Bundle Branch Re-entry Ventricular Tachycardia (VT)

Bundle branch re-entry is a relatively rare form of ventricular tachycardia (VT), usually in patients with significant left ventricular impairment and distal conduction system disease, the latter providing the slow conduction necessary to sustain re-entry. The surface ECG in sinus rhythm (SR) characteristically shows intra-ventricular conduction defects and the tachycardia usually has a left bundle branch block (LBBB) morphology.(1) Patients often have a history of syncope or cardiac arrest.(2) Although rare it is an important diagnosis because ablation is the first line therapy.(1)

Clinical characteristics

Clinical features associated with bundle branch re-entrant VT (BBR VT) include:

• Dilated cardiomyopathy, both ischemic and non-ischemic. (The relative contribution of the BBR mechanism to inducible sustained monomorphic VT is significantly higher in non-ischemic (up to 40%) than in ischaemic aetiology (up to 6%).(2-5) The high mortality often reported in BBR VT patients may be due to the severity of the underlying heart disease in many patients.(1)

• Valvular disease. (6)

• Patients with myotonic myocardial dystrophy. (7)

• The arrhythmia has also been reported in patients with idiopathic isolated conduction system disease and no apparent structural heart abnormalities.(8-11)

Electrophysiological background

A potential for re-entrant circuits is inherent in the structure of the His-Purkinje system (HPS). Classical concepts of re-entry require the presence of two connected pathways - in the HPS these could be provided by the left and right bundle branches which are connected by the His bundle (the His emerges from the compact AV node and traverses the AV ring in the region of the fibrous septum before dividing to give rise to right and left bundle branches). See fig 1.

After a depolarisation excitable cells have a refractory period during which they cannot be re-stimulated. For a re-entrant circuit to sustain there must be sufficiently slow conduction in at least a portion of the circuit to allow cells time to recover from the preceding activation. In common atrial flutter for example this slow region is the cavo-tricuspid isthmus. One would not expect re-entry circuits comprised of distal conduction system tissue to sustain as this tissue is specialised for rapid distribution of the impulse and usually has the fastest conduction in the heart. If conduction is too rapid the circulating wave catches up with refractory tissue and the circuit is broken. When bundle branch re-entry does occur it does so in the context of conduction system disease and facilitated by slowly conducting bundles.

• Figure 1 Figure 1
• Figure 2 Figure 2
• Figure 3 Figure 3
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Another variant of His-Purkinje macro re-entry which utilizes the two ramifications of the left bundle branch (the anterior and posterior fascicles) is referred to as inter-fascicular re-entrant tachycardia and can also occur in patients with BBR VT.(1)

The last two beats of a pacing drive train from the RV apex are followed by a shortly coupled extra. After the extra a His potential can be seen as the next event, preceding the first QRS complex of tachycardia and again before the second beat – characteristic of BBR VT. There is probably V-A conduction of the first beat of tachycardia (His A precedes HRA – compare with sinus activation evident just before the second beat of the drive). A prolonged HV interval during sinus rhythm is found in the majority of patients with BBR VT (2-7) but in this case RB conduction was reasonably slick with slow conduction provided by the retrograde LB.

During the drive train the His spike is not clearly seen because retrograde conduction over the right bundle is reasonably rapid and the His spike is concealed within the large and complex ventricular electrogram.

Why does tachycardia initiate with the extra stimulus?

In classical re-entry, tachycardias start because unidirectional block occurs in one of the two pathways. The extra exceeds the retrograde refractory period of the RB but is conducted with delay by the left bundle to the His, revealing the retrograde His spike (fig 4.) This slow conduction in the left LB allows the right bundle to recover in time to conduct the impulse anterogradely to activate the ventricles (the block is unidirectional).

Note in fig 3 that the signal on the right ventricular apical catheter (RVA) is at QRS onset – the “exit site” of the VT circuit is the insertion of the RB. The impulse is then conducted through the ventricular myocardium until it retrogradely enters the LB bundle to complete the circuit (fig 5). Some additional conduction slowing may be provided by diseased myocardium.

• Figure 4 Figure 4
• Figure 5 Figure 5
• Figure 6a. Figure 6a.
• Figure 6b. Figure 6b.
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As with many re-entrant circuits, although the possibility exits for the circuit to rotate in the opposite direction (anterograde conduction via the LB with retrograde via the RB) one direction dominates and BBR VT with a right bundle branch block (RBBB) morphology is rarely seen.

Features suggestive of BBR VT

VT in patients with structural heart disease often has RBBB morphology - consistent with a left ventricular origin. BBR VT almost always has a LBBB pattern which may be similar to typical LBBB and may be virtually identical to sinus rhythm if the patient has resting LBBB.1 Electrophysiological features consistent with BBR VT include:

• Reproducible initiation of tachycardia with critical V-H interval prolongation (suggesting induction depends on conduction delay within the HPS).

• A stable His or bundle branch potential preceding each ventricular activation.

• An activation sequence of His followed by RB followed by V

• Changes in the H-H interval during VT precede changes in the VV interval. Reproducible termination of VT with block in the HPS.

• Inability to induce VT after ablation of the right (or left) bundle branch.(1)

Ablation of BBR VT

The VT circuit in structural heart disease is more complex than for many other arrhythmias and is usually formed from areas of scar tissue and regions of functional block within the ventricular myocardial substrate. It is prudent in ablation to target a narrow isthmus to minimise the number of energy deliveries required to achieve success. Traditionally, VT ablation in the setting of structural heart disease has involved pinpointing the location of the critical isthmus within the vast landscape of the ventricular mass by activation and entrainment mapping.

However if a diagnosis of BBR VT can be made then the majority of the re-entrant path becomes known and a narrow isthmus immediately presents itself. The proximal RB remains a discrete structure for a significant portion of its course and can be located and if necessary ablated. Radiofrequency catheter ablation of the RB can cure BBR VT and is currently regarded as the first line therapy.(1) In contrast the LB quickly splits into two fans of fibres (the anterior and posterior fascicles) and it is more difficult to eliminate left bundle conduction by discrete RF lesions. RB potentials in sinus rhythm look like His potentials but are later and more closely associated with the ventricular signal. Ablation in the right ventricle targeting RB potentials can eliminate RB conduction and is therefore curative for BBR VT. Some patients with BBR VT may have inducible VTs other than BBR VT and an ICD may be indicated.(1)

• Figure 7 Figure 7
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After ablation of the RB in the featured patient here, LB conduction was revealed to be intact but abnormal and the patient required permanent pacing. Due to the severity of left ventricular dysfunction and conduction system disease in these patients biventricular pacing may be indicated following right bundle ablation.

References:

1. Mazur A, Kusniec J and Strasberg B. Bundle Branch Reentrant Ventricular Tachycardia Indian Pacing and Electrophysiology Journal 2005 5(2): 86-95
2. Caceres J, Jazayeri M, McKinnie J, Avitall B, Denker ST, Tchou P, Akhtar M. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation 1989;79:256-270.
3. Cohen TJ, Chien WW, Lurie KG, Young C, Goldberg HR, Wang YS, Langberg JJ, Lesh MD, Lee MA, Griffin JC, Scheinman MM. Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: Results and long-term follow-up. J Am Coll Cardiol 1991;18:1767 – 1773.
4. Blank Z, Dhala A, Deshpande S, Sra J, Jazayeri M, Akhtar M. Bundle branch reentrant ventricular tachycardia: Cumulative experience in 48 patients. J Cardiovasc Electrophysiol 1993;4:253 – 262.
5. Mehdirad AA, Keim S, Rist K, Tchou P. Long-term clinical outcome of right bundle branch radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia. Pacing Clin Electrophysiol 1995;18:2135-2143.
6. Narasimhan C, Jazayeri M, Sra J, Dhala A, Deshpande S, Biehl M, Akhtar M, Blank Z. Ventricular tachycardia in valvular heart disease: Facilitation of bundle-branch reentry by valvesurgery. Circulation 1997;96:4307-4313.
7. Merino JL, Carmona JR, Fernandez-Lozano I, Peinado R, Basterra N, Sobrino JA. Mechanisms of sustained ventricular tachycardia in myotonic dystrophy: Implications for catheter ablation. Circulation 1998;98:541-546.
8. Blank Z, Jazayeri M, Dhala A, Deshpande S, Sra J, Akhtar M. Bundle branch reentry: a mechanism of ventricular tachycardia in the absence of myocardial or valvular dysfunction. J Am Coll Cardiol 1993;22:1718-1722.
9. Simons GR, Sorrentino RA, Zimerman LI, Wharton MJ, Natale A. Bundle branch reentry tachycardia and possible sustained interfascicular reentry tachycardia with a shared unusual induction pattern. J Cardiovasc Electrophysiol 1996;7:44-50.
10. Gupta AK, Vajifdar BU, Vora AM. Bundle branch re-entrant ventricular tachycardia in a patient with structurally normal heart. Indian Heart J 1999;51:80-82.
11. Mazur A, Iakobishvili Z, Kusniec J, Strasberg B. Bundle branch reentrant ventricular tachycardia in a patient with the Brugada electrocardiographic pattern. A.N.E. 2003;8:252-255.