Catheter Ablation of Bundle Branch Re-entrant Tachycardia

Find out how this EP lab treated this rarely seen arrhythmia in a 43-year-old patient. The authors discuss how to differentiate the distinguishing characteristics of the arrhythmia.
Sgt. Albert N. Paul, Jr., RCIS; Thomas M. Wiley, MD, FACC; Walter Reed Army Medical Center, Washington, DC

Bundle branch re-entrant tachycardia is rarely seen in the electrophysiology lab. Patients who are susceptible to this arrhythmia will generally present with a baseline incomplete left or right bundle branch block (LBBB or RBBB) on electrocardiogram. The most common underlying cardiac disease associated with bundle branch re-entry (BBR) is dilated cardiomyopathy of either ischemic or idiopathic etiology.¹

Case Report

A 43-year-old male presented with an episode of weakness and palpitations after walking. An ECG taken during this episode showed a wide complex tachycardia with LBBB pattern, left axis deviation and a cycle length of 265 ms. The patient stated that he had had many similar episodes during strenuous activity and recently had begun to have the episodes at rest. The patient had no past medical history relevant to this condition. There was no family history of sudden cardiac death. Baseline electrocardiogram revealed normal sinus rhythm with RBBB present since at least 1985. A trans-thoracic echocardiogram, performed prior to the electrophysiology study, revealed normal left-ventricular size and function. For the initial electrophysiology study (EPS), the patient was brought to the electrophysiology lab and extra-stimulus pacing was performed at the right ventricular apex and right ventricular outflow tract. Ventricular fibrillation was induced with triple extra-stimulus pacing at the right ventricular apex. The patient was converted to normal sinus rhythm with a single 200 Joule countershock. The clinical impression following this study was spontaneous ventricular tachycardia without inducible ventricular tachycardia at EPS, and right bundle branch block. It was recommended that a cardiac magnetic resonance imaging study and coronary angiography be performed. Possible differential diagnoses were arrhythmogenic right ventricular dysplasia (ARVD) (an inherited genetic disorder wherein fat deposits infiltrate the right ventricular myocardium and cause the patient to be more susceptible to arrhythmias), atherosclerotic coronary artery disease (ASCAD), Brugada syndrome (The syndrome of ST-segment elevation in V1-V3, right bundle branch block, and sudden cardiac death is a genetically inherited disease associated with increased susceptibility to ventricular tachyarrhythmias in the absence of cardiac structural abnormalities3), and BBR. A notable minor complication of this EPS was that transient complete RBBB that resolved after the study was induced with catheter introduction. Following a normal cardiac MRI, left heart selective coronary angiography and left ventriculography were performed. This study revealed normal epicardial coronary arteries; normal left heart pressures, and normal left ventricular systolic function with an ejection fraction of 65%. Figure 1. Findings of this tracing include: initial H-H interval measured 260 ms, while initial V-V interval is 285 ms. As the tachycardia progresses, the V-V interval becomes equal to the H-H interval. This demonstrates that ventricular activation follows activation of the His-Purkinje system. Baseline H-V interval is 75 ms when tachycardia begins, H-V interval is prolonged to 125 ms. After the MRI and coronary angiogram, it was possible to rule out ASCAD and ARVD as causes of the patient's tachycardia. The primary focus was now on BBR. This determination was made because of the patient's baseline incomplete RBBB, and because tachycardia could not be induced during the last EPS after complete RBBB was induced during catheter introduction. The second EPS was performed and extra-stimulus pacing was begun in the right ventricular apex. Up to 2 beats of ventricular tachycardia were inducible in the baseline state; sustained ventricular tachycardia with a cycle length of 280 milliseconds was induced after an isoproterenol infusion was begun at 1.5 micrograms per minute. This tachycardia was identified as BBR because of H-V prolongation when tachycardia is induced, and V-V times correlating with H-H times (Figure 1). A 6 French ablation catheter was then introduced into the right ventricle and positioned to obtain a right bundle branch potential. Radio frequency energy was then applied to a temperature of 60 degrees Celsius for 60 seconds. RBBB was evident after the first ablation attempt. Two additional lesions were placed in this area to ensure that the right bundle branch was completely ablated. Ventricular tachycardia was no longer inducible with or without isoproterenol infusion. Extra stimulus pacing was again performed 25 minutes after the final lesion was placed, with no evidence of tachycardia.

Distinguishing characteristics. The characteristics of BBR that distinguish it from other forms of ventricular tachycardia are tachycardia cycle length of less than 300 ms, and an increase in H-V interval from baseline.

Another distinguishing characteristic is that any change in V-V interval is preceded by a change in H-H interval. This tells us that the His-Purkinje system is driving the tachycardia. In non-BBR ventricular tachycardias, changes in V-V interval are followed by changes in H-H interval.

In the normal heart, the electrophysiologic characteristics of the His-Purkinje system (rapid conduction and long refractory periods) preclude the formation of a re-entrant pathway.² Patients with a conduction delay in either bundle branch may slow the electrical impulse enough to allow activation of the opposite bundle branch in a retrograde fashion, thereby creating a re-entrant circuit.

Discussion. While catheter ablation of either the right or left bundle branch will result in cessation of the tachycardia, it is less complicated to ablate the right bundle branch than it is to ablate the left. In order to ensure proper catheter position on the right bundle, first locate a His bundle potential on the ablation catheter and then advance the catheter along the His-Purkinje axis until the atrial electrogram becomes small or non-existent.⁴

While this patient did not meet the usual clinical criteria for BBR (i.e., dilated cardiomyopathy or other structural abnormality), the conduction delay down the right bundle branch was significant enough to create a re-entrant circuit. Although the initiation of transient complete right bundle branch block during the first procedure prevented the induction of tachycardia, and thereby delayed treatment, it was clinically useful in making the correct diagnosis in this patient. Without this valuable clue, it may have been impossible to differentiate this tachycardia from a non-ablatable ventricular tachycardia.

Although bundle branch re-entry is seldom seen, it is important to be able to recognize its characteristics, so that appropriate therapy can be delivered. At the time of this writing, the patient is once again leading an extremely active life as a soldier in the United States Army. Because the appropriate diagnosis was made, the implantation of a cardioverter/defibrillator was avoided, to the great relief of the patient, and cost savings that may have exceeded $30,000 for the initial implantation of a cardioverter-defibrillator.

REFERENCES

1. Moulton K. Order and disorder in the cardiac rhythm: Electrophysiology training program. Springfield, Illinois: Critical Care Ed., 2001.
2. Huang SKS, Wilber DJ. Radiofrequency catheter ablation of cardiac arrhythmias: Basic concepts and clinical applications. 2nd Edition. Armonk, New York: Futura Publishing Company, Inc., 2000: pp. 653.
3. Priori SG, Napolitano C, Giordano U, et al. Brugada syndrome and sudden cardiac death in children. Lancet 2000;355:808.
4. Hummel JD, Kalbfleisch SJ, Dillon JM. Pocket guide for cardiac electrophysiology. Philadelphia: W.B. Saunders Company, 2000: pp. 225.