In this artcle, the authors present a case that illustrates the importance of keeping an open mind while evaluating SVTs.
Case PresentationA 53-year-old morbidly obese Caucasian female with past medical history of paroxysmal palpitations, hypertension, diastolic heart failure, and chronic bronchitis was admitted for pneumonia and respiratory failure. She initially had to be mechanically ventilated, and was subsequently extubated. Post-extubation, she was noted to have multiple episodes of narrow complex tachycardia (Figure 1), resulting in hypotension, chest discomfort, and shortness of breath. During narrow complex tachycardia (rates ranging from 170–185 beats/min), RP interval was less than PR interval and the p-waves were positive in V1 and inferior leads and were negative in lead I and aVL. The tachycardia reproducibly responded to adenosine (Figure 2); however, marked hemodynamic instability necessitated electrical cardioversion on two occasions. Given the near-incessant nature of the arrhythmia, hemodynamic intolerance, and inability to tolerate effective doses of beta-blockers or calcium channel blockers, the patient was brought for an electrophysiology study and possible catheter ablation. Baseline rhythm was sinus. PR interval was 196 msec. Baseline HV interval was 40 msec. There was no antegrade preexcitation. Electrode catheters were placed in the high right atrium, His bundle, coronary sinus, and right ventricular outflow tract. A narrow complex tachycardia with cycle length of 390 msec was inducible during catheter manipulation, with ventricular decremental pacing from the right ventricle (Figure 3), during atrial or coronary sinus burst pacing as well as by atrial extrastimuli. During atrial extrastimulus testing, initiation of tachycardia was not dependent on a critical AH interval prolongation. HV interval during tachycardia was 40 msec, same as that during sinus rhythm. The tachycardia always terminated with a ventricular electrogram. Isoproterenol, up to 4 mcg/min, was infused to sustain tachycardia to perform pacing maneuvers. During tachycardia, progressive AH interval prolongation (AH interval ranging from 160 msec to 330 msec) resulting in Wenckebach AV block was seen (Figure 4). This ruled out orthodromic AV reciprocating tachycardia (ORT). Near simultaneous AV relationship was noted intermittently during tachycardia (septal VA interval ≤0 msec), resembling typical AV node reentry tachycardia (AVNRT). However, p-waves were positive in the inferior leads during tachycardia, which was inconsistent with typical AVNRT. Moreover, there was no consistent AV or VA relationship during changes in tachycardia cycle length (AA did not predict HH and HH did not predict AA either) (Figure 4). Any attempt at determining a ‘jump’ in the AV nodal function curve was offset by initiation of tachycardia. All the above-mentioned findings suggested a diagnosis of atrial tachycardia. Ventricular overdrive pacing during tachycardia demonstrated a VAAV response,1 confirming the diagnosis of atrial tachycardia (Figure 5). With the available catheters, the earliest atrial activation during tachycardia was noted in the His bundle catheter. Coronary sinus activation during tachycardia appeared near simultaneous. The p-wave morphology during tachycardia (positive in V1 and inferior leads and negative in I and aVL) and near-simultaneous atrial activation in the coronary sinus were suggestive of a superior and lateral location in the left atrium.2 The earliest atrial activation being in the His bundle catheter rather than in the coronary sinus suggested an anterior left atrial location. Transseptal catheterization was performed and a left atrial activation mapping during tachycardia was performed using a 3.5 mm tip, externally irrigated ablation catheter (ThermoCool, Biosense Webster Inc., a Johnson & Johnson company, Diamond Bar, CA) using the Carto 3 electroanatomic mapping system (Biosense Webster Inc.). Earliest atrial activation during tachycardia was located to the superior mitral annulus (43 msec earlier than atrial activation in the His bundle catheter; Figure 6). Radiofrequency ablation at this location terminated the tachycardia with return of sinus rhythm (Figure 7). Post-ablation, with the ablation catheter still in the left atrium, burst pacing from the proximal coronary sinus in the presence of isoproterenol resulted in induction of a narrow complex tachycardia, this time with a cycle length of 330 msec, and near simultaneous A and V activation. There was a His before each QRS. The AH interval during tachycardia was 250 msec and the HV interval was the same as during sinus rhythm. The septal VA interval was was no evidence for AH interval variability or AV block during this tachycardia. Typical AVNRT was suspected. Ventricular overdrive pacing from the right ventricle entrained the tachycardia and a VAV response (not shown) was seen on cessation of pacing. Burst ventricular pacing for 3–6 beats terminated the tachycardia without conduction to the atria. This ruled out atrial tachycardia. Septal VA interval Discussion This case demonstrates the importance of keeping an open mind while evaluating and ablating supraventricular tachycardias (SVT) in the electrophysiology lab. Radiofrequency ablation resulted in apparent termination of the left atrial tachycardia, which was the patient’s presenting arrhythmia. Re-induction of a narrow complex tachycardia, with similar atrial activation sequence to the rhythm just ablated, may bias the operator to think of recurrence of the same arrhythmia. The knee-jerk reaction in such situations is to continue to deliver radiofrequency energy at the same location, at times with more power and temperature, hoping for a more complete lesion. This approach, more often than not, leads to complications. It pays great dividends, however, to keep an open mind as to the possibility that an SVT induced following an atrial tachycardia ablation may be a different arrhythmia. It is critical to take the time to systematically analyze this arrhythmia to identify its mechanism. One of the keys in this case that helped differentiate the first and second tachycardias was the p-wave morphology on the surface electrocardiogram. Positive p-waves in inferior leads are inconsistent with AVNRT. Once atrial tachycardia was diagnosed, further analysis of the p-wave morphology (positive p-wave in lead V1 and negative p-waves in leads I and aVL) helps to immediately localize the arrhythmia to the superolateral aspect of the left atrium and help direct detailed activation mapping to that area.2 Similarly, during the second tachycardia (induced after ablation), inspection of the surface electrocardiogram revealed negative p-waves in the inferior leads, which would be inconsistent with recurrent atrial tachycardia from a superior left atrial location. Another clue that the second tachycardia is not a recurrence of the atrial tachycardia can be found on careful review of Figure 8. In this figure, coronary sinus burst pacing induces a narrow complex tachycardia with near simultaneous A and V activation, but the atrial activation on the distal ablation catheter (ABL d), which was still located in the superior mitral annulus, is now later than the atrial activation in the His bundle and the coronary sinus catheters. If this was recurrent atrial tachycardia, one would have expected the ABL d to have the earliest atrial activation. In this case, the patient’s clinical arrhythmia was a short RP tachycardia that reproducibly terminated with adenosine administration. The response to adenosine would make one think that an AV node-dependent arrhythmia (AVNRT or ORT) is more likely. Adenosine, however, has been shown to suppress and/or terminate a subgroup of atrial tachycardias with a focal origin.3 Mechanistically, these atrial tachycardias can be automatic or of triggered origin. Thus, termination of a narrow complex tachycardia with adenosine can rule out a macroreentrant atrial tachycardia but does not necessarily rule out a focal atrial tachycardia. A biatrial activation map performed during atrial tachycardia (Figure 10) shows the activation to spread from a focal area of earliest activation in the superior mitral annulus (white arrow) to the rest of the atria in a centrifugal fashion. This supported the diagnosis of an adenosine-sensitive focal atrial tachycardia in our patient. During the first tachycardia, AVNRT and ORT were excluded by the following findings:
• ORT: Presence of AV block during SVT (Figure 4) is incompatible with ORT. AV node is an integral part of the ORT circuit and any AV block will terminate ORT. Also, ORT exhibits consistent VA linking, i.e., the HH interval predicts the subsequent AA interval during tachycardia cycle length changes. VAAV response following ventricular overdrive pacing is inconsistent with ORT. • AVNRT: Although response to adenosine makes one suspicious of an AV node-dependent arrhythmia, positive p-waves in the inferior leads during SVT goes against AVNRT. For short stretches during the initial SVT, septal VA interval was Ventricular overdrive pacing during SVT with demonstration of a VAV or VAAV response is a very useful maneuver to differentiate atrial tachycardia from ORT and AVNRT. However, one should make sure that the atria are captured and advanced to the pacing cycle length. An example where ventricular overdrive pacing does not advance the atria to the pacing cycle length is shown in Figure 11. In this situation, the VAAV response is not valid. During the second tachycardia, atrial tachycardia and ORT were excluded by the following findings:• Atrial tachycardia: Ventricular burst pacing during SVT terminated the tachycardia without conducting to the atrium. This excludes the atrium as part of the circuit and thus rules out atrial tachycardia. VAV response upon cessation of ventricular overdrive pacing during SVT is inconsistent with atrial tachycardia. • ORT: Initiation of the tachycardia dependent on AH prolongation as well as a VAV response following ventricular overdrive pacing can be seen with both ORT and AVNRT. A septal VA interval It may be possible that ablation of atrial tachycardia facilitated induction of AVNRT. The patient did have dual AV nodal physiology at baseline but when atrial tachycardia was present, antegrade depolarization of the AV node with varying AH intervals might have prevented sustained retrograde fast pathway conduction, thus suppressing induction and maintenance of AVNRT. Ablation of atrial tachycardia may have eliminated this varying frequency of AV nodal depolarization, resulting in recovery of retrograde fast pathway conduction and initiation of AVNRT.4 For challenging cases in which SVT persists despite repeated ablation attempts, the following critical issues should be kept in mind:1. The first step is to make sure that the catheters are in the appropriate positions so as to avoid working with wrong data. 2. Secondly, always think whether this is the same arrhythmia or a different SVT, albeit, with a similar cycle length and similar activation sequence in the available catheters. It is essential to systematically analyze the SVT to confirm the mechanism. Use more catheters and/or electroanatomic mapping as necessary to clarify the mechanism. 3. Once the mechanism is proved beyond doubt and the ablation electrode is at the appropriate location, one should make sure that the ablation system is working properly and that the ablation catheter has adequate tissue contact. Consideration should be given to using alternate ablation techniques and/or using special sheaths for catheter stability.
References1. Kistler PM, Roberts-Thomson KC, Haqqani HM, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol 2006;48:1010–1017. 2. Iwai S, Markowitz SM, Stein KM, et al. Response to adenosine differentiates focal from macroreentrant atrial tachycardia: Validation using three-dimensional electroanatomic mapping. Circulation 2002;106:2793–2799. 3. 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. 4. Gopinathannair R, Sandesara CM, Olshansky B. Not so innocent bystander(s). Europace 2009;11:1230–1234.