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Paradoxical delay in accessory pathway conduction during long R-P′ tachycardia after interpolated ventricular premature complexes
April 15. 1985
amil every 8 hours and a well-tolerated pressure of 90 mm Hg.
systolic
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 55
1223
blood
Verapamil, a calcium channel antagonist, has been __ reported by several investigators to be efficacious in the termination of reentrant SVTs when administered acutely.2-4 In all reported cases of SVT using an AV bypass tract, whether concealed or with overt WolffParkinson-White syndrome, termination of the arrhythmia by verapamil occurred by way of a direct effect on the AV node by increasing the AV node effective refractory period and prolonging AV node conduction time.2-4 In no instance was a significant effect on either anterograde or retrograde conduction properties of the accessoryAV pathway noted after acute administration of verapamil. Recently, Horio et al5 described 2 patients with catecholamine-induced ventricular preexcitation, in whom verapamil blocked anterograde conduction in the accessory pathway after catecholamine administration. Our patient was not given isoproterenol during the study, and therefore, we cannot comment on the relevance of these findings to our case. This case constitutes the only report of verapamilinduced conduction block in a concealed AV bypass tract. Histologic studies have found anomalous AV connections to be composed of either myocardial fibers or Purkinje cells.6 These cells primarily depend on the fast sodium channel for action potential initiation and propagation and are usually not affected by calcium channel blockade. This case illustrates that concealed bypass tracts may rarely be composed of tissue, either normal or diseased, that uses slow channel conduction for impulse propagation. The exact nature of this tissue remains to be defined. Because most patients with SVT and no evidence of preexcitation never come to electrophysiologic study, the findings in this patient may be more widespread among the subset of patients with SVT and a concealed bypass tract, in whom empiric calcium channel antagonist therapy is successful. Acknowledgment: We thank Brenda Williams, Carol Ginyard and Elizabeth Rose Isidro for assistancein preparing this manuscript and Lance LaForteza for preparation of artwork.
Paradoxical Delay in Accessory Pathway Conduction During Long R-P’ Tachycardia After Interpolated Ventricular Premature Complexes
From the Department of Medicine, Division of Cardiology, Duke University Medical Center, Durham, North Carolina. This study was sup ported in part by Research Training Grant HL-07101, SCOR HL-17670, RCDA HL-00546, and HL-15190 from the National lnstiiutes of Health, Bethesda, Maryland. Manuscript received June 4, 1984; revised manuscript received January 4, 1985, accepted January 5, 1985.
HFIA ““A
HBE
+6oomsec
---cI
FIGURE 2. Loss of retrograde accessory pathway conduction during right ventricular pacing after the administration of intravenous verapamil. Simultaneous recordings from surface electrocardiographic leads I, aVF and VI and intracardiac electrograms from the high right atrium (HRA), His bundle region (HBE), and the mid- and distal coronary sinus (CSm and CSd) at a paper speed of 100 mm/s. This figure demonstrates a loss of ventrlculoatrial conduction during right ventricular pacing at a cycle Ien& of 600 ms. Note the normal anterograds atrial activation sequence of spontaneous sinus beats. Abbreviations as in Figure 1.
References 1. Josephson ME? Sektes S. Clinical Cardiac Electrophysiology. Techniques and Interpretations. Philadelphia: Lea 8 Febiger. 1979:163. 2. Hamef A, Peter T, Platt M, Yandel WJ. Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-ParkinsonWhite syndrome. Am Heart J 1981;101:600-612. 3. Spurrell RAJ, Krlkler DY, Sowton E. Effects of verapamil on electrophysiological properties of anomolous atrioventricular connection in Wolff-Parkinson-White s ndrome. Br Heari J 1974;36:256-264. f 4. Wellens HJJ, an SL, Frits WHS, Duren DR, Lie KL, Dohmen HM. Effect of verapamil studies by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia. Br Heart J 1977;39:1056-1066. 5. Horlo Y, Maisuyame K, Morlkaml Y, Rokutanda M, Hirata A, Okumura K, Takaoka A, Uchlda H, Kuglyama K, Arakl S. Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exerciseinduced Wolff-Parkinson-White syndrome. JACC 1984;4:166-191. 6. Anderson RH, Becker AE. Gross anatomy and microscopy of the conducting system. In: Mandel WJ, ed. Cardiac Arrhythmia-Their Mechanisms, Diagnosis and Management. Philadelphia: J.B. Lippincott, 1960;12-54.
GUST H. BARDY, MD DOUGLAS L. PACKER, MD LAWRENCE D. GERMAN, MD FERNANDO COLTORTI, MD JOHN J. GALLAGHER, MD
The introduction of a ventricular premature complex (VPC) into reciprocating tachycardia is a technique used to confirm the presence of an accessory ptrioventricular (AV) pathway.1-3 Retrograde atria1 preexcitation after a VPC introduced during reciprocating tachycardia when the His bundle is refractory to retrograde conduction is evidence that an accessory pathway is present.3 The failure of an appropriately
1224
BRIEF REPORTS
L&m
AVR,AVL, AVF
VI # v2
I v3
v4#vs#V6 FIGURE 1. Electrocardllam during tachycardia showing teristically inverted P’-waves II, Ill and aVF associated with /R-R’ ratio of 0.55.
_ ____.
recorded characin leads an R-P’-
.
FIGURE 2. A ventricular premature complex (WC) is delivered into the right ventricular apex when the His bundle is refractory (no change in HH interval). A, the VPC paradoxically delays retrograde atrial activation via the accessory pathway by 15 ms. B, the VPC is delivered earlier in diastole but still during refractoriness of the His bundle. There is now a 33-m~ paradoxical delay in retrograde atria1 activation consistent with a decrementally conducting posterior septal accessory pathway. There is no evldent intraventrlcular delay to account for thls magnitude of delay, as evidenced by the similar timing relation between all recorded ventricular electrograms during Interpolated VPCs and during orthodromically conducted beats. Furthermore, this delay occurred at longer coupling Intervals than when latency was observed durlng refractory period determinations. CS-UP 4 through CS-UP 1 = coronary sinus unipoles. proximal to distal; DCS = distal coronary sinus bipole; HBE = His bundle electrogram; PCS = proximal coronary sinus bipole (at the orifice); RA = right atrium; RV = right ventricle.
April 15, 1985
timed VPC to alt.er the timing of atria1 activation implies that either an accessory pathway conducting in the retrograde direction is not present or that the accessory pathway is relatively far from the site of premature stimulation3 This latter possibility can occur when VPCs are inserted into the right ventricular apex in patients with a left lateral accessory pathway. The finding that an accessory pathway can show a paradoxical delay in retrograde atria1 activation during reciprocating tachycardia with this maneuver has not been described. We report a patient with a posterior septal accessory pathway with decremental conduction properties characteristic of the “permanent form of junctional reciprocating tachycardia.” Paradoxical delay in retrograde atria1 activation was observed after the introduction of a VPC into reciprocating tachycardia when the His bundle was refractory. A 16-year-old girl had narrow complex tachycardia since age 6 years. The sinus rhythm electrocardiogram was normal. During tachycardia the electrocardiogram showed negative P’ waves in leads II, III and aVF which occurred closer to the succeeding than to the preceding QRS complex (long R-P tachycardia) with an R-P//R-R ratio of 0.55 (Fig. 1). Recause of refractory tachycardia, an electrophysiologic evaluation was performed according to techniques previously described. 24 Spontaneous initiation of reciprocating tachycardia occurred after gradual acceleration of the sinus rate, with no change in the A-H in.terval. Over the first several cycles of tachycardia there was a gradual increase in the ventriculoatrial interval. Reciprocating tachycardia initiated with atria1 pacing also resulted in a gradual increase in ventriculoatrial conduction time while the A-H interval remained relatively constant. Spontaneous termination of reciprocating tachycardia occurred with a ventricular depolarization and was preceded by prolongation of the ventriculoatrial conduction time. Right ventricular decremental pacing resulted in progressive prolongation of ventriculoatrial intervals over the accessory pathway as the pacing cycle length was decreased. During reciprocating tachycardia ea.rliest retrograde atria1 activation was at the coronary sinus orifice. Single VPCk were inserted into the right ventricular apex during reciprocating tachycardia when the His bundle was refractory (i.e., the pacing stimulus was delivered concurrently with or immediately before the His deflection such that the H-H interval was not altered). The VPC paradoxically delayed retrograde atria1 activation by 15 to 35 ms (Fig. 2). The degree of atria1 delay increased as the prematurity of the VPC increased, consistent with the decremental nature of the accessory pathway. There was no evidence of intramyocardial delay to account for these findings.
The use of VPCs for analysis of tachycardia was initially described by Durrer et a15and Coumel et ale in 1967. However, not until 1974 did Zipes et all describe premature retrograde atria1 activation after a VPC during reciprocating tachycardia while recording the His potential, thereby demonstrating that retrograde depolarization of the His bundle did not occur. This observation was initially postulated to represent retrograde atria1 conductoin over a perinodal bypass fiber as described by James. Review of the electrograms,
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 55
1225
however, suggests that retrograde conduction occurred over a concealed AV accessory pathway. These findings were enlarged upon by Tonkin et al2 and Sellers et al3 who reported that atria1 preexcitation without altering the retrograde atria1 activation sequence after a VPC in reciprocating tachycardia effectively eliminates AV nodal reentry as a diagnostic considerat.ion, and substantiates that the accessory pathway participates in tachycardia. This patient had several of the findings of the “permanent form of junctional reciprocating tachycardia” initially described by Coumel et al in 1967.6Since then, this entity has been shown to result from a posterior septal accessory pathway that manifests decremental conduction properties.4 Our patient’s tachycardia demonstrated a long R-P’ interval, negative P’ waves in II, III and aVF and prolonged ventriculoatrial conduction times over a decrementally conducting accessory pathway located in the typical posterior septal position. These findings are consistent with both earlier and later descriptions of the permanent form of junctional reciprocating tachycardia. That our patient did not preexcite the atria, but rat,her paradoxically delayed retrograde atria1 activation, is unusual. In nearly 500 patients seen at Duke University with accessory pathways, including 9 patients with the permanent form of junctional reciprocating tachycardia, this phenomenon has not previously been observed. One might invoke intraventricular delay as the reason for the late atria1 activation. However, the similar timing relation between the right ventricular electrogram, the His bundle ventricular electrogram and the unipolar and bipolar ventricular electrograms recorded from the coronary sinus catheter argue against this. Furthermore, the VPCs were not inserted at a coupling interval where intraventricular delay would be expected. Latency during a right ventricular refractory period occurred only at coupling intervals of less than 220 ms. Nevertheless, given the difficulty in choosing the onset of the VPC, a small intraventricular conduction could indeed be present. However, such a delay would, by definition, not account for the relatively large 35ms delay seen. We therefore believe that the delay did occur in the accessorypathway and may prove to be a feature of the permanent form of junctional reciprocating tachycardia in some patients. References 1. Zipes DP, De Joseph RL, Rothbaum DA. Unusual properties of accessory pathways. Circulation 1974;49:1200-1211. 2. Tonkln AM, Gallagher JJ, Svemon RH, Wallace AG, Scaly WC. Anterogade block in accessory Pathways with retrograde conduction in reciprocating tachycardia. Eur J Cardiol 1975;3: 143-152. 3. Sellers TD, Gallagher JJ, Cope GD, Tonkin AM, Wallace AG. Retrograde atrial preexcitation following premature ventricutar beats during reciprocating tachycardia in the Wolff-Parkinson-White syndrome. Eur J Cardiol 19764: 283-294. 4. Gallagher JJ, Scaly WC. The permanent form of junctional reciprocating tachycardia: further elucidation of the underlying mechanism. Eur J Cardiol 1978;0:413-430. 5. Durrer D, Schoo L, Schullenburg FM, Wellew HJJ. The role of premature beats in the initiation and the termination of supraventricular tachycardia in the Wolff-Parkinson-White syndrome. Circulation 1967;36:644-662. 6. Coumel P, Cabrol C, Fablato A, Gourgon R, Slama R. Tachycardie permanente par rythme reciproqua. I. Preuves du diagnosti ue par stimulation aurlculaire et ventriculaire. Arch Mal Coeur 1967;60:16 s O-1864.
amil every 8 hours and a well-tolerated pressure of 90 mm Hg.
systolic
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 55
1223
blood
Verapamil, a calcium channel antagonist, has been __ reported by several investigators to be efficacious in the termination of reentrant SVTs when administered acutely.2-4 In all reported cases of SVT using an AV bypass tract, whether concealed or with overt WolffParkinson-White syndrome, termination of the arrhythmia by verapamil occurred by way of a direct effect on the AV node by increasing the AV node effective refractory period and prolonging AV node conduction time.2-4 In no instance was a significant effect on either anterograde or retrograde conduction properties of the accessoryAV pathway noted after acute administration of verapamil. Recently, Horio et al5 described 2 patients with catecholamine-induced ventricular preexcitation, in whom verapamil blocked anterograde conduction in the accessory pathway after catecholamine administration. Our patient was not given isoproterenol during the study, and therefore, we cannot comment on the relevance of these findings to our case. This case constitutes the only report of verapamilinduced conduction block in a concealed AV bypass tract. Histologic studies have found anomalous AV connections to be composed of either myocardial fibers or Purkinje cells.6 These cells primarily depend on the fast sodium channel for action potential initiation and propagation and are usually not affected by calcium channel blockade. This case illustrates that concealed bypass tracts may rarely be composed of tissue, either normal or diseased, that uses slow channel conduction for impulse propagation. The exact nature of this tissue remains to be defined. Because most patients with SVT and no evidence of preexcitation never come to electrophysiologic study, the findings in this patient may be more widespread among the subset of patients with SVT and a concealed bypass tract, in whom empiric calcium channel antagonist therapy is successful. Acknowledgment: We thank Brenda Williams, Carol Ginyard and Elizabeth Rose Isidro for assistancein preparing this manuscript and Lance LaForteza for preparation of artwork.
Paradoxical Delay in Accessory Pathway Conduction During Long R-P’ Tachycardia After Interpolated Ventricular Premature Complexes
From the Department of Medicine, Division of Cardiology, Duke University Medical Center, Durham, North Carolina. This study was sup ported in part by Research Training Grant HL-07101, SCOR HL-17670, RCDA HL-00546, and HL-15190 from the National lnstiiutes of Health, Bethesda, Maryland. Manuscript received June 4, 1984; revised manuscript received January 4, 1985, accepted January 5, 1985.
HFIA ““A
HBE
+6oomsec
---cI
FIGURE 2. Loss of retrograde accessory pathway conduction during right ventricular pacing after the administration of intravenous verapamil. Simultaneous recordings from surface electrocardiographic leads I, aVF and VI and intracardiac electrograms from the high right atrium (HRA), His bundle region (HBE), and the mid- and distal coronary sinus (CSm and CSd) at a paper speed of 100 mm/s. This figure demonstrates a loss of ventrlculoatrial conduction during right ventricular pacing at a cycle Ien& of 600 ms. Note the normal anterograds atrial activation sequence of spontaneous sinus beats. Abbreviations as in Figure 1.
References 1. Josephson ME? Sektes S. Clinical Cardiac Electrophysiology. Techniques and Interpretations. Philadelphia: Lea 8 Febiger. 1979:163. 2. Hamef A, Peter T, Platt M, Yandel WJ. Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-ParkinsonWhite syndrome. Am Heart J 1981;101:600-612. 3. Spurrell RAJ, Krlkler DY, Sowton E. Effects of verapamil on electrophysiological properties of anomolous atrioventricular connection in Wolff-Parkinson-White s ndrome. Br Heari J 1974;36:256-264. f 4. Wellens HJJ, an SL, Frits WHS, Duren DR, Lie KL, Dohmen HM. Effect of verapamil studies by programmed electrical stimulation of the heart in patients with paroxysmal re-entrant supraventricular tachycardia. Br Heart J 1977;39:1056-1066. 5. Horlo Y, Maisuyame K, Morlkaml Y, Rokutanda M, Hirata A, Okumura K, Takaoka A, Uchlda H, Kuglyama K, Arakl S. Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exerciseinduced Wolff-Parkinson-White syndrome. JACC 1984;4:166-191. 6. Anderson RH, Becker AE. Gross anatomy and microscopy of the conducting system. In: Mandel WJ, ed. Cardiac Arrhythmia-Their Mechanisms, Diagnosis and Management. Philadelphia: J.B. Lippincott, 1960;12-54.
GUST H. BARDY, MD DOUGLAS L. PACKER, MD LAWRENCE D. GERMAN, MD FERNANDO COLTORTI, MD JOHN J. GALLAGHER, MD
The introduction of a ventricular premature complex (VPC) into reciprocating tachycardia is a technique used to confirm the presence of an accessory ptrioventricular (AV) pathway.1-3 Retrograde atria1 preexcitation after a VPC introduced during reciprocating tachycardia when the His bundle is refractory to retrograde conduction is evidence that an accessory pathway is present.3 The failure of an appropriately
1224
BRIEF REPORTS
L&m
AVR,AVL, AVF
VI # v2
I v3
v4#vs#V6 FIGURE 1. Electrocardllam during tachycardia showing teristically inverted P’-waves II, Ill and aVF associated with /R-R’ ratio of 0.55.
_ ____.
recorded characin leads an R-P’-
.
FIGURE 2. A ventricular premature complex (WC) is delivered into the right ventricular apex when the His bundle is refractory (no change in HH interval). A, the VPC paradoxically delays retrograde atrial activation via the accessory pathway by 15 ms. B, the VPC is delivered earlier in diastole but still during refractoriness of the His bundle. There is now a 33-m~ paradoxical delay in retrograde atria1 activation consistent with a decrementally conducting posterior septal accessory pathway. There is no evldent intraventrlcular delay to account for thls magnitude of delay, as evidenced by the similar timing relation between all recorded ventricular electrograms during Interpolated VPCs and during orthodromically conducted beats. Furthermore, this delay occurred at longer coupling Intervals than when latency was observed durlng refractory period determinations. CS-UP 4 through CS-UP 1 = coronary sinus unipoles. proximal to distal; DCS = distal coronary sinus bipole; HBE = His bundle electrogram; PCS = proximal coronary sinus bipole (at the orifice); RA = right atrium; RV = right ventricle.
April 15, 1985
timed VPC to alt.er the timing of atria1 activation implies that either an accessory pathway conducting in the retrograde direction is not present or that the accessory pathway is relatively far from the site of premature stimulation3 This latter possibility can occur when VPCs are inserted into the right ventricular apex in patients with a left lateral accessory pathway. The finding that an accessory pathway can show a paradoxical delay in retrograde atria1 activation during reciprocating tachycardia with this maneuver has not been described. We report a patient with a posterior septal accessory pathway with decremental conduction properties characteristic of the “permanent form of junctional reciprocating tachycardia.” Paradoxical delay in retrograde atria1 activation was observed after the introduction of a VPC into reciprocating tachycardia when the His bundle was refractory. A 16-year-old girl had narrow complex tachycardia since age 6 years. The sinus rhythm electrocardiogram was normal. During tachycardia the electrocardiogram showed negative P’ waves in leads II, III and aVF which occurred closer to the succeeding than to the preceding QRS complex (long R-P tachycardia) with an R-P//R-R ratio of 0.55 (Fig. 1). Recause of refractory tachycardia, an electrophysiologic evaluation was performed according to techniques previously described. 24 Spontaneous initiation of reciprocating tachycardia occurred after gradual acceleration of the sinus rate, with no change in the A-H in.terval. Over the first several cycles of tachycardia there was a gradual increase in the ventriculoatrial interval. Reciprocating tachycardia initiated with atria1 pacing also resulted in a gradual increase in ventriculoatrial conduction time while the A-H interval remained relatively constant. Spontaneous termination of reciprocating tachycardia occurred with a ventricular depolarization and was preceded by prolongation of the ventriculoatrial conduction time. Right ventricular decremental pacing resulted in progressive prolongation of ventriculoatrial intervals over the accessory pathway as the pacing cycle length was decreased. During reciprocating tachycardia ea.rliest retrograde atria1 activation was at the coronary sinus orifice. Single VPCk were inserted into the right ventricular apex during reciprocating tachycardia when the His bundle was refractory (i.e., the pacing stimulus was delivered concurrently with or immediately before the His deflection such that the H-H interval was not altered). The VPC paradoxically delayed retrograde atria1 activation by 15 to 35 ms (Fig. 2). The degree of atria1 delay increased as the prematurity of the VPC increased, consistent with the decremental nature of the accessory pathway. There was no evidence of intramyocardial delay to account for these findings.
The use of VPCs for analysis of tachycardia was initially described by Durrer et a15and Coumel et ale in 1967. However, not until 1974 did Zipes et all describe premature retrograde atria1 activation after a VPC during reciprocating tachycardia while recording the His potential, thereby demonstrating that retrograde depolarization of the His bundle did not occur. This observation was initially postulated to represent retrograde atria1 conductoin over a perinodal bypass fiber as described by James. Review of the electrograms,
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume 55
1225
however, suggests that retrograde conduction occurred over a concealed AV accessory pathway. These findings were enlarged upon by Tonkin et al2 and Sellers et al3 who reported that atria1 preexcitation without altering the retrograde atria1 activation sequence after a VPC in reciprocating tachycardia effectively eliminates AV nodal reentry as a diagnostic considerat.ion, and substantiates that the accessory pathway participates in tachycardia. This patient had several of the findings of the “permanent form of junctional reciprocating tachycardia” initially described by Coumel et al in 1967.6Since then, this entity has been shown to result from a posterior septal accessory pathway that manifests decremental conduction properties.4 Our patient’s tachycardia demonstrated a long R-P’ interval, negative P’ waves in II, III and aVF and prolonged ventriculoatrial conduction times over a decrementally conducting accessory pathway located in the typical posterior septal position. These findings are consistent with both earlier and later descriptions of the permanent form of junctional reciprocating tachycardia. That our patient did not preexcite the atria, but rat,her paradoxically delayed retrograde atria1 activation, is unusual. In nearly 500 patients seen at Duke University with accessory pathways, including 9 patients with the permanent form of junctional reciprocating tachycardia, this phenomenon has not previously been observed. One might invoke intraventricular delay as the reason for the late atria1 activation. However, the similar timing relation between the right ventricular electrogram, the His bundle ventricular electrogram and the unipolar and bipolar ventricular electrograms recorded from the coronary sinus catheter argue against this. Furthermore, the VPCs were not inserted at a coupling interval where intraventricular delay would be expected. Latency during a right ventricular refractory period occurred only at coupling intervals of less than 220 ms. Nevertheless, given the difficulty in choosing the onset of the VPC, a small intraventricular conduction could indeed be present. However, such a delay would, by definition, not account for the relatively large 35ms delay seen. We therefore believe that the delay did occur in the accessorypathway and may prove to be a feature of the permanent form of junctional reciprocating tachycardia in some patients. References 1. Zipes DP, De Joseph RL, Rothbaum DA. Unusual properties of accessory pathways. Circulation 1974;49:1200-1211. 2. Tonkln AM, Gallagher JJ, Svemon RH, Wallace AG, Scaly WC. Anterogade block in accessory Pathways with retrograde conduction in reciprocating tachycardia. Eur J Cardiol 1975;3: 143-152. 3. Sellers TD, Gallagher JJ, Cope GD, Tonkin AM, Wallace AG. Retrograde atrial preexcitation following premature ventricutar beats during reciprocating tachycardia in the Wolff-Parkinson-White syndrome. Eur J Cardiol 19764: 283-294. 4. Gallagher JJ, Scaly WC. The permanent form of junctional reciprocating tachycardia: further elucidation of the underlying mechanism. Eur J Cardiol 1978;0:413-430. 5. Durrer D, Schoo L, Schullenburg FM, Wellew HJJ. The role of premature beats in the initiation and the termination of supraventricular tachycardia in the Wolff-Parkinson-White syndrome. Circulation 1967;36:644-662. 6. Coumel P, Cabrol C, Fablato A, Gourgon R, Slama R. Tachycardie permanente par rythme reciproqua. I. Preuves du diagnosti ue par stimulation aurlculaire et ventriculaire. Arch Mal Coeur 1967;60:16 s O-1864.