythmias, the precise catheter localization of reentrant pathways has taken on new importance . Currently, the proximity of a cathether to a reentrant pathway is assessed by analyzing the timing of the local electrogram recorded from that catheter. The lack of reliable success of attempted endocardial ablation, especially for ventricular tachycardia (1,2) , is indicative of the need for new methods of localizing critical segments of reentrant pathways. Recently, Prystowsky and Zipes (3) showed that electrical stimuli delivered during the ventricular or atrial refractory period can prolong refractoriness. Because these subthreshold stimuli have only a very local effect (4), the demonstration that a subthreshold stimulus affects a reentrant tachycardia may indicate that the catheter is adjacent to a portion of the reentrant circuit. Patients with incessant atrioventricular (AV) reentrant tachycardia utilizing a posteroseptaI accessory pathway are particularly well suited for testing this hypothesis because the atrial insertion of this accessory AV connection has been well localized to the rim of the coronary sinus (5,6), and electrical shocks delivered to that site have been successful in abolishing conduction by the accessory pathway (7). We present the first example of advancement of a reentrant circuit by apparently subthreshold stimuli delivered to the

From the Divisions of Cardiology of the Departments of Medicine and Pediatrics. University of California at Los Angeles School of Medicine. Center for the Health Sciences, Los Angeles. California . Manuscript received March 24, 1986; revised manuscript received May 13, 1986. accepted May 30, 1986. Address for reprints: William G. Stevenson. MD. Division of Cardiology, UCLA School of Medicine. 47-123 Center for the Health Sciences, Los Angeles, California 90024. © 1987 by the American College of Cardiology

tachycardia utilizing a posteroseptal pathway. Mechanisms by which these stimuli could influence the tachycardia circuit are proposed, and the potential usefulness of this finding for mapping tachyarrhythmias is discussed. (J Am Coli CardioI1987;9:455-8)

os of the coronary sinus during orthodromic reentrant tachycardia in a child with a posteroseptal pathway .

Case Report Clinical data and methods. The patient is a 6 year old boy with supraventricular tachycardia refractory to digitalis and propranolol. After informed parental consent was obtained , the patient was taken in a fasting drug-free state to the catheterization laboratory and sedated with diazepam, meperidine, promethazine and chlorpromazine. Local anesthesia was obtained with I % lidocaine. Four quadripolar electrode catheters (USCI) with a I em interelectrode distance were placed transvenously in the right ventricular apex, across the tricuspid valve in position to record the His bundle. high right atrium, and coronary sinus electrograms. Surface electrocardiographic leads I. aVF and V I and intracardiac recordings filtered at 30 to 500 Hz were recorded at paper speeds of 50 to 150 mmls on an Electronics for Medicine VR 16 chart recorder. Pacing was performed with a programmable stimulator (Bloom Associates, Ltd.). After the initial recordings, the proximal electrode pair of the coronary sinus catheter was positioned at the os of the coronary sinus . Bipolar pacing near the accessory pathway was performed using the proximal electrode pair of the coronary sinus catheter while recording from the distal electrode pair, which was then at the proximal coronary sinus location . Bipolar pacing distant to the accessory pathway was performed from the distal electrode pair of a right atrial catheter positioned at a site on the atrial septum midway between the coronary sinus os and the His bundle catheter. 0735-1097/87/$3.50

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Effect of atrial premature stimuli. To evaluate the effect of high amplitude stimuli delivered during atrial refractoriness on the tachycardia, stimuli with a pulse width of 9 ms and strength of lOrnA were used to scan atrial diastole in 10 ms decrements coupled to the coronary sinus atrial electrogram. Stimuli delivered at the coronary sinus os captured the atrium when the coupling interval (AS) was 85 ms or greater (Fig. 2A). As the coupling interval decreased to 65 ms (Fig. 28), the stimulus encountered atrial refractoriness and produced no change in the tachycardia. As the coupling interval decreased further to 55 ms (Fig. 2C), no evidence of atrial or ventricular capture was observed in the surface or endocardial electrograms, but the AA interval shortened from 290 to 260 as a result of a decrease in the VA interval, with no change in AH and HV intervals. Thus, the tachycardia rate advanced by 30 ms. As the coupling interval was decreased further to 35 ms (Fig. 20) , the tachycardia rate was again advanced by 30 ms. In contrast, identical stimuli of up to 25 ms less than the atrial effective refractory period and delivered distant to the reentrant circuit at the lower right atrial septum had no effect on the tachycardia.

Discussion Patients with incessant narrow QRS tachycardias with longer RP than PR intervals often have a slowly conducting paraseptal accessory pathway that inserts at the rim of the coronary sinus (5- 7). Although extensive mapping of the AV ring during tachycardia was not performed in our patient, the observation that the earliest retrograde atrial activation during tachycardia occurred at the os of the coronary sinus is consistent with such a posterior paraseptal accessory pathway location. We demonstrated that premature extrastimuli delivered at this location advanced atrial activation by decreasing the VA interval without evidence of atrial or ventricular capture. Identical stimuli delivered to other sites in the right atrium. presumably more distant from the accessory pathway, had no effect on the VA interval of the tachycardia. Hence. nonspecifi c effects of the relatively high amplitude diastolic stimuli are unlikely to account for this observation. Mechanism. Shortening of the VA interval by apparently subthreshold atrial extrastimuli could be explained by several mechanisms. The first is capture of the atrium. ventricle or accessory pathway. Atrial capture with a latency of up to 170 ms is unlikely. Capture of the accessory pathway or adjacent ventricle by the atrial stimuli could also advance the atrial activation. However , as seen in Figure 2, there is no evidence for ventricular capture by the atrial extrastimulus in the surface or intracardiac electrograms. Specifically, there is no change in the configuration or relative timing of the ventricular electrogram recorded from the right ventricular apex, coronary sinus or His bundle

lACC Vol. 9. No.2 February 1987:455-8

ROTHSCHILD ET AL. REFRACTORY STIMULI RESET TACHYCARDIA

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catheter immediately after the stimulus. However, it is possible that the extrastimulus captured a very small portion of the ventricle near the ventricular insertion of the accessory pathway or the accessory pathway itself, and entrained the tachycardia for one beat (8). That is, the stimulated impulse penetrated the reentrant circuit and advanced the tachycardia. This explanation is only tenable if the catheter is in close proximity to the accessory pathway because a more distant position would require capture of some intervening atrial or ventricular tissue with conduction to the reentrant circuit and would alter the recorded electrograms. An alternative explanation is that the noncaptured atrial extrastimulus advanced atrial activation by inducing supernormal conduction in the accessory pathway or adjacent myocardium. During the noncaptured bipolar extrastimulus, tissue in the vicinity of the anode would be subjected to hyperpolarizing current which, by facilitating repolarization of the tissue, may enhance conduction of the next impulse. Alternatively, in the vicinity of the cathode, depolarizing current would tend to prolong the duration of the action potential. If the action potential was sufficiently prolonged, the next impulse might arrive during phase 3 (rapid repolarization) of the action potential, which might facilitate rapid supernormal conduction (9, 10). We did not investigate the effects of unipolar anodal and cathodal stimulation to determine which of these mechanisms may have been op-

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erative. Because these electronic effects occur only in the immediate vicinity of the anode and cathode, this explanation is feasible only if the pacing leads were very close to the accessory pathway. High amplitude stimuli can also cause local catecholamine release, which can alter regional conduction velocity and refractoriness (II). However, in contrast to our observations, we would have expected local catecholamine release to alter regional conduction for more than just one cycle. Conclusion. We report a case in which apparently noncaptured atrial stimuli advanced circus movement tachycardia when delivered near a posteroseptal accessory pathway. This effect was not seen when identical stimuli were delivered farther away from the accessory pathway. This observation may be useful in the precise catheter localization of reentrant pathways.

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Anatomic and electrophysiologic substrate of the permanent form of junctional reciprocating tachycardia. J Am Coil CardioI1984;4:60I-IO. 7. Morady F, Scheinman MM, Winston SA, et al. Efficacy and safety of transcatheter ablation of posteroseptal accessory pathways. Circulation 1985;72:170-7. 8. Brugada P, Wellens H11. Entrainment as an electrophysiologic phenomenon. J Am Coil Cardiol 1984;3:451-4. 9. Spear JF, Moore EN. Supernormal excitability and conduction. In: Wellens H11, Lie KI, Janse MJ, eds. The Conduction System of the Heart. Philadelphia: Lea & Febiger, 1976:111-25. 10. Antzelevitch C, Moe GK. Electrotonically mediated delayed conduction and reentry in relation to "slow responses" in mammalian ventricular conducting tissue. Circ Res 1981;49:1129-39. II. Vincenz FF, West TC. Release of autonomic mediators in cardiac tissue by direct subthreshold electrical stimulation. J Pharmacol Exp Ther 1963;141:185-94.