Repetitive multiform narrow complex tachycardia

Abstract

A 73-year-old man presented to the emergency department with palpitations. After experiencing transient exertional palpitations and dyspnea a few months earlier, investigation revealed moderate left ventricular dysfunction and extensive coronary artery disease with evidence of prior inferior infarction. He underwent bypass grafting and remained symptom free with normalization of his ejection fraction until the current presentation. Figure 1 demonstrates his presenting rhythm that did not respond to adenosine but terminated with intravenous diltiazem. What is the most likely mechanism of the tachycardia? Figure 1 shows a regular narrow complex tachycardia with 3 distinct alternating QRS morphologies: (1) right bundle branch block (RBBB), V1 R 120 ms, V4 precordial transition, left superior axis; (2) RBBB, V1 rsRʹ 100 ms, positive precordial concordance, left superior axis; and (3) RBBB, V1 R 100 ms, positive precordial concordance, left superior axis. The RBBB and left superior axis of all 3 morphologies suggest that the ventricles are activated via the left posterior fascicle, or at the very least, there is early engagement of this fascicle. While supraventricular tachycardia with aberrant conduction is theoretically possible, varying ventricular morphologies in this fashion, lack of termination with adenosine, and the relatively narrow QRS duration (<130 ms) would make this less likely. Together with the response to diltiazem, the overall evidence suggests ventricular tachycardia involving the left posterior fascicle. The classic form of idiopathic fascicular ventricular tachycardia involves the left posterior fascicle, in which there is slow antegrade conduction along abnormal Purkinje fibers in the mid-septum (resulting in P1 potentials) and conduction over the left posterior fascicle (resulting in P2 potentials).1Nogami A. Naito S. Tada H. et al.Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia.J Am Coll Cardiol. 2000; 36: 811-823Crossref PubMed Scopus (218) Google Scholar In any individual patient, variable relationships of the abnormal Purkinje fiber to the left posterior fascicle can result in a more basal or apical site of breakout to the left ventricle; these differences can often be suggested on the surface electrocardiogram by the width of the QRS complex and the precordial transition.2Liu Q. Shehata M. Jiang R. et al.Macroreentrant loop in ventricular tachycardia from the left posterior fascicle: new implications for mapping and ablation.Circ Arrhythm Electrophysiol. 2016; 9e004272Crossref Scopus (7) Google Scholar,3Ma W. Lu F. Shehata M. et al.Catheter ablation of idiopathic left posterior fascicular ventricular tachycardia: predicting the site of origin via mapping and electrocardiography.Circ Arrhythm Electrophysiol. 2017; 10e005240Crossref PubMed Scopus (1) Google Scholar Sung et al4Sung R.K. Kim A.M. Tseng Z.H. et al.Diagnosis and ablation of multiform fascicular tachycardia.J Cardiovasc Electrophysiol. 2013; 24: 297-304Crossref PubMed Scopus (29) Google Scholar described multiform fascicular QRS complexes due to alternate conduction over the left anterior fascicle and the left posterior fascicle from the septal fascicle, but the QRS forms described in the present report are different. Idiopathic fascicular ventricular tachycardia typically occurs in patients with structurally normal hearts, which was not the case in the present report. However, abnormal Purkinje fibers have also been implicated in a minority of patients with ischemic ventricular tachycardia and extension of inferoposterior scar to the left posterior fascicle.5Bogun F. Good E. Reich S. et al.Role of Purkinje fibers in post-infarction ventricular tachycardia.J Am Coll Cardiol. 2006; 48: 2500-2507Crossref PubMed Scopus (121) Google Scholar In this case, it was hypothesized that different QRS morphologies were due to varying sites of left ventricular breakout (Figure 2). The patient underwent electrophysiology study, where multiple episodes of ventricular tachycardia were able to be induced with ventricular extrastimuli similar to those seen on presentation. Ablation of the left posterior fascicle was undertaken, with subsequent noninducibility and no further episodes after 12 months of follow-up.