EP 101: Wide Complex Tachycardia Case Study – Part 1

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 the first installment of this multi-part series for the EP 101 section, the authors discuss evaluation and proper diagnosis of a wide complex tachycardia in the setting of coronary artery disease. Case Presentation A 53-year-old man with hypertension, hyperlipidemia and coronary artery disease (s/p stent placement in 2001) presented to the emergency room with chest pain radiating to the jaw associated with tachycardia, dyspnea and diaphoresis. An electrocardiogram indicated the presence of a wide complex tachycardia (WCT) 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 (VT) 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 (Figure 2). Cardiac biomarkers were negative, and with the clinical presentation suggestive of acute coronary syndrome (unstable angina), coronary angiography was performed and showed severe three-vessel coronary artery disease. An echocardiogram showed preserved left ventricular function. The patient underwent three-vessel coronary bypass surgery and no further WCT occurred during hospitalization. This scenario raises questions as to whether the WCT was monomorphic VT, whether ischemia was responsible, and whether this patient requires an implantable defibrillator before discharge even though he was revascularized and has preserved left ventricular function. To address these issues, an electrophysiology study was performed. The primary reason to perform an EP study was to diagnose the mechanism of the WCT (thought to be VT) but not to ablate the tachycardia. Therefore, a two-catheter study was performed (His bundle, right ventricular/right atrial catheters). No consent for ablation was obtained. The baseline rhythm was sinus with normal sinus node, atrial, AV nodal, His-Purkinje, and ventricular function. No evidence for dual AV nodal physiology was noted by atrial extrastimulus testing. No arrhythmias were inducible by atrial stimulation. Right ventricular (RV) stimulation from the outflow tract using triple extrastimuli resulted in a narrow complex tachycardia with a cycle length (CL) ranging from 270 to 320 ms (Figure 3). During tachycardia, His bundle activation preceded QRS with a constant HV interval. No retrograde His bundle activation was seen. This tachycardia terminated spontaneously with a ventricular electrogram (Figure 4). During narrow complex tachycardia (CL 319 msec), the HA interval was 204 msec and the AH interval was 115 msec. Burst pacing from the RV apex resulted in induction of a WCT with a LBBB, left axis morphology, resembling the patient’s clinical tachycardia (Figure 5). During WCT (CL 310 msec), the HA interval was 255 msec and the AH interval shortened to 55 msec. There was no other inducible WCT and no induced ventricular fibrillation. At this point, it was decided to place a coronary sinus (CS) catheter to better understand the tachycardia. Repeat attempts at tachycardia induction only resulted in transient narrow complex tachycardia, not WCT. During narrow complex tachycardia, the earliest atrial activity was seen in the proximal CS (Figure 6). Right ventricular pacing during the tachycardia showed continuous VA conduction in a similar pattern as the tachycardia with earliest atrial activation at the proximal CS. Differential diagnoses entertained were orthodromic AV reciprocating tachycardia (AVRT) using a right-sided or a septal accessory pathway versus an AV nodal reciprocating tachycardia (AVNRT). The fact that the tachycardia CL was the same if not shorter during WCT with a LBBB pattern, a left-sided pathway was considered unlikely. As the tachycardia stopped spontaneously, delivery of ventricular ectopic beats during tachycardia was not possible. During RV pacing at a CL of 400 msec, 1:1 concentric VA conduction was noted. Six mg of IV adenosine was given at this point to better define the presence of an accessory pathway. This was associated with two retrograde activation patterns with retrograde VA block in a repetitive fashion (Figure 7). The tachycardia CL varied considerably. However, the HA interval was always constant and the preceding HH interval predicted the subsequent AA interval. The AH interval, though, continued to vary and at times demonstrated marked beat-to-beat variation, consistent with dual AV node physiology (Figure 8). Since the WCT was not re-inducible and the transient nature of the tachycardia did not allow further diagnostic maneuvers, it was decided to bring the patient back the next day for a detailed study and possible ablation after discussion with the patient. Discussion This case brings about several important points. A WCT in a middle-aged male with known coronary artery disease is of major concern and requires careful evaluation. In this situation, a WCT is ventricular tachycardia approximately 90% of the time.1 EP testing is indicated in patients with a WCT of undiagnosed cause to rule out VT. Since the patient was hemodynamically stable and mentally alert, and his tachycardia was regular, the option of lidocaine as an initial anti-arrhythmic agent was an appropriate one. It turned out the tachycardia was supraventricular tachycardia and not ventricular tachycardia. It is likely that tachycardia initiated the anginal symptoms rather than ischemia triggering the tachycardia. Lidocaine termination of a WCT is not indicative of VT as the cause. Lidocaine can also affect accessory pathways. In retrospect, the most likely cause for the initial clinical tachycardia was orthodromic AVRT with LBBB aberrancy that stopped due to conduction block in the accessory pathway from lidocaine. Studies on lidocaine effects on accessory pathways have shown mixed results. Josephson et al reported that lidocaine increases refractory period in an antegrade-conducting accessory pathway,2 whereas a study by Barrett et al3 found that lidocaine used in patients with Wolff-Parkinson-White syndrome did not terminate AVRT and had no appreciable effects on the effective refractory periods of the antegrade or retrograde accessory pathway. Although likely, it could not be proved whether lidocaine indeed had a therapeutic effect on the tachycardia in this case. Choosing to perform an EP study in this setting is most appropriate as there is no clear answer to whether this patient requires an implantable defibrillator before discharge. The finding of WCT in the setting of an acute coronary syndrome also has an impact on how you choose to do the EP study. If inducible VT is your primary concern, only a two-catheter (His bundle and a quadripolar catheter for atrium/RV) study is needed. However, this needs to be upgraded to a three- or four-catheter study (His bundle, RV, atrium, CS) if a supraventricular tachycardia is induced. During atrial extrastimulus testing, the presence of dual AV nodal physiology is demonstrated by a >50 msec increase in AH interval for a 10 msec decrement in the A1A2 coupling interval. This is called a “jump” and it indicates shift in antegrade conduction from the fast pathway to the slow pathway. In this case, this was not demonstrated by single extrastimulus testing, as the atrial effective refractory period was achieved before the AV nodal effective refractory period. However, this finding does not rule out dual AV node physiology — it was easily demonstrable during narrow complex tachycardia as shown in Figure 8. The ways to overcome this problem include using double atrial extrastimuli or to use isoproterenol to shorten the atrial effective refractory period. During the initial electrophysiology evaluation, a narrow complex tachycardia as well as a WCT was induced with RV pacing, with similar His bundle activation (His preceding QRS). Although the tachycardia CL varied considerably, the HA timing remained constant and the preceding HH interval predicted the subsequent AA interval; this was true for both the narrow complex tachycardia and WCT. This finding demonstrates AV nodal dependency for the tachycardia and rules out atrial tachycardia. The use of HA timing becomes especially important in this case, as the WCT had a shorter CL than the narrow complex tachycardia. Assuming that this is an orthodromic AVRT with LBBB aberrancy and the pathway is on the left free wall, LBBB should have increased the CL of the AVRT, proving that the affected bundle branch is part of the circuit. In this case, tachycardia with the LBBB morphology was associated with a shorter CL. However, this does not rule out a left free wall accessory pathway, as there was significant prolongation of the HA interval and the CL 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. Looking at Figure 5, it appears that rapid RV pacing initiated the WCT. However, on closer review, it appears the tachycardia started somewhere during rapid pacing and continued rapid pacing during WCT sped the tachycardia up to the pacing CL (250 msec), resulting in constant fixed fusion (arrows). Upon termination of pacing, the last paced beat is still at the pacing cycle length (entrained), but the surface ECG morphology is not fused (block arrow). This represents the first criterion for manifest entrainment and proves reentry as a mechanism for the WCT.4 During narrow complex tachycardia, the earliest retrograde atrial activation was seen at proximal CS. This raises suspicion as to whether this was a posteroseptal accessory pathway on the right side. However, when reviewing the HA interval for both WCT and narrow complex tachycardia, the HA interval appeared to be markedly prolonged (an increase of ~50 msec) when LBBB happened during the tachycardia. Bundle branch block during an orthodromic AVRT with a septal accessory pathway should not be expected to prolong the AVRT CL by more than 15 msec. HA prolongation with a bundle branch block, despite overall shortening of tachycardia CL, raises suspicion of a free wall accessory pathway located on the same side as the bundle branch block. Once the CS catheter was placed, we were unable to induce the WCT again. Therefore, it was not clear at this point whether the CS activation for the WCT was the same as that for the narrow complex tachycardia. Thus, despite consensus that the narrow complex tachycardia was an orthodromic AVRT and that the WCT was the same tachycardia with LBBB aberrancy, the presence and location of the accessory pathway could not be conclusively proved. Adenosine, in this case, caused VA block during ventricular pacing by blocking in the AV node and accessory pathway. Even though adenosine has been used to assess accessory pathway conduction, adenosine can also block accessory pathway conduction in select patients. 5,6 However, VA block induced by adenosine during ventricular pacing does not necessarily rule out a non-decremental accessory pathway. Ventricular pacing was performed for a sufficient period of time at a CL well above the tachycardia CL with consistent 1:1 VA conduction before adenosine administration to ascertain whether VA block was truly a drug effect and related to accessory pathway refractoriness. Ultimately, the data obtained from the electrophysiology study helped rule out: • Ventricular tachycardia: The finding that there was a narrow and a wide QRS complex tachycardia present with similar HV activation and 1:1 VA relationship makes VT highly unlikely. His bundle activation with a similar HV interval to sinus rhythm during tachycardia essentially rules out VT. 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. • Atrial tachycardia: Cycle length irregularity can be a feature of atrial tachycardia, but atrial tachycardia does not exhibit AV nodal dependency. In an irregular atrial tachycardia, the HH interval does not predict the succeeding AA interval, and the HA timing will not be constant. Also, the AA interval only approximately predicts the HH interval, as the AV node response to the tachycardia varies as the node is not part of the tachycardia circuit. Also ventricular pacing during tachycardia did not demonstrate the V-A-A-V response typical for atrial tachycardia. • AVNRT: Adenosine administration during ventricular pacing demonstrated concentric and eccentric retrograde atrial activation consistent with accessory pathway and AV nodal conduction. Although there was evidence for dual AV node physiology antegrade, the presence of variable AH intervals during both WCT and narrow complex tachycardia makes AVNRT unlikely. Retrograde conduction of a His-refractory premature stimulus during tachycardia preexciting the atrium would have been confirmatory for an accessory pathway in this situation. Conclusions This case demonstrates several important points, including evaluation and management of a WCT in the setting of an acute coronary syndrome, and electrophysiological techniques used in differentiating VT from supraventricular tachycardia and in differential diagnosis of supraventricular tachycardia. Typical orthodromic AVRT is narrow complex but can present as a WCT with bundle-branch aberrancy, which can be confusing and often difficult to distinguish from VT, especially in a patient with known coronary artery disease. A carefully performed electrophysiology evaluation, including pharmacological maneuvers, is needed for proper diagnosis and guide therapy. Acknowledgement The authors acknowledge the assistance of Renee Sullivan, MD in this manuscript.