Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Emile G. Daoud, MD


A 68-year-old woman is admitted for an evaluation of sudden syncope resulting in a head laceration. She has a 4-year history of a nonischemic cardiomyopathy with stable NYHA class II symptoms and left ventricular ejection fraction of 40%, treated with lisinopril and Toprol XL. Laboratory studies were unremarkable, and surface echocardiography demonstrates no change in the ejection fraction. The 12-lead ECG shows sinus bradycardia with a left bundle branch block (LBBB) pattern (Figure 25-1).


FIGURE 25.1 Sinus bradycardia with a left bundle branch block pattern.


This is a worrisome history. Sudden syncope associated with an injury, especially in the setting of structural heart disease, implies an abrupt drop in blood pressure with subsequent cerebral hypoperfusion and loss of consciousness. The evaluation should be based on the assumption that the mechanism is a malignant dysrhythmia.

• Differential: Ventricular tachycardia (VT); findings from the ECG suggests sinus node disease, infra-Hisian conduction block.

• Neurological etiologies and vasodepressor mechanisms of syncope are unlikely in the absence of prior neurologic disease or symptoms of vagal discharge.

• Evaluation: Electrophysiology study (EPS) to evaluate for a mechanism of syncope. Since the accuracy of electrophysiology testing in the setting of a nonischemic cardiomyopathy is low, if the EPS does not reveal the etiology of syncope, there should be a consideration for empiric implantation of a defibrillator (ICD).


At EPS, VT was reproducibly induced with programmed stimulation of the ventricle. The tracing (Figure 25-2) shows surface leads V1 and aVF and intracardiac tracings from the His catheter and the radiofrequency ablation (RFA) catheter, positioned at the right bundle. The mechanism of the tachycardia is bundle branch reentrant ventricular tachycardia (BBR-VT). The hallmark features are:


FIGURE 25.2 Surface and intracardiac tracing during induced sustained bundle branch reentry VT.

• VA dissociation. The single atrial beat is marked with an A on the His mid electrode.

• QRS morphology during the VT is identical to the QRS morphology of the patient’s native LBBB during sinus rhythm.

• There is significant infra-Hisian conduction delay during the VT with an H-V interval of 124 ms.

• The activation sequence is from His bundle→right bundle→right ventricular myocardium. The right bundle potential is highlighted with an arrow.

• Changes in the H-H interval precede changes in the V-V interval (compare the H-H interval measurements on His ds to V-V intervals on the RFA recording).

The mechanism of BBR-VT is significant conduction disease within the His-Purkinje system establishing the substrate for reentry. The most common form of BBR-VT utilizes antegrade conduction over the right bundle (Figure 25-3). The tachycardia is often initiated by retrograde block in the right bundle, slow concealed retrograde conduction over the left bundle-His (curved dashed line), allowing adequate time for recovery and then antegrade conduction over the right bundle. Activation of the myocardium (the asterisk *) is with a QRS morphology identical to a left bundle branch block pattern. The VT was successfully eliminated by ablation of the right bundle. Postablation, infranodal conduction was unreliable, and a biventricular pacing ICD was subsequently implanted.


FIGURE 25.3 (A) and (B) demonstrate the mechanism of bundle branch reentry VT; (C) demonstrates the mechanism of interfascicular VT.

Features of Bundle Branch Reentrant VT

• BBR-VT is an unusual reentrant VT utilizing both bundles and is due to conduction disease within the His-Purkinje system; it is more commonly induced in patients with nonischemic CM (up to 40%) than ischemic CM (4%-6%).

• Also reported in patients with prior aortic/mitral valve surgery due to proximity of surgery to conduction system, myotonic dystrophy, and with a Class I sodium channel-blocking antiarrhythmic medication. Each of these can result in slow conduction in the His-Purkinje system.

• Patients often present with syncope, near-syncope, or sudden cardiac death.

• The morphology of the VT is usually a LBBB pattern with an identical morphology as the patient’s native QRS conduction during sinus rhythm; it can also be a right bundle branch block VT.

• Findings at EPS often include: (1) prolongation of the HV interval; (2) tachycardia induction is dependent upon critical prolongation of the V-H interval; (3) during VT, the HV interval is usually longer than baseline conduction, but can be unchanged or slightly shorter; (4) during VT, a stable His potential is recorded prior to each QRS and changes in the H-H interval precede changes in the V-V interval (Figure 25-2).

• Tachycardia can be eliminated by ablation of one of the bundles—most often and easily the right bundle. Successful ablation, however, may result in complete or high-grade AV block.

• Another form of His-Purkinje VT is interfascicular VT. This reentrant circuit is contained within the left anterior and left posterior fascicles. Thus, the VT morphology often has a right bundle/left anterior or posterior fascicular block pattern (Figure 25-3).


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2. Cohen TJ, Chien WW, Lurie KG, et al. 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.

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