Dan Blendea MD, PhD, E. Kevin Heist MD, PhD, Jeremy N. Ruskin, MD, Moussa Mansour, MD
An 84-year-old woman with history of hypertension presented with palpitations, dizziness, and dyspnea. Upon arrival in the emergency department (ED) the ECG showed a wide-complex tachycardia at a rate of 155 bpm. This was a short RP tachycardia with left bundle branch block (LBBB) QRS morphology similar to that in sinus rhythm (Figure 10-1). The patient received 6 mg of adenosine IV and converted to sinus rhythm. The ECG in sinus rhythm revealed LBBB. There was no evidence of ventricular preexcitation.
FIGURE 10-1 Twelve-lead ECG during tachycardia (A) with LBBB QRS morphology similar to that in sinus rhythm (B).
In the ED the patient recalled having episodes of palpitations for the past 3 years. Initially she described intermittent “blips” in her chest without associated chest pain or dyspnea. Later, episodes of palpitations became more frequent and more protracted, prompting two prior visits to the ED. Each time tachycardia, thought to be supraventricular tachycardia, resolved with adenosine. The patient received diltiazem, with limited improvement in the frequency and duration of the episodes of palpitations. Three years prior to the current presentation she was diagnosed with LBBB. At that time the workup included an echocardiogram that revealed left atrial enlargement and normal left ventricular systolic function, and an exercise myocardial perfusion imaging stress test without evidence of ischemia or infarction.
Given the recurrent episodes of symptomatic supraventricular tachycardia, the patient underwent an electrophysiology (EP) study. With ventricular pacing, the atrial activation was eccentric—earliest at the distal dipole of the coronary sinus catheter situated in a lateral position (CS 1-2; Figure 10-2) suggesting retrograde conduction via a lateral accessory pathway (AP). With atrial pacing, conduction was decremental, via the AV node. The retrograde effective refractory period of the AP was 330 ms at a 600 ms driving train. At baseline, single echos were seen (Figure 10-3). Supraventricular tachycardia with a cycle length of 400 ms (heart rate 150 bpm) was induced with atrial extrastimuli (Figure 10-4). The surface ECG was similar to the ECG on presentation in the ED. The earliest atrial activation was again at the CS 1-2 electrode. Ventricular entrainment revealed a VAV response. His-synchronous PVCs advanced the subsequent A as well as the tachycardia (Figure 10-5). These maneuvers were consistent with orthodromic atrioventricular reentrant tachycardia (AVRT), using a concealed left lateral AP. A transseptal puncture was performed, and radiofrequency applications were delivered to the area of the earliest activation at the left lateral region during ventricular pacing. Pathway conduction was abolished at the successful site after 3 seconds of RF application (Figure 10-6). Postablation there was midline and decremental AV conduction with no evidence for dual AV nodal physiology. There was no retrograde VA conduction. The patient tolerated the procedure well. At follow-up there has been no recurrence of arrhythmia symptoms, and the ECG remained unchanged.
FIGURE 10-2 With ventricular pacing the atrial activation was eccentric—earliest at the distal dipole of the coronary sinus catheter (CS 1-2) suggesting retrograde conduction via a left lateral accessory pathway. Tracings are shown from surface leads I, aVF, and V1 as well as HRA, His proximal (HISp), mid (HISm), and distal (HISd), coronary sinus (CS) proximal (9,10) to distal (1,2), and right ventricular apex (RVa).
FIGURE 10-3 Single atrial echo beats were seen with atrial extrastimuli. Tracings are shown from surface leads I, aVF, and V1 as well as HRA, His proximal (HISp), mid (HISm), and distal (HISd), ablation catheter distal (ABLd) and proximal (ABLp), coronary sinus (CS) proximal (9,10) to distal (1,2), and right ventricular apex (RVa).
FIGURE 10-4 Supraventricular tachycardia with cycle length of 400 ms (heart rate 150 bpm) was induced with an atrial extrastimulus. Tracings are shown from surface leads I, aVF, and V1 as well as HRA, His proximal (HISp), mid (HISm), and distal (HISd), coronary sinus (CS) proximal (9,10) to distal (1,2), and right ventricular apex (RVa).
FIGURE 10-5 His-synchronous PVCs advanced the subsequent A as well as the tachycardia. Tracings are shown from surface leads I, aVF, and V1 as well as HRA, His proximal (HISp), mid (HISm), and distal (HISd), coronary sinus (CS) proximal (9,10) to distal (1,2), and right ventricular apex (RVa).
FIGURE 10-6 Pathway conduction was abolished at the successful site after 3 seconds of radiofrequency ablation. Tracings are shown from surface leads I, aVF, and V1 as well as HRA, His proximal (HISp), mid (HISm), and distal (HISd), ablation catheter distal (ABLd) and proximal (ABLp), coronary sinus (CS) proximal (9,10) to distal (1,2), and right ventricular apex (RVa).
EPIDEMIOLOGY, ETIOLOGY, AND PATHOGENESIS
AVRT is the second most common cause of paroxysmal supraventricular tachycardia, but the etiology of AP formation remains largely unknown.1,2 It is not clear whether the development of atrioventricular connections is genetically determined,3 due to some environmental exposure, or due to other factors.1
The APs are located in the left free wall in approximately 60% of patients undergoing RF ablation, in or adjacent to the interventricular septum in 20% to 30% of patients, and in the right free wall in about 10% of patients.4,5
There are gender differences in the clinical characteristics of the APs. Women seem have more concealed accessory pathways (59%) than men (50%).5 Orthodromic AVRT is more frequent than antidromic AVRT in both men and women.5 The left free wall locations are similarly encountered in men and in women.4
With advancing age, there is a higher prevalence of left-sided APs and a longer duration of the arrhythmia compared to young patients.6 The incidence of concealed APs and orthodromic AVRT increases with age. The tachycardia cycle length, antegrade and retrograde AP effective refractory periods, antegrade AV node effective refractory periods, and atrial and ventricular effective refractory periods lengthen as the age increases.6
Importance of the LBBB
In the present case, it was only after the onset of LBBB at age 81 that the patient started to have palpitations. It is likely that the electrical delay in ventricular conduction caused by LBBB allowed recovery of the retrograde conduction in the left-sided AP and thus initiation and perpetuation of orthodromic AV reentry.
There are reports in the literature of othodromic AVRT using concealed APs facilitated by the onset of ipsilateral bundle branch block. Calo et al described an onset incessant orthodromic AVRT, using a concealed right-sided accessory pathway, after iatrogenic right bundle branch block during an EP study.7 Another report by Stanke and colleagues described the association between LBBB and development of orthodromic AVRT using a concealed left-sided accessory pathway.8
Preexcitation of the ventricles in patients with Wolff-Parkinson-White (WPW) syndrome results in distinctive changes of the 12-lead ECG configuration with characteristic polarity of the delta wave, QRS polarity, and R/S ratio, respectively, depending on the AP location. Based on these characteristics, several algorithms have been developed to predict AP location from the surface ECG in patients with WPW syndrome. Unfortunately, there are only limited possibilities to predict the localization of concealed atrioventricular APs from a 12-lead surface ECG by analyzing retrograde P-wave polarity during AVRT.9-11The analysis of retrograde P-wave polarity during AVRT is often difficult due to the superimposing repolarization. Typically a negative P wave in lead I is indicative of a left free wall location with a 95% positive predictive value.9 The presence of negative P waves in inferior leads suggests an inferior/posterior location, while positive P waves in all inferior leads indicate a superior/anterior location. Isoelectric or biphasic P waves in any of the inferior leads suggest a left lateral location. A combination of negative P waves in lead I, positive P waves in aVR and V1, and isoelectric P waves in aVL indicate a left lateral location of the AP with 100% positive predictive value.10 In the present case, the P waves during tachycardia were negative in lead I, positive in lead II, and biphasic in lead III (Figure 10-7), morphology consistent with atrial activation via a left lateral AP.
FIGURE 10-7 P-wave morphology during supraventricular tachycardia (SVT) and during sinus rhythm.
During EP study, the hallmark of orthodromic AVRT is the requirement of a 1:1 atrial and ventricular activation for maintaining tachycardia. The diagnosis of orthodromic AVRT using a left free wall AP requires demonstration of an eccentric atrial activation sequence earliest along the left atrial free wall. In addition, in orthodromic AVRT there is a constant ventricle-to-atrium conduction time despite changes in the tachycardia cycle length, and typically one can advance the atrial activation by a premature ventricular stimulus delivered during His bundle refractoriness. A left lateral AP is typically associated with a preexcitation index greater than 70 ms.12 The preexcitation index is defined as the difference between the tachycardia cycle length and the longest coupling interval of a right ventricular apical premature stimulus that advances the atrium.12,13 A diagnostic feature suggestive of a left free wall pathway is the prolongation of the QRS-to-atrium time during orthodromic AVRT by 35 to 40 ms or longer with the onset of LBBB.14 Another diagnostic criterion for orthodromic AVRT is the ability to reproducibly terminate the tachycardia with a premature ventricular stimulus delivered during His bundle refractoriness.
Orthodromic AVRTs using left free wall APs must be differentiated from atrial tachycardias originating from areas close to the mitral annulus, which is best accomplished by dissociating the ventricles from the tachycardia.13 For example, a VAAV response after termination of ventricular pacing that entrains the atrium excludes orthodromic AVRT and confirms atrial tachycardia.13 About 6% of AV nodal reentrant tachycardias are associated with an eccentric atrial activation sequence earliest in the distal or posterior CS with the shortest VA time with an atrial activation pattern that can be confused with a left-sided concealed AP. The diagnostic criteria that suggest AV nodal reentrant tachycardia rather than AVRT are demonstration of dual AV nodal physiology, inability to advance the atrium with ventricular extrastimuli during His refractoriness, decremental VA conduction, and ability to dissociate the atria and the ventricles from the tachycardia.13,15
MAPPING AND ABLATION
Mapping and ablation of left free wall APs may be performed via a transseptal or transaortic approach, the latter facilitating access to the ventricular insertion sites of the APs, but being usually avoided in patients with peripheral vascular disease, aortic stenosis, or small left ventricular dimensions. The transseptal approach allows mapping of the atrial side of the mitral annulus or the annulus itself.13 Several electrogram characteristics predict successful ablation of a left free wall AP, when mapping is performed during orthodromic AVRT or during ventricular pacing: presence of presumed AP potential, continuous electrical activity, and local VA interval of 25 to 50 ms.13,16
Before delivering radiofrequency energy it is important to obtain a stable catheter position. Catheter stability during ablation of left-sided APs is enhanced by use of preformed sheaths. With ventricular pacing to entrain the orthodromic AVRT, the risk of catheter dislodgement with termination of the arrhythmia is diminished. Loss of AP conduction should occur in 1 to 6 seconds after radiofrequency energy delivery, longer times to successful ablation being associated with higher recurrence rates.13,16,17 In the case of resistant Aps, irrigated catheters can help delivering higher energies.18 Epicardial left-sided APs can be approached from within the CS or using direct epicardial mapping and ablation.19,20
1. Hsu JC, Tanel RE, Lee BK, et al. Differences in accessory pathway location by sex and race. Heart Rhythm. 2010;7(1):52-66.
2. Ganz LI, Friedman PL. Supraventricular tachycardia. N Eng J Med. 1995;332:162-173.
3. Vidaillet HJ, Jr, Pressley JC, Henke E, Harrell FE, Jr, German LD. Familial occurrence of accessory atrioventricular pathways (preexcitation syndrome). N Eng J Med. 1987;317:65-69.
4. Birati EY, Eldar M, Belhassen B. Gender differences in accessory connections location: an Israeli study. J Interv Card Electrophysiol. 2012;34:227-229.
5. Huang SY, Hu YF, Chang SL, et al. Gender differences of electrophysiologic characteristics in patients with accessory atrioventricular pathways. Heart Rhythm. 2011;8:571-574.
6. Li CH, Hu YF, Lin YJ, et al. The impact of age on the electrophysiological characteristics and different arrhythmia patterns in patients with Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol. 2011;22:274-279.
7. Calo L, Lamberti F, Golia P, et al. Facilitation of atrioventricular reentrant tachycardia by iatrogenic right bundle branch block. Ital Heart J. 2001;2:468-471.
8. Stanke A, Storti C, De Ponti R, Salerno-Uriarte JA. Spontaneous incessant AV reentrant tachycardia related to left bundle branch block and concealed left-sided accessory AV pathway. J Cardiovasc Electrophysiol. 1994;5:777-781.
9. Fitzgerald DM, Hawthorne HR, Crossley GH, Simmons TW, Haisty WK, Jr. P wave morphology during atrial pacing along the atrioventricular ring. ECG localization of the site of origin of retrograde atrial activation. J Electrocardiol. 1996;29:1-10.
10. Rostock T, Sydow K, Steven D, et al. A new algorithm for concealed accessory pathway localization using T-wave-subtracted retrograde P-wave polarity during orthodromic atrioventricular reentrant tachycardia. J Interv Card Electrophysiol. 2008;22:55-63.
11. Tai CT, Chen SA, Chiang CE, et al. A new electrocardiographic algorithm using retrograde P waves for differentiating atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway. J Am Coll Cardiol. 1997;29:394-402.
12. Miles WM, Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia and localizing accessory pathways. Circulation. 1986;74:493-500.
13. Huang SK, Wood MA. Catheter Ablation of Cardiac Arrhythmias. Philadelphia, PA: W.B. Saunders; 2006.
14. Yang Y, Cheng J, Glatter K, Dorostkar P, Modin GW, Scheinman MM. Quantitative effects of functional bundle branch block in patients with atrioventricular reentrant tachycardia. Am J Cardiol. 2000;85:826-831.
15. Hwang C, Martin DJ, Goodman JS, et al. Atypical atrioventricular node reciprocating tachycardia masquerading as tachycardia using a left-sided accessory pathway. J Am Coll Cardiol. 1997;30:218-225.
16. Chen X, Borggrefe M, Shenasa M, Haverkamp W, Hindricks G, Breithardt G. Characteristics of local electrogram predicting successful transcatheter radiofrequency ablation of left-sided accessory pathways. J Am Coll Cardiol. 1992;20:656-665.
17. Twidale N, Wang XZ, Beckman KJ, et al. Factors associated with recurrence of accessory pathway conduction after radiofrequency catheter ablation. Pacing Clin Electrophysiol. 1991;14:2042-2048.
18. Yamane T, Jais P, Shah DC, et al. Efficacy and safety of an irrigated-tip catheter for the ablation of accessory pathways resistant to conventional radiofrequency ablation. Circulation. 2000;102:2565-2568.
19. Ho I, d’Avila A, Ruskin J, Mansour M. Images in cardiovascular medicine. Percutaneous epicardial mapping and ablation of a posteroseptal accessory pathway. Circulation. 2007;115:e418-e421.
20. Haissaguerre M, Gaita F, Fischer B, Egloff P, Lemetayer P, Warin JF. Radiofrequency catheter ablation of left lateral accessory pathways via the coronary sinus. Circulation. 1992;86:1464-1468.