- Email: [email protected]
Preexcitation masking underlying aberrant conduction: An atriofascicular accessory pathway functioning as an ectopic right bundle branch
Preexcitation masking underlying aberrant conduction: An atriofascicular accessory pathway functioning as an ectopic right bundle branch Ernest W. Lau, MD, Martin S. Green, MD, David H. Birnie, MD, Robert Lemery, MD, Anthony S.L. Tang, MD From the University of Ottawa Heart Institute, Ottawa, Ontario, Canada. Preexcitation and aberrant conduction both cause a broad QRS complex. An unusual case of an atriofascicular accessory pathway effectively functioning as an ectopic right bundle branch and responsible for both physiologically normal ventricular activation and pathologic preexcited tachycardias as part of a split AV node-bundle branch system is presented. KEYWORDS Atriofascicular accessory pathway; Mahaim; Ectopic bundle branch © 2004 Heart Rhythm Society. All rights reserved.
Case Presentation A 26-year-old woman suffered from a left bundle branch block (LBBB) pattern broad QRS tachycardia easily terminated with adenosine. The ECG recorded in sinus rhythm appeared normal with no suggestion of preexcitation (Figure 1a). Cardiovascular examination and echocardiogram revealed no abnormalities. The patient underwent electrophysiologic (EP) study, with a decapolar catheter in the coronary sinus and three quadripolar catheters at the right ventricular apex, the high right atrium, and the His-bundle position. At a baseline cycle length of 704 ms, A-H interval was 76 ms, H-V interval was 52 ms, and QRS duration was 76 ms. Incremental atrial pacing produced a right bundle branch block (RBBB) pattern on the ECG. There was little change in either the ECG pattern or the H-V interval as cycle length decreased. Reducing the coupling interval to a 600-ms drive train of a single atrial extrastimulus from 340 to 330 ms resulted in an RBBB pattern QRS complex preceded by a His potential. In contrast, reducing the coupling interval to a 400-ms drive train of a single atrial extrastimulus from 330 to 320 ms resulted in an LBBB pattern QRS complex with no discernible His potential.
Address reprint requests and correspondence: Dr. Martin S. Green, University of Ottawa Heart Institute, Room H145, 40 Ruskin Street, Ottawa, Ontario K1Y 4W7, Canada. E-mail address: [email protected]. (Received April 28, 2004; accepted June 16, 2004.)
The patient’s clinical tachycardia could be initiated by programmed atrial and ventricular stimulation. During the tachycardia, ventricular activation at the right ventricular apex was simultaneous with the onset of the QRS complex. Retrograde atrial activation was central and compatible with conduction over the atrioventricular node (AVN) (Figure 2). In the distal His channel, the His potential followed the local ventricular electrogram but preceded the local atrial electrogram. A critically timed extrastimulus delivered from the right atrium that did not penetrate the anatomic AVN (i.e., without advancing the local atrial electrogram recorded at either the proximal His or coronary sinus channel in the same cycle) was able to advance the next ventricular activation and reset the tachycardia. Pacing the right ventricular apex at the clinical tachycardia’s cycle length produced a retrograde activation sequence identical to that of the clinical tachycardia, with a stimulus-A interval equal to the corresponding V-A interval. An atriofascicular accessory pathway (AP) causing an antidromic AV reentrant tachycardia (AVRT) was suspected, and a search was made for the sharp, high-frequency AP (“Mahaim”) potential between the local atrial and ventricular electrograms around the tricuspid annulus.1 An exhaustive search around the posterior and lateral aspects of the tricuspid annulus did not reveal any such potential. Contact with the anteroseptal aspect of the tricuspid annulus by the mapping catheter (Figure 3a) produced a transient RBBB pattern on ECG. More detailed exploration of the region revealed a sharp potential between the local atrial and ventricular electrograms at a site just superior and lateral to the His catheter
1547-5271/$ -see front matter © 2004 Heart Rhythm Society. All rights reserved. doi:10.1016/j.hrthm.2004.06.017
Heart Rhythm (2004) 4, 497– 499
498
Figure 1 Surface ECGs recorded in sinus rhythm before (a) and after (b) ablation of atriofascicular accessory pathway.
(Figure 3b). At this site, the local ventricular electrogram was later than either the surface QRS complex or the local ventricular electrogram at the right ventricular apex. Application of radiofrequency energy at the site produced an accelerated rhythm with an LBBB pattern that might have originated from heating of AVN-like tissue within the atriofascicular AP.2 Afterwards, there was a permanent RBBB pattern on the ECG (Figure 1b), and tachycardia was no longer inducible.
Commentary The features observed during EP study were suggestive of an atriofascicular AP mediating antidromic AVRT. An anteroseptal or midseptal atrioventricular AP was unlikely because the local ventricular electrogram at the successful ablation site was later than the surface QRS complex and the ventricular electrogram at the right ventricular apex. No attempt was made to identify the distal insertion of the atriofascicular AP, as such a site usually is less preferable as
Figure 2 Intracardiac electrograms recorded during antidromic AV reentrant tachycardia. Surface ECG leads I, II, III, V1, and V6 and intracardiac tracings from the high right atrium (HRA), His bundle (His), coronary sinus (CS), and right ventricular apex (RVA) are shown. During AV reentrant tachycardia, RVA activation was simultaneous with the onset of the QRS complex, and the retrograde His occurred after the local ventricular electrogram.
Heart Rhythm, Vol 1, No 4, October 2004
Figure 3 Electrograms (right [b]) and fluoroscopic image (left [a]) of the successful ablation site. At the successful ablation site depicted, a sharp deflection representing an accessory pathway potential (AP) could be seen between the local atrial and ventricular electrograms. The local ventricular electrogram recorded at the right ventricular apex preceded the sharp deflection components of the local ventricular electrogram recorded at the base of the right ventricle by the His-bundle catheter. CS ⫽ coronary sinus; HB ⫽ His bundle; RA ⫽ high right atrium; RVA ⫽ right ventricular apex.
an ablation target than the site the AP crosses the tricuspid annulus. The atrial insertion site of the atriofascicular AP in this case was unusual, being high in the anterior septum close to the AVN and His-bundle position rather than around the free wall of the tricuspid annulus. Judging by the spatial proximity of the successful ablation site to the His-bundle position (Figure 3a), the atrial component of the antidromic AVRT circuit would have been small. Contact by the mapping catheter at that site, far from the right ventricular cavity, produced a transient RBBB pattern on ECG. Thus, when the atriofascicular AP became transiently blocked due to mechanical trauma, supraventricular impulses could only reach the ventricles through the anatomic AVN and left bundle branch. This suggests that the right bundle branch was antegradely disconnected from the anatomic AVN and solely supplied by the atriofascicular AP, even before ablation. This view is further strengthened by the fact that when the atriofascicular AP blocked at an atrial extrastimulus with a coupling interval of 330 ms to a drive train of 600 ms (during baseline EP study before any ablation catheter was introduced), what emerged was an RBBB pattern QRS complex preceded by a His potential. The right bundle branch also appeared to be disconnected from the anatomic AVN retrogradely. Because conduction through the His-Purkinje system usually is rapid and atriofascicular APs insert directly into the distal right bundle branch or adjacent right ventricular myocardium, the V-A interval usually is short and the retrograde His potential generally precedes the local ventricular electrogram in the His channels during antidromic AVRT mediated by atriofascicular APs.1 The exception to this rule is when there is RBBB, such as produced by mechanical trauma to
Lau et al
Preexcitation and Aberrant Conduction
the right bundle branch during catheter manipulation. In this case, the right bundle branch was not available for retrograde conduction to the atria during either antidromic AVRT or right ventricular apex pacing. In both situations, the retrograde activation sequence and conduction times were similar and showed considerable delay, suggesting that any impulse originating from near the right ventricular apex had to traverse the interventricular septum before it could engage the left bundle branch and reach the His bundle and anatomic AVN. Combining all the observations made during the EP study, it was deduced that the right bundle branch was totally disconnected from the anatomic AVN, both antegradely and retrogradely, and its only connection to the atria was through the atriofascicular AP. However, the observed phenomena also were compatible with the alternative explanation that an atriofascicular AP simply coexisted with underlying RBBB. In this particular case, “preexcitation” caused by the atriofascicular AP was essential to physiologically normal ventricular activation, as comparison of the ECGs recorded before and after ablation revealed (Figure 1). It can even be argued that the atriofascicular AP functioned effectively as a “nodoventricular” or “nodofascicular” AP3 in a split AV conduction system composed of two halves: one comprising the anatomic AVN, His bundle, and left bundle branch, and the other comprising the atriofascicular AP and right bundle branch. The antegrade effective refractory periods (ERPs) of the two systems must have been very close. Thus, the atriofascicular AP/right bundle branch system had a longer antegrade ERP than the anatomic AVN/His bundle/left bundle branch system at an atrial drive train of 600 ms but a shorter ERP at an atrial drive train of 400 ms. The closeness in the antegrade ERPs of the two systems explains why incremental atrial pacing produced a paradoxical RBBB
499 pattern rather than the classic LBBB pattern expected in the presence of an atriofascicular AP. Theoretically, it should be possible to eliminate the patient’s antidromic AVRT by ablating the anatomic AVN instead of the atriofascicular AP, even though postablation ECG then would show an LBBB instead of an RBBB pattern. It seems paradoxical that the same atriofascicular AP could be responsible for both supporting physiologically normal ventricular activation and causing pathologic preexcited tachycardias. Whereas normalization of the surface QRS complex in the presence of underlying RBBB by preexcitation mediated by a right-sided atriofascicular AP was previously described in Ebstein’s anomaly,4 the current case is different in that the patient had a structurally normal heart. A split AV conduction system including an atriofascicular AP appears to be compatible with near-normal electrical and mechanical functioning of the heart, but at the cost of susceptibility to preexcited tachycardias.
References 1. McClelland JH, Wang X, Beckman KJ, Hazlitt HA, Prior MI, Nakagawa H, Lazzara R, Jackman WM. Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials. Circulation 1994;89:2655–2666. 2. Heald SC, Davies DW, Ward DE, Garratt CJ, Rowland E. Radiofrequency catheter ablation of Mahaim tachycardia by targeting Mahaim potentials at the tricuspid annulus. Br Heart J 1995;73:250 –257. 3. Klein GJ, Guiraudon GM, Kerr CR, Sharma AD, Yee R, Szabo T, Wah JA. “Nodoventricular” accessory pathway: evidence for a distinct accessory atrioventricular pathway with atrioventricular node-like properties. J Am Coll Cardiol 1988;11:1035–1040. 4. Vora AM, Lokhandwala YY. Pre-excited tachycardia in a patient with Ebstein’s anomaly: is the preexcitation manifest during sinus rhythm? J Cardiovasc Electrophysiol 1998;9:1012–1014.
Case Presentation A 26-year-old woman suffered from a left bundle branch block (LBBB) pattern broad QRS tachycardia easily terminated with adenosine. The ECG recorded in sinus rhythm appeared normal with no suggestion of preexcitation (Figure 1a). Cardiovascular examination and echocardiogram revealed no abnormalities. The patient underwent electrophysiologic (EP) study, with a decapolar catheter in the coronary sinus and three quadripolar catheters at the right ventricular apex, the high right atrium, and the His-bundle position. At a baseline cycle length of 704 ms, A-H interval was 76 ms, H-V interval was 52 ms, and QRS duration was 76 ms. Incremental atrial pacing produced a right bundle branch block (RBBB) pattern on the ECG. There was little change in either the ECG pattern or the H-V interval as cycle length decreased. Reducing the coupling interval to a 600-ms drive train of a single atrial extrastimulus from 340 to 330 ms resulted in an RBBB pattern QRS complex preceded by a His potential. In contrast, reducing the coupling interval to a 400-ms drive train of a single atrial extrastimulus from 330 to 320 ms resulted in an LBBB pattern QRS complex with no discernible His potential.
Address reprint requests and correspondence: Dr. Martin S. Green, University of Ottawa Heart Institute, Room H145, 40 Ruskin Street, Ottawa, Ontario K1Y 4W7, Canada. E-mail address: [email protected]. (Received April 28, 2004; accepted June 16, 2004.)
The patient’s clinical tachycardia could be initiated by programmed atrial and ventricular stimulation. During the tachycardia, ventricular activation at the right ventricular apex was simultaneous with the onset of the QRS complex. Retrograde atrial activation was central and compatible with conduction over the atrioventricular node (AVN) (Figure 2). In the distal His channel, the His potential followed the local ventricular electrogram but preceded the local atrial electrogram. A critically timed extrastimulus delivered from the right atrium that did not penetrate the anatomic AVN (i.e., without advancing the local atrial electrogram recorded at either the proximal His or coronary sinus channel in the same cycle) was able to advance the next ventricular activation and reset the tachycardia. Pacing the right ventricular apex at the clinical tachycardia’s cycle length produced a retrograde activation sequence identical to that of the clinical tachycardia, with a stimulus-A interval equal to the corresponding V-A interval. An atriofascicular accessory pathway (AP) causing an antidromic AV reentrant tachycardia (AVRT) was suspected, and a search was made for the sharp, high-frequency AP (“Mahaim”) potential between the local atrial and ventricular electrograms around the tricuspid annulus.1 An exhaustive search around the posterior and lateral aspects of the tricuspid annulus did not reveal any such potential. Contact with the anteroseptal aspect of the tricuspid annulus by the mapping catheter (Figure 3a) produced a transient RBBB pattern on ECG. More detailed exploration of the region revealed a sharp potential between the local atrial and ventricular electrograms at a site just superior and lateral to the His catheter
1547-5271/$ -see front matter © 2004 Heart Rhythm Society. All rights reserved. doi:10.1016/j.hrthm.2004.06.017
Heart Rhythm (2004) 4, 497– 499
498
Figure 1 Surface ECGs recorded in sinus rhythm before (a) and after (b) ablation of atriofascicular accessory pathway.
(Figure 3b). At this site, the local ventricular electrogram was later than either the surface QRS complex or the local ventricular electrogram at the right ventricular apex. Application of radiofrequency energy at the site produced an accelerated rhythm with an LBBB pattern that might have originated from heating of AVN-like tissue within the atriofascicular AP.2 Afterwards, there was a permanent RBBB pattern on the ECG (Figure 1b), and tachycardia was no longer inducible.
Commentary The features observed during EP study were suggestive of an atriofascicular AP mediating antidromic AVRT. An anteroseptal or midseptal atrioventricular AP was unlikely because the local ventricular electrogram at the successful ablation site was later than the surface QRS complex and the ventricular electrogram at the right ventricular apex. No attempt was made to identify the distal insertion of the atriofascicular AP, as such a site usually is less preferable as
Figure 2 Intracardiac electrograms recorded during antidromic AV reentrant tachycardia. Surface ECG leads I, II, III, V1, and V6 and intracardiac tracings from the high right atrium (HRA), His bundle (His), coronary sinus (CS), and right ventricular apex (RVA) are shown. During AV reentrant tachycardia, RVA activation was simultaneous with the onset of the QRS complex, and the retrograde His occurred after the local ventricular electrogram.
Heart Rhythm, Vol 1, No 4, October 2004
Figure 3 Electrograms (right [b]) and fluoroscopic image (left [a]) of the successful ablation site. At the successful ablation site depicted, a sharp deflection representing an accessory pathway potential (AP) could be seen between the local atrial and ventricular electrograms. The local ventricular electrogram recorded at the right ventricular apex preceded the sharp deflection components of the local ventricular electrogram recorded at the base of the right ventricle by the His-bundle catheter. CS ⫽ coronary sinus; HB ⫽ His bundle; RA ⫽ high right atrium; RVA ⫽ right ventricular apex.
an ablation target than the site the AP crosses the tricuspid annulus. The atrial insertion site of the atriofascicular AP in this case was unusual, being high in the anterior septum close to the AVN and His-bundle position rather than around the free wall of the tricuspid annulus. Judging by the spatial proximity of the successful ablation site to the His-bundle position (Figure 3a), the atrial component of the antidromic AVRT circuit would have been small. Contact by the mapping catheter at that site, far from the right ventricular cavity, produced a transient RBBB pattern on ECG. Thus, when the atriofascicular AP became transiently blocked due to mechanical trauma, supraventricular impulses could only reach the ventricles through the anatomic AVN and left bundle branch. This suggests that the right bundle branch was antegradely disconnected from the anatomic AVN and solely supplied by the atriofascicular AP, even before ablation. This view is further strengthened by the fact that when the atriofascicular AP blocked at an atrial extrastimulus with a coupling interval of 330 ms to a drive train of 600 ms (during baseline EP study before any ablation catheter was introduced), what emerged was an RBBB pattern QRS complex preceded by a His potential. The right bundle branch also appeared to be disconnected from the anatomic AVN retrogradely. Because conduction through the His-Purkinje system usually is rapid and atriofascicular APs insert directly into the distal right bundle branch or adjacent right ventricular myocardium, the V-A interval usually is short and the retrograde His potential generally precedes the local ventricular electrogram in the His channels during antidromic AVRT mediated by atriofascicular APs.1 The exception to this rule is when there is RBBB, such as produced by mechanical trauma to
Lau et al
Preexcitation and Aberrant Conduction
the right bundle branch during catheter manipulation. In this case, the right bundle branch was not available for retrograde conduction to the atria during either antidromic AVRT or right ventricular apex pacing. In both situations, the retrograde activation sequence and conduction times were similar and showed considerable delay, suggesting that any impulse originating from near the right ventricular apex had to traverse the interventricular septum before it could engage the left bundle branch and reach the His bundle and anatomic AVN. Combining all the observations made during the EP study, it was deduced that the right bundle branch was totally disconnected from the anatomic AVN, both antegradely and retrogradely, and its only connection to the atria was through the atriofascicular AP. However, the observed phenomena also were compatible with the alternative explanation that an atriofascicular AP simply coexisted with underlying RBBB. In this particular case, “preexcitation” caused by the atriofascicular AP was essential to physiologically normal ventricular activation, as comparison of the ECGs recorded before and after ablation revealed (Figure 1). It can even be argued that the atriofascicular AP functioned effectively as a “nodoventricular” or “nodofascicular” AP3 in a split AV conduction system composed of two halves: one comprising the anatomic AVN, His bundle, and left bundle branch, and the other comprising the atriofascicular AP and right bundle branch. The antegrade effective refractory periods (ERPs) of the two systems must have been very close. Thus, the atriofascicular AP/right bundle branch system had a longer antegrade ERP than the anatomic AVN/His bundle/left bundle branch system at an atrial drive train of 600 ms but a shorter ERP at an atrial drive train of 400 ms. The closeness in the antegrade ERPs of the two systems explains why incremental atrial pacing produced a paradoxical RBBB
499 pattern rather than the classic LBBB pattern expected in the presence of an atriofascicular AP. Theoretically, it should be possible to eliminate the patient’s antidromic AVRT by ablating the anatomic AVN instead of the atriofascicular AP, even though postablation ECG then would show an LBBB instead of an RBBB pattern. It seems paradoxical that the same atriofascicular AP could be responsible for both supporting physiologically normal ventricular activation and causing pathologic preexcited tachycardias. Whereas normalization of the surface QRS complex in the presence of underlying RBBB by preexcitation mediated by a right-sided atriofascicular AP was previously described in Ebstein’s anomaly,4 the current case is different in that the patient had a structurally normal heart. A split AV conduction system including an atriofascicular AP appears to be compatible with near-normal electrical and mechanical functioning of the heart, but at the cost of susceptibility to preexcited tachycardias.
References 1. McClelland JH, Wang X, Beckman KJ, Hazlitt HA, Prior MI, Nakagawa H, Lazzara R, Jackman WM. Radiofrequency catheter ablation of right atriofascicular (Mahaim) accessory pathways guided by accessory pathway activation potentials. Circulation 1994;89:2655–2666. 2. Heald SC, Davies DW, Ward DE, Garratt CJ, Rowland E. Radiofrequency catheter ablation of Mahaim tachycardia by targeting Mahaim potentials at the tricuspid annulus. Br Heart J 1995;73:250 –257. 3. Klein GJ, Guiraudon GM, Kerr CR, Sharma AD, Yee R, Szabo T, Wah JA. “Nodoventricular” accessory pathway: evidence for a distinct accessory atrioventricular pathway with atrioventricular node-like properties. J Am Coll Cardiol 1988;11:1035–1040. 4. Vora AM, Lokhandwala YY. Pre-excited tachycardia in a patient with Ebstein’s anomaly: is the preexcitation manifest during sinus rhythm? J Cardiovasc Electrophysiol 1998;9:1012–1014.