EP 101: A Tale of Two Wide Complex Tachycardias

Rakesh Gopinathannair, MD, MA, Alexander Mazur, MD†, Brian Olshansky, MD, FHRS† Division of Cardiovascular Medicine, University of Louisville, Louisville, Kentucky †Division of Cardiovascular Medicine, University of Iowa Hospital, Iowa City, Iowa
Rakesh Gopinathannair, MD, MA, Alexander Mazur, MD†, Brian Olshansky, MD, FHRS† Division of Cardiovascular Medicine, University of Louisville, Louisville, Kentucky †Division of Cardiovascular Medicine, University of Iowa Hospital, Iowa City, Iowa

In this article, the authors describe a case involving two different wide complex tachycardias. The authors also highlight the importance of a thorough electrophysiological evaluation when evaluating a wide complex tachycardia in a young patient.

Case Report

A 38-year-old Caucasian male presented to the emergency room with rapid palpitations and was noted to be in wide QRS tachycardia at 216 beats per minute. The tachycardia terminated with intravenous adenosine. Review of the electrocardiogram showed a typical left bundle branch block (LBBB) pattern with QRS duration of 160 msec and no clearly discernible P waves (Figure 1). A 12-lead electrocardiogram following tachycardia termination showed normal sinus rhythm with no evidence of preexcitation.

Echocardiogram showed a structurally normal heart with normal left ventricular systolic function. Coronary angiogram revealed normal coronary arteries. Patient reported paroxysmal palpitations in the past that lasted for a few minutes and subsided spontaneously, with most of the episodes triggered by bending over. Symptoms persisted despite being on metoprolol. Patient worked as a welder and was otherwise physically active with no limitations. Given frequent symptomatic arrhythmic episodes affecting his lifestyle and employment, it was decided to perform an electrophysiology study with the goal of ablating the tachycardia.

Baseline rhythm was sinus with a cycle length (CL) of 705 msec. PR, QRS, and QT intervals were all within normal limits. AH interval at baseline was 74 msec. There was no evidence for antegrade preexcitation or dual AV node physiology. His-Purkinje function was intact with baseline HV interval of 45 msec.

Decremental ventricular pacing demonstrated eccentric, non-decremental retrograde activation with earliest atrial activity in the proximal-mid coronary sinus (CS 7-8) electrode, suggestive of a posteroseptal accessory pathway (Figure 2). Accessory pathway effective refractory period was 290 msec. Atrial extrastimulus testing as well as decremental atrial pacing from the coronary sinus reproducibly induced a narrow complex tachycardia with a CL of 281 msec and 1:1 AV conduction. Earliest atrial activation during tachycardia was noted on CS 7-8 and was similar to that observed during ventricular pacing (Figure 3). During tachycardia, septal VA time was 110 msec, AH interval was 125 msec, HV interval was 50 msec, and QRS to the local A in CS 7-8 was 78 msec. Both LBBB and right bundle branch block (RBBB) were noted during tachycardia. RBBB did not affect the tachycardia CL or VA conduction (Figure 4) whereas occurrence of LBBB prolonged the VA interval by ~20 msec (Figure 5). No significant change was noted in tachycardia CL secondary to reciprocal shortening of AH interval. LBBB pattern was similar to clinical wide complex tachycardia.

Ventricular premature extrastimulus (PVC) delivered when the His bundle was refractory yielded the following observations: A His refractory PVC advanced the next atrial activation, confirming the presence of an accessory pathway (Figure 5). Next, a His refractory PVC reproducibly terminated the tachycardia without conducting to the atrium (Figure 6), confirming orthodromic reciprocating tachycardia (ORT). Pre-excitation index during ORT was ~35 msec, suggestive of a septal accessory pathway.

Mapping was initially performed along the septal tricuspid annulus and in the proximal coronary sinus during ORT as well as during ventricular pacing. Earliest atrial activation was consistently noted in CS 7-8. Attempted ablation within proximal CS failed to eliminate accessory pathway conduction. Following transseptal catheterization, earliest atrial activation during ventricular pacing was noted at the posteroseptal aspect of the mitral valve annulus. Ablation at this location resulted in concentric atrial activation during ventricular pacing, suggesting elimination of left posteroseptal accessory pathway conduction. Decremental atrial pacing from the coronary sinus, however, resulted in induction of a narrow complex tachycardia with 1:1 AV association and CL of 256 msec (Figure 7). Atrial activation during this tachycardia appeared to be concentric with the distal His bundle electrode being the earliest. Septal VA interval was 107 msec. A His refractory PVC reproducibly terminated this tachycardia without atrial activation, confirming ORT (Figure 8). Repeat induction resulted in a wide complex tachycardia with a LBBB morphology, 1:1 AV conduction and CL of 280 msec with similar, concentric atrial activation. LBBB did not affect the VA interval during the tachycardia, further supporting a different accessory pathway. The earliest atrial activation during tachycardia was close to the most prominent His bundle electrogram. Thus, it was decided to use cryoablation to minimize the risk of AV block. Four cryoablation lesions were delivered using a Freezor cryo catheter (Medtronic CryoCath, Inc.) at the location of the earliest atrial activation during ORT. During the last cryoablation lesion, second-degree AV block was noted. Ablation was immediately discontinued with complete recovery of AV nodal conduction. Ventricular pacing demonstrated no VA conduction, suggesting elimination of the accessory pathway (Figure 9). Following a 30-minute waiting period, there was no evidence of accessory pathway conduction. Tachycardia was not inducible and VA conduction was concentric and decremental. Post ablation AH interval was similar to baseline. At three-month follow-up, the patient has remained asymptomatic without tachycardia recurrence.

Discussion

This case describes a 38-year-old male who had two different wide complex tachycardias. ORT with LBBB aberrancy was the mechanism in both instances. The case also highlights the importance of a thorough electrophysiological evaluation, while keeping all possibilities open, when evaluating a wide complex tachycardia in a young patient.

Rapid wide complex tachycardia in a young male is concerning and requires careful assessment. Structural heart disease needs to be ruled out. Following acute termination of the tachycardia, an echocardiogram as well as evaluation for coronary artery disease are appropriate next steps.

Tachycardia termination with adenosine is suggestive of an AV node dependent rhythm and points toward supraventricular tachycardia (SVT) with aberrancy. However, ventricular tachycardias originating from the right ventricular outflow tract are adenosine-sensitive and can have LBBB morphology. Lack of ventricular preexcitation in a baseline EKG following tachycardia termination argues against antidromic tachycardia. Given recurrent episodes and uncertainty with diagnosis, proceeding with an electrophysiology study in this situation is appropriate.

Since there was no evidence of structural heart disease or coronary artery disease, the differential diagnoses entertained at the beginning of the study included SVT with aberrancy (AV nodal reentrant tachycardia [AVNRT], atrial tachycardia, or ORT), idiopathic ventricular tachycardia, and antidromic tachycardia. Ventricular pacing demonstrated eccentric atrial activation, earliest in CS 7-8, suggesting presence of an accessory pathway. Atrial decremental pacing did not show any evidence of antegrade preexcitation, thus ruling out a manifest accessory pathway and the diagnosis of antidromic tachycardia.

During the study, decremental atrial pacing induced a narrow complex tachycardia with a CL of 281 msec (SVT1) and atrial activation sequence similar to that seen during ventricular pacing. There was spontaneous LBBB during tachycardia closely resembling the patient’s clinical arrhythmia QRS morphology. Transition from a narrow to wide complex tachycardia with similar CL, HV interval and identical atrial activation sequence points out to SVT with aberrant conduction as the mechanism of clinical tachycardia. Thus, the differential diagnoses were narrowed down to three: ORT, atypical AVNRT, and an atrial tachycardia.

There were two diagnostic findings that confirmed SVT1 to be an ORT:

  1. A His-refractory PVC reproducibly terminated the tachycardia without conducting to the atrium. A PVC delivered from the right ventricular apex within 50 msec of the expected His bundle activation is considered a His-refractory or His-synchronous PVC. The only way a His-refractory PVC can conduct to the atrium is through an accessory pathway. Advancement of the subsequent atrial beat following a His-refractory PVC confirms presence of an accessory pathway but does not prove pathway participation in the tachycardia circuit. In contrast, reproducible termination of the tachycardia with a His-refractory PVC that does not conduct to the atrium is diagnostic of accessory pathway mediated tachycardia.1
  2. Development of LBBB during tachycardia resulted in an increase in VA interval by ~20 msec. Bundle branch block occurring ipsilateral to an accessory pathway prolongs the VA interval proving that the concealed pathway is an integral part of the circuit. Whereas ipsilateral bundle branch block during an ORT using a septal accessory pathway prolongs the VA interval by 10–25 msec, VA interval prolongation >35 msec indicates presence of an ipsilateral free wall pathway.1

Thus, these two findings proved accessory pathway participation in the arrhythmia circuit.

Another useful piece of information that can help determine location of an accessory pathway is the measurement of pre-excitation index, which is based on the fact that the further away the accessory pathway is from the site of pacing, the greater the prematurity needed for a PVC to reach the pathway. Pre-excitation index is defined as the prematurity of the latest right ventricular PVC that can advance the next atrial activity,1 and is usually measured as the difference between tachycardia CL and the PVC coupling interval that advances the next atrial beat. Pre-excitation index <45 msec (~35 msec in our patient) suggests a septal pathway, whereas >75 msec is suggestive of a left free wall pathway.

Other observations further confirmed ORT as the mechanism of the induced tachycardia. Eccentric atrial activation during tachycardia similar to that during ventricular pacing usually argues against AVNRT and atrial tachycardia. Ventricular overdrive pacing from the right ventricular apex entrained the tachycardia and upon cessation of pacing, resulted in a VAV response (not shown), which excluded an atrial tachycardia of septal or coronary sinus origin.2 The measured post-pacing interval minus tachycardia CL (PPI-TCL) was <115 msec, suggesting that the right ventricular apex is a part of the circuit, arguing against atypical AVNRT.3 In summary, careful electrophysiological assessment demonstrated the mechanism of the clinical wide complex tachycardia (SVT1) to be ORT with LBBB aberrancy utilizing a posteroseptal accessory pathway.

Mapping of a concealed posteroseptal pathway is done by locating the earliest atrial activation during ORT or right ventricular pacing during sinus rhythm if the atrial activation sequence is identical to that observed during ORT. One important decision to make in posteroseptal accessory pathways is whether to approach from the right side of the septum, coronary sinus, or the left side of the septum. Since posteroseptal pathways usually traverse the inferior pyramidal space, they can be in close proximity to the ostium of the coronary sinus on the right atrial side, to the proximal coronary sinus or the middle cardiac vein, to the posterior septum on the left side, or rarely, can be in the posterior epicardial aspect of the heart.

An increase in VA interval of 10–25 msec with development of LBBB during SVT is consistent with a left posteroseptal accessory pathway as right posteroseptal pathways are usually unaffected by LBBB.1 Confirmation of accurate positioning of the coronary sinus catheter cannot be emphasized enough in this situation. It is critical to verify that the proximal coronary sinus electrode pair is at the os of the coronary sinus. Failure to recognize a posteroseptal pathway as being left-sided instead of right-sided is one of the main reasons for prolonged or failed attempts at catheter ablation of accessory pathways.4

During mapping and ablation, difficulties that can be encountered, especially in the left posteroseptal location, include catheter instability not allowing adequate catheter-tissue contact as well as inability to position the catheter at the effective site.4 These can be overcome by using various pre-formed sheaths such as the SL and SR series of sheaths (St. Jude Medical), as well as trying ablation catheters of different curves. Alternative approaches (retrograde versus transseptal) should also be considered.

In our case, once the posteroseptal pathway was ablated, atrial activation appeared concentric. Just having this change in atrial activation is not enough, as this does not rule out the presence of a concealed mid- or anteroseptal accessory pathway. It is important to make sure that the retrograde conduction is concentric and decremental by ventricular extrastimulus testing and to rule out a second septal accessory pathway (as happened in our case) by maneuvers such as para-Hisian pacing or differential pacing from the right ventricular apex and base.

When a wide complex tachycardia with similar CL (SVT2) was re-induced following left posteroseptal accessory pathway ablation, it is important to avoid the urge to re-ablate at the same location. Instead, careful evaluation of the arrhythmia is warranted to establish the mechanism. In our case, change in the atrial activation sequence in the coronary sinus was important to recognize the presence of a second pathway, although both tachycardias had somewhat similar CLs and LBBB morphology. SVT2 was diagnosed to be an ORT based on the finding that a His-synchronous PVC reproducibly terminated the tachycardia without conducting to the atrium. VA interval in mid- and anteroseptal pathway mediated ORT is unaffected by development of LBBB.1

Mapping earliest atrial activation in an anteroseptal pathway should be done during ORT as it is difficult to separate retrograde AV nodal conduction versus pathway conduction when mapped during ventricular pacing. Avoiding injury to the compact AV node and the His bundle is critical. If junctional beats are noted during radiofrequency ablation, energy delivery should be immediately stopped as it is difficult to determine whether these are junctional beats conducted retrograde, i.e., up the accessory pathway or the AV nodal fast pathway. Cryoablation is a safer, albeit possibly less effective, alternative if there is concern for potential AV conduction system injury. In difficult cases, alternative approaches such as access from the superior vena cava in an attempt to keep the catheter on the ventricular side of the tricuspid annulus and ablation from the non-coronary cusp of the aortic valve should be considered.5

Thus concludes a tale of two concealed accessory pathway mediated tachycardias presenting as highly symptomatic wide complex tachycardias in the same patient. In our opinion, the following should be ‘take home’ points from this discussion:

  1. Wide complex tachycardia in a young patient is concerning and needs a careful and thorough electrophysiological evaluation to establish the mechanism.
  2. Careful attention to baseline variables and tachycardia characteristics along with employment of directed pacing maneuvers can enable accurate determination of tachycardia mechanism and guide ablation.
  3. It is important to differentiate a left from a right posteroseptal accessory pathway to avoid difficulties with mapping and ablation.
  4. Recurrent tachycardia with similar CL post-ablation should not be assumed to have the same mechanism. Close attention to subtle activation changes and a comprehensive evaluation is needed to establish mechanism of tachycardia.
  5. Common difficulties during mapping and ablation of septal accessory pathways include proximity to the AV conduction system, catheter instability, and inability to accurately identify the target site and position the ablation catheter at that location. Use of different catheter curves and pre-shaped sheaths, employing alternative approaches (transseptal versus retrograde aortic versus superior vena cava) and well as energy sources (radiofrequency versus cryoablation) can, for the most part, help overcome these problems.

References

  1. Murgatroyd FD, Krahn AD. Handbook of Cardiac Electrophysiology. Remedica Books, London, 2002.
  2. Knight BP, Zivin A, Souza J, et al. A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol 1999;33:775–781.
  3. Knight BP, Ebinger M, Oral H, et al. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol 2000;36:574–582.
  4. Morady F, Strickberger AS, Man C, et al. Reasons for prolonged or failed attempts at radiofrequency catheter ablation of accessory pathways. J Am Coll Cardiol 1996;27:683–689.
  5. Macedo PG, Patel SM, Bisco SE, et al. Septal accessory pathway: Anatomy, causes for difficulty, and an approach to ablation. Indian Pacing Electrophysiol J 2010;10:292–309.