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A wide QRS complex tachycardia: What is the mechanism?

Lena Teischinger, MD,*† Christian Plass, MD,*† Harald Mayr, MD,*† Bernhard Frey, MD, FESC*†‡

From the *LKH St. Poelten, 3. Medizinische Abteilung, St. Poelten, Austria, †Karl Landsteiner Institut zurErforschung ischaemischer Herzerkrankungen und Rhythmologie, St. Poelten, Austria, and ‡Klinik für InnereMedizin 2, Abteilung für Kardiologie, Medizinische Universitaet Wien, Wien, Austria.

Case presentationAn 86-year-old man with incessant tachycardia and anischemic cardiomyopathy underwent an electrophysiologicalprocedure. During sinus rhythm, the 12-lead electrocardio-gram showed a complete left bundle branch block with aprolonged PR interval. During tachycardia, the QRS mor-phology was identical; however, no P waves were visible(Figure 1). The cycle length during tachycardia variedbetween 440 and 490 ms.

The intracardiac recordings showed a prolonged His-ventricular (HV) interval of 102 ms during sinus rhythm aswell as of 102 ms during tachycardia. Of note, the HV intervalremained constant during the various tachycardia cycle lengthsand changes in the His-His interval preceded changes in theventriculo-ventricular interval. There was no splitting of the Hispotential. Furthermore, the recordings revealed an atrioventric-ular (AV) dissociation during tachycardia (Figure 1).

Owing to the nearly incessant nature of the tachycardia,limited maneuvers were performed. Ventricular overdrivepacing terminated tachycardia reliably, so that classicalentrainment could not be evaluated. Therefore, ventricularresetting response was studied by using a ventricular drive of 3consecutive beats, thus ensuring that at least the last beatcaptured the ventricle without terminating the tachycardia.Resetting of tachycardia from the right ventricular apex isshown in Figure 2; resetting from the basal mid-septum isshown in Figure 3. What is the mechanism of the tachycardia?

CommentaryThe differential diagnosis of a wide QRS complex tachy-cardia with left bundle branch block and AV dissociation in

KEYWORDS Accessory pathway; Bundle branch ventricular tachycardia;Catheter ablation; Entrainment; Nodoventricular; Resetting; Supraventricu-lar tachycardiaABBREVIATIONS AV ¼ atrioventricular; BB-VT ¼ bundle branch

ventricular tachycardia; HV ¼ His-ventricular (Heart Rhythm2014;11:1079–1081)

Address reprint requests and Correspondence: Dr Bernhard Frey, MD,FESC, Klinik für Innere Medizin 2, Abteilung für Kardiologie, MedizinischeUniversitaet Wien, Waehringer Guertel 18-20, 1090 Wien, Austria. E-mailaddress: bernhard.frey@meduniwien.ac.at.

1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.

a patient with ischemic cardiomyopathy and His-Purkinjedisease is mainly ventricular tachycardia. When the QRScomplex during tachycardia is identical to the QRS complexin sinus rhythm, bundle branch ventricular tachycardia(BB-VT) is a likely diagnosis, in particular when theinvolvement of the Purkinje system in the antegrade axisof the tachycardia can be established, for example, changesin His-His intervals precede changes in the ventriculo-ventricular interval. However, to our knowledge, BB-VThas not been reported to be incessant and BB-VT usually hasa shorter cycle length than 490 ms.1 In fact, these observa-tions cast doubts on the diagnosis of BB-VT. Therefore,the tachycardia was reset from the right ventricular apex(Figure 2).

Figure 2 shows that the third premature beat delivered atthe right ventricular apex was captured at a time of Hisrefractoriness and advanced the subsequent His potentialwithout any change in the HV interval (which remainedconstant 102 ms), that is, it demonstrated orthodromiccapture of the His bundle. Furthermore, the post-pacinginterval was 72 ms longer than the tachycardia cycle length(Figure 2). The maneuver was repeated several times,ensuring an apical position fluoroscopically, but it revealedthe same information.

The response to apical ventricular resetting is notexpected with BB-VT in mind:

1.

A long post-pacing interval indicates that the rightventricular apex is far away from the circuit, thus makingbundle branch reentry an unlikely diagnosis.2

2.

Furthermore, the HV interval, being prolonged butidentical to sinus rhythm, during a range of tachycardiacycle lengths and during the resetting response does notmake bundle branch reentry any likelier.3

3.

A His refractory premature ventricular beat that resets thetachycardia and advances the His potential effectivelyexcludes all tachycardia circuits confined to the AVjunction or the His bundle.

4.

A His refractory premature ventricular beat that capturesthe His bundle orthodromically while resetting tachycar-dia makes BB-VT an unlikely diagnosis.4 In bundlebranch reentry, the His bundle is activated retrogradely

http://dx.doi.org/10.1016/j.hrthm.2013.12.009

Figure 1 Tachycardia and sinus rhythm. The format of the tracings in all 3 figures: the 12-lead electrocardiogram, a catheter at the right atrial appendage(RAA), a catheter recording the His (H) potential, a catheter positioned at right ventricular mid-septum, and the radiofrequency (RF) ablation catheter positionedin the right atrium in Figure 1. In this tracing, 5 ventricular beats are depicted: the first 3 are tachycardia beats and the last 2 are sinus rhythm beats. The last Hpotential at the right end of the figure (the sixth H) marks the beginning of the next nonsustained tachycardia run. RV¼right ventricular.

Heart Rhythm, Vol 11, No 6, June 20141080

from a tachycardia circuit confined to the bundlebranches. Therefore, ventricular resetting is expected todissociate the His bundle recording from the ventricularrecording, leading to a change in the virtual HV interval.However, this was not the case. On the contrary, the HVrelation remained constant at 102 ms during variousconditions (sinus rhythm, tachycardia with multiple cyclelengths, and after resetting), suggesting that the antegradeaxis of the tachycardia includes the His bundle.

antegrade axis includes the His bundle and if all tachycardiacircuits above the His bundle are excluded, then an ortho-

So what is the mechanism of the tachycardia? If the

dromic tachycardia with a retrograde axis consisting of anunidentified pathway is the most likely diagnosis. Of note,the exit of this retrograde pathway has to be above the levelof the His bundle because of its orthodromic capture duringtachycardia but below the level of the atrium because of AVdissociation during tachycardia.

Figure 2 Resettingof the right ventricular(RV) apex. The radio-frequency (RF) cathe-ter is positioned at theRV apex. A train of 3beats is delivered witha cycle length of 402ms during tachycardia;cycle length¼ 426 ms.The third beat resetsthe tachycardia. Thepost-pacing interval is430 ms longer thanthe tachycardia cyclelength. H ¼ His;RAA ¼ right atrialappendage.

Figure3 Resettin-g of the right ventri-cular (RV) basalseptum. The radiofre-quency (RF) catheteris positioned at thebasal septum. A trainof 3 beats is deliveredwith a cycle length of410 ms during tachy-cardia; cycle length¼ 437 ms. The thirdbeat resets the tachy-cardia. The post-pacing interval is only13 ms longer thanthe tachycardia cyclelength. H ¼ His;RAA ¼ right atrialappendage.

1081Teischinger et al Wide QRS Complex Tachycardia

Differential resetting was performed as the next step.The ventricular drive was delivered at the basal septum of theright ventricle (Figure 3). Pacing at this site resulted inminimal fusion, with only slight changes in QRS complex ascompared with apical pacing. Again, the last beat advancedthe subsequent His potential without any change in the HVinterval, which remained constant at 102 ms. However, thedifference between the post-pacing interval and the tachy-cardia cycle length shortened to 13 ms.

Minimal fusion combined with a short post-pacing intervalshowed that the basal septum was near the tachycardia circuit,with the orthodromic wave front (of the tachycardia) depolariz-ing a substantial portion of the ventricles whereas the anti-dromic wave front (of the pacing stimulus) depolarizing only asmall portion of the ventricles. Thus, the location of the pacingstimulus was near the point of collision between the anti- andorthodromic wave fronts, immediately proximal to the zone ofslow conduction, and far away from the exit of the slowconduction zone. This finding excludes BB-VT in which theleft bundle branch functions as the slow conducting retrogradetachycardia axis. In BB-VT, the basal septum is, therefore, nearthe exit of the slow conducting pathway. This was clearly notthe case in this patient.

So, after differential resetting, the diagnosis of a supra-ventricular tachycardia, namely an orthodromic tachycardiadue to a retrogradely conducting nodoventricular pathway wasmade. The pathway did not conduct antegradely, as evidencedby a long HV interval and a complete left bundle branch blockwith typical morphology during sinus rhythm. In fact, theventricular exit of the pathway could not be identified.

Mapping of the septal tricuspid annulus during tachy-cardia did not reveal an accessory potential. Therefore,the antegrade axis was targeted and catheter ablation of

the proximal right bundle branch terminated tachycardiaand resulted in complete AV block necessitating ventric-ular pacing. The patient underwent cardiac resynchroni-zation therapy-defibrillator implantation during the sameprocedure right after ablation. A 10-month follow-upremained uneventful.

Why was the tachycardia near incessant and why did thepatient have no tachycardia for more than 85 years? It can beassumed that the accessory pathway has been present sincebirth. For induction of tachycardia, however, a critical delayin the anterograde and/or retrograde axis conduction isrequired. Most likely, His-Purkinje disease with slowing ofinfra-His conduction contributed to tachycardia develop-ment. The combination therapy of amiodarone and β-blockerpresumably further slowed the AV nodal conduction and theretrograde pathway conduction and thus enabled the criticalconduction delay so that tachycardia started spontaneously.Of note, the AV dissociation during tachycardia preventedsupraventricular beats from entering the circuit and thereforestabilized the tachycardia.4

References1. Blanck Z, Dhala A, Deshpande S, et al. Bundle branch reentrant ventricular tachycardia:

cumulative experience in 48 patients. J Cardiovasc Electrophysiol 1993;4:253–262.2. Merino JL, Peinado R, Fernandez-Lozano I, et al. Bundle-branch reentry and the

postpacing interval after entrainment by right ventricular apex stimulation: a newapproach to elucidate the mechanism of wide-QRS-complex tachycardia withatrioventricular dissociation. Circulation 2001;103:1102–1108.

3. Fisher JD. Bundle branch reentry tachycardia: why is the HV interval often longerthan in sinus rhythm? The critical role of anisotropic conduction. J Interv CardElectrophysiol 2001;5:173–176.

4. Quinn FR, Mitchell LB, Mardell AP, et al. Entrainment mapping of a concealednodoventricular accessory pathway in a man with complete heart block andtachycardia-induced cardiomyopathy. J Cardiovasc Electrophysiol 2008;19:90–94.