EP 101: Wide Complex Tachycardia Case Study – Part II

Rakesh Gopinathannair, MD, MA, and Brian Olshansky, MD Division of Cardiovascular Medicine University of Iowa Hospitals and Clinics Iowa City, Iowa
Rakesh Gopinathannair, MD, MA, and Brian Olshansky, MD Division of Cardiovascular Medicine University of Iowa Hospitals and Clinics Iowa City, Iowa
In this article, the authors provide Part 2 of a wide complex tachycardia case study (Part 1 was published in EP Lab Digest’s November 2008 issue). Case Presentation A 53-year-old man with coronary artery disease (s/p stent placement in 2001) presented to the emergency room with chest pain radiating to the jaw associated with palpitations, dyspnea and diaphoresis. An electrocardiogram showed a wide complex tachycardia at 190 bpm with a left bundle branch block (LBBB) morphology and normal QRS axis (Figure 1). Blood pressure was 139/60 mmHg. Ventricular tachycardia was presumed and lidocaine 100 mg IV was given, which terminated the tachycardia and symptoms. A subsequent ECG showed sinus rhythm with a narrow QRS, normal intervals, and inferior Q-waves. With the clinical presentation suggestive of acute coronary syndrome (unstable angina), coronary angiography was performed and showed severe three-vessel coronary artery disease. Echocardiogram showed preserved left ventricular function. The patient underwent three-vessel coronary bypass surgery, and no further wide complex tachycardia occurred during hospitalization. Given suspicion for ventricular tachycardia, an electrophysiology (EP) study was performed. In Part 1 of this case study, published in the November 2008 edition of EP Lab Digest, we discussed the potential differential diagnoses, pharmacological maneuvers attempted for diagnosis and their effects on the tachycardia, and results and discussion of the initial EP testing. In brief, right ventricular (RV) outflow tract stimulation using triple extrastimuli resulted in a narrow complex tachycardia with a cycle length ranging from 270 msec to 320 msec. Burst pacing from the RV apex resulted in induction of a wide complex tachycardia with a LBBB, normal axis morphology, resembling the patient’s clinical tachycardia. During the tachycardias, His bundle activation preceded QRS with a constant HV and HA interval. During narrow complex tachycardia (cycle length = 319 msec), the HA interval was 204 msec and AH interval was 115 msec. During wide complex tachycardia (cycle length = 310 msec), the HA interval was 255 msec and AH interval was 55 msec. Cycle length variation during both narrow and wide complex tachycardia was due to differences in the AH interval. Tachycardia terminated spontaneously with ventricular activation. During this study, the cycle length of the LBBB tachycardia was not longer than the narrow complex tachycardia. There were no other inducible wide complex tachycardias. During narrow complex tachycardia, the earliest atrial activity was seen in the proximal coronary sinus electrode (Figure 2). Right ventricular pacing during tachycardia showed continuous VA conduction in a similar pattern as the tachycardia, with earliest atrial activation noted at the proximal coronary sinus electrode. Differential diagnoses entertained were orthodromic AV reciprocating tachycardia (AVRT) using a right-sided or septal accessory pathway versus AV nodal reciprocating tachycardia (AVNRT) with intermittent LBBB aberrancy. Since the tachycardia cycle length was the same, if not shorter, during wide complex tachycardia with a LBBB pattern, a left-sided pathway was initially considered unlikely. Bracketing of retrograde atrial activation was not seen in the coronary sinus. Since sustained wide complex tachycardia was not reinducible, and as the transient nature of the tachycardia did not allow further diagnostic maneuvers, the patient was brought back the next day for a detailed EP study and possible ablation, the details of which are discussed below. A tricuspid annulus decapolar catheter (Halo, Biosense Webster Inc., a Johnson & Johnson company, Diamond Bar, CA) with the distal poles in the coronary sinus, along with a His bundle, RV, and right atrial catheters were utilized. LBBB morphology wide complex tachycardia was easily induced by burst pacing from the RV outflow tract. During the study, the tachycardia shifted spontaneously to a narrow complex morphology. The earliest atrial activity during tachycardia was noted in Halo 2, which was inside the coronary sinus on the left atrial side (Figure 3). Retrograde activation was the same during narrow and wide complex tachycardia, and appeared different from the previous day where the earliest retrograde atrial activity was noted in the proximal coronary sinus electrode. During wide complex tachycardia (cycle length = 275 msec), the HA interval was 220 msec and the AH interval was 55 msec. During narrow complex tachycardia (cycle length = 275 msec), the HA interval was 185 msec and the AH interval was 90 msec. The tachycardia cycle length varied considerably during narrow and wide complex tachycardia. For the majority of the time, the cycle length of the LBBB tachycardia was not longer than the narrow complex tachycardia. However, for each tachycardia, the HA interval remained constant but the preceding HH interval predicted the subsequent AA interval. This latter finding was explained by variability in the AH interval. There was marked beat-to-beat variation at times, consistent with dual antegrade AV node physiology. Pacing from the RV apex during both wide and narrow complex tachycardia demonstrated similar retrograde activation patterns. A His-refractory ventricular premature beat (ventricular premature beat delivered within 50 msec of the expected His bundle activation) during tachycardia reset the tachycardia and preexcited the atria, with the tachycardia cycle length shortening from 307 msec to 275 msec (Figure 4). This finding was consistent with the presence of a retrograde conducting accessory pathway, the location of which was a posterior, left-sided, free wall accessory pathway as noted at Halo 2 (Figure 5). Atrial pre-excitation occurred with a single His-refractory premature ventricular beat during both wide and narrow complex tachycardia. Thus, the findings from the EP study were indicative of the presence of an orthodromic AVRT using a left posterior free wall accessory pathway with intermittent LBBB aberrancy — this was the patient’s clinical tachycardia. After trans-septal catheterization, six radiofrequency applications were delivered in the region of the posterior AV ring on the left side, where the earliest retrograde atrial activity (earlier than Halo 2) during ventricular premature stimulation was noted (Figure 6). A 4-mm-tip ablation catheter was used for this purpose, with an average power of 50 W and average temperature of 50 degrees. Following ablation, coronary sinus activation during RV pacing was consistent with retrograde AV nodal conduction. Orthodromic AVRT was not inducible again, and shorter coupling intervals during ventricular pacing resulted in retrograde block in AV node without any eccentric activation (Figure 7). There was no inducible tachycardia with atrial or ventricular extrastimuli with and without use of isoproterenol. Discussion During the initial EP study, a narrow complex tachycardia was induced with RV pacing with earliest retrograde atrial activation seen at proximal coronary sinus electrode. Although a right-sided septal accessory pathway was suspected, the mechanism remained unclear as the transient nature of the tachycardia made further diagnostic maneuvers difficult. During the second EP study, a similar RV pacing protocol induced tachycardia, and this time the earliest retrograde atrial activity was noted on the left atrial side of the septum. This apparent paradox was resolved by observing one of the fundamental aspects of electrophysiology, namely, catheter positioning. After review of the cine pictures from the previous day, it was clear that the coronary sinus catheter was positioned deep in the coronary sinus such that the proximal coronary sinus electrode bipole was not at the os of the coronary sinus but was on the left side. No bracketing was seen. Because of this, the earliest atrial activity was misinterpreted as coming from the right side of the septum near the coronary sinus os, when it actually happened at the posterior aspect of left atrium. As is classically taught, bundle branch block occurring ipsilateral to an accessory pathway increases the tachycardia cycle length and the local HA interval, proving that the affected retrograde pathway is consistently part of the circuit. Bundle branch block during an orthodromic AVRT with a septal accessory pathway should be not be expected to prolong the AVRT cycle length or HA interval by more than 15 msec. Significant cycle length and HA interval prolongation with a bundle branch block should raise suspicion of an ipsilateral free wall accessory pathway being utilized during AVRT. The fact that a LBBB during this AVRT utilizing a left-sided pathway resulted in a similar or shorter tachycardia cycle length does not contradict the rules of electrophysiology. However, it does not rule out a left free wall accessory pathway, as there was significant prolongation of the HA interval (>30 msec). Cycle length shortening happened only because of the markedly shortened AH interval during LBBB, probably resulting from the antegrade activation switching from the slow to fast pathway in the AV node. In fact, the conversion from wide to narrow complex tachycardia may be a function of the antegrade limb of the AVRT with AV nodal conduction (and the AH interval) being influenced by catecholamines and the presence of dual AV node physiology. Tachycardia cycle length in this case varied considerably. The most important measurement in this case would be the HA interval. It is best to measure cycle length and HA interval during the same tachycardia as it transitions from one to another rate and QRS morphology. The HA interval, with and without aberration, is a better predictor of pathway location than is tachycardia cycle length. Ventricle to earliest A timing can also be used, but is less reliable given changing morphology of the tachycardia. Autonomic fluctuations can affect, in particular, AV nodal conduction that can change the cycle length even for the same tachycardia. During narrow complex tachycardia with cycle length variation, when the HH interval predicts the subsequent AA interval, this proves AV node dependency for the reentrant tachycardia circuit. The data obtained from the second day’s study helped rule out the following potential differential diagnoses. Ventricular tachycardia: The presence of a narrow and a wide QRS complex tachycardia with similar HV activation and 1:1 VA relationship makes ventricular tachycardia highly unlikely. His bundle activation with a similar HV interval to sinus rhythm during wide complex tachycardia essentially rules out ventricular tachycardia. Rarely, HH interval can precede and predict the subsequent AA interval in the setting of bundle branch reentry tachycardia with 1:1 retrograde conduction. However, the presence of both narrow and wide complex tachycardia with similar His bundle activation plus a normal baseline HV interval makes bundle branch reentry unlikely. Orthodromic AVRT using a septal accessory pathway: Earliest retrograde atrial activation during tachycardia in the posterior left atrium (as demonstrated in this case at Halo 2, which was located in mid coronary sinus) and not at the proximal coronary sinus argues against a septal accessory pathway. Delivery of a His-refractory premature beat during tachycardia resulted in atrial preexcitation with a similar activation pattern, confirming the location of the accessory pathway to the left posterior free wall. Significant prolongation of the HA interval (>30 msec) during LBBB argues against a septal pathway. AV node reentry tachycardia: Although there was evidence for dual AV node physiology, the presence of variable AH intervals during wide and narrow complex tachycardia makes AVNRT unlikely (although not impossible). A His-refractory ventricular premature stimulus during tachycardia conducted retrograde and preexcited the atria. This makes AVNRT unlikely. Alternatively, a retrograde “innocent bystander” pathway could potentially explain this, but the fact that the atrial activation did not change during delivery of the premature extrastimulus makes this highly unlikely. During tachycardia, the earliest retrograde atrial activity occurred at a posterior left atrial location inconsistent with AVNRT, as retrograde activation during typical (“slow-fast”) AVNRT would occur at the anterior septum (recorded by His bundle catheter) and atypical (“fast-slow”) AVNRT would occur near the coronary sinus os. Locating the accessory pathway to guide ablation (Figure 8) can be achieved as follows: After trans-septal catheterization, a steerable ablation catheter is placed in the region of the mitral annulus in a posterior location. The presence of atrial and ventricular electrograms in the distal pole of the ablation catheter and alignment with the coronary sinus catheter indicates an annular position. Since there is no antegrade preexcitation, the best way to identify the retrograde conducting accessory pathway is to map the mitral annulus for the earliest atrial activity during tachycardia. However, the nonsustained nature of tachycardia precludes mapping during tachycardia in some instances. In these situations, earliest atrial activity can be mapped during ventricular pacing or during single ventricular extrastimulus testing, as long as it can be assured that conduction is proceeding only up the accessory pathway. If single ventricular extrastimulus testing is employed for mapping, it is important to identify an S1S2 coupling interval where retrograde conduction of the extrastimulus (S2) is solely through the accessory pathway. This is achieved by progressively decrementing the S1S2 interval until retrograde block is seen in the AV node and retrograde conduction of S2 shifts to the accessory pathway. Minor adjustments in the S1S2 coupling interval are then made so that S2 consistently demonstrates retrograde accessory pathway conduction. Using the ablation catheter, the location of the earliest atrial activity conducting up the accessory pathway is then mapped. The earliest local atrial activity thus noted usually corresponds to the atrial insertion of the pathway. The ventricular and atrial electrograms at this location can be close to each other or even superimpose (Figure 6). However, the local VA timing as a measure of the accessory pathway insertion is unreliable, as conduction on both sides of the AV ring through atrial and ventricular tissue can provide a short VA interval that appears to be but is not a representation of VA conduction. Occasionally, an accessory pathway potential can be seen. In this case, as tachycardia was non-sustained, it did not allow detailed mapping during AVRT. An alternative approach will be to perform mapping while pacing the ventricle at a faster rate to ensure retrograde conduction through the accessory pathway alone and/or mapping while pacing the ventricle nearby the accessory pathway. Isoproterenol may not help, as it can increase retrograde conduction through the AV node as well as the accessory pathway. Adenosine in this case caused retrograde block in the accessory pathway. This limited its utility in identifying the accessory pathway location. The successful endpoint for ablation was reached when the tachycardia was no longer inducible and when ventricular pacing showed block in the accessory pathway. Since there was evidence for dual AV node physiology, the question arises whether to ablate the slow pathway along with the accessory pathway in this case. This was not necessary, as the AV node was only utilized for orthodromic AVRT. There was no inducible AVNRT with or without isoproterenol. Ablation of slow pathway may incur risk and provide no benefit. The timing of the left-sided accessory pathway ablation after bypass surgery is a matter of further discussion. There is risk of trans-septal catheterization and intraprocedural anticoagulation in the immediate perioperative period. This case shows that this can be safely done as long as adequate precautions are in place. An alternative approach would be to perform the EP study to identify the tachycardia mechanism, and if ventricular tachycardia is ruled out and if the tachycardia is tolerated hemodynamically, bring the patient back for an ablation at a later time when the risk of anticoagulation is less. Conclusions In Part II of this case study, several additional concepts used for the diagnosis and treatment of a wide complex tachycardia in the setting of an acute coronary syndrome are highlighted. Electrophysiological techniques used to differentiate ventricular from supraventricular tachycardia and the differential diagnosis of supraventricular tachycardia are explained. Common pitfalls encountered during the procedure are discussed. Mapping and ablation techniques involved in typical orthodromic AVRT with a left free wall pathway are described. Typical orthodromic AVRT can present as a wide complex tachycardia secondary to bundle-branch aberrancy. This wide complex tachycardia can have a similar surface electrocardiographic appearance as ventricular tachycardia, and is often difficult to distinguish from ventricular tachycardia, particularly in a patient with known coronary artery disease, and especially if the classic rules of electrophysiology do not seem to pertain. An EP study performed carefully and with meticulous attention to diagnostic findings and catheter position can lead toward the right diagnosis and successful ablation. To see Part I of the article, please visit: http://eplabdigest.com/articles/EP-101-Wide-Complex-Tachycardia-Case-Study-%E2%80%93-Part-1