Bundle Branch Reentry Vt

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Catheter ablation plays a role in the management of selected patients with mono-morphic ventricular tachycardia. The efficacy and safety depend on the type and location of origin of the ventricular arrhythmia, which can be predicted from the nature of the underlying heart disease and tachycardia characteristics (Table 1).

The QRS morphology identifies a ventricular tachycardia (VT) as either polymorphic or monomorphic. Polymorphic ventricular tachycardias (PVTs) are those in which the QRS morphology is continuously changing because of a changing sequence of ventricular activation. With PVT, a consistent site of origin that can be targeted for ablation is unlikely.

Monomorphic ventricular tachycardias are those in which the morphology of each QRS complex resembles that of the preceding and following QRS. The ventricles are repetitively activated in the same sequence. An arrhythmia focus or structural substrate is present, which can potentially be targeted for catheter ablation. The QRS morphology provides an indication of the probable location of the arrhythmogenic region (1) (Fig. 1). Tachycardias that have a left bundle-branch block (LBBB)-like configuration in V1 have an origin in the right ventricle or the interventricular septum (either the right or left side of the septum). Conversely, a right bundle-branck block (RBBB)-like morphology in V1 suggests a left ventricular origin. A frontal plane axis directed inferiorly (dominant R-waves in leads II, III, AVF) indicates an origin in the cranial aspect of the heart, such as the anterior wall of the left ventricle or the right ventricular outflow tract

From: Contemporary Cardiology: Management of Cardiac Arrhythmias Edited by: L. I. Ganz © Humana Press Inc., Totowa, NJ

Table 1

Catheter Ablation of Ventricular Tachycardia: Approximate Effectiveness and Risks of

Major Complications

Efficacy

Risk

Incessant VT Idiopathic VT RV Outflow Tract Left ventricular verapamil-sensitive Post-MI slow VT Reduction of VT episodes Prevention of all VT Post-MI fast VT Other scar-related VTs RV dysplasia + RV dilation Nonischemic cardiomyopathy Bundle-Branch reentry VT

High

Palliative ~50% 100%

Low, but rare fatalities Low

?Low

Low-pacemaker

Bundle Branch Reentry
Fig. 1. The QRS morphology suggests the probable origin and often the type of VT. The morphology of V1 is illustrated at left. See text for discussion LV = left ventricle, RV = right ventricle, OT = outflow tract.

(RVOT). A frontal-plane axis directed superiorly (dominant S-waves in leads II, III, and AVF), indicates initial depolarization of the inferior wall of the left or right ventricle. Dominant R-waves in leads V3-V4 favor a location of the focus nearer the base of the heart than the apex. Dominant S-waves in these leads favor a more apically placed focus. The QRS morphology is an excellent marker of the arrhythmia site of origin when the ventricles are structurally normal, but much less reliable when tachycardia is associated with regions of infarction or scar.

Precise localization of the arrhythmia origin requires catheter mapping. The specific approach to mapping is determined by the nature of the arrhythmia. Ideally, mapping requires that the tachycardia be stable and sustained, allowing a catheter to be moved from point to point during the tachycardia. This is facilitated by hemodynamic stability during tachycardia. Tachycardias that produce hemodynamic collapse requiring immediate termination are not amenable to point-by-point mapping of the activation sequence, but can sometimes be targeted by other approaches.

Once the region giving rise to the tachycardia has been located, ablation of the tissue in the region is accomplished by radiofrequency current application that heats the tissue. A temperature in excess of 48°C irreversibly damages the tissue (2). A fibrous scar forms at the ablation site (3-5). The ablation lesion is initially accompanied by some edema and hemorrhage into the tissue. With time, healing occurs accompanied by resolution of the edema. Occasionally, healing of the lesion is followed by recovery of the tissue in the border of the lesion, and the arrhythmia returns. Alternatively, microvascular damage produced by the lesion can cause it to expand during the healing phase, increasing lesion size. Individual radiofrequency ablation lesions are typically less than 1 cm in diameter. Small focal lesions are ideal for ablation of supraventricular tachycardias (SVT) and small foci. However, VTs that are related to areas of scar often require larger lesions. When a large number of radiofrequency lesions is required to ablate a large region, late changes are not uncommon. Occasionally, an arrhythmia recurs early and then disappears. Ablation failure is often caused by inadequate lesion size or penetration.

Whether VT can be ablated depends on the location and size of the region that causes the arrhythmia. Most VTs originate from sites on the endocardial surface of the heart, which can be reached with an electrode catheter. For the purposes of ablation, VTs can be divided into three types: focal origin, bundle-branch reentry, and scar-related (Table 2). Focal-origin tachycardias arise from a small region; the excitation wavefront spreads out across the ventricles from a focal point that is often amenable to ablation. Most VTs in patients who do not have structural heart disease (idiopathic ventricular tachycardias (IVTs)) are of this type. The mechanism may be automaticity or reentry. Bundle-branch reentry is caused by circulation of the excitation wavefronts through the bundle branches; a bundle branch can be targeted for ablation. Scar-related reentry circuits occur in various configurations and locations, and are the most challenging to ablate.

Patients with VT also fall into three major groups according to underlying heart disease: patients without structural heart disease, in whom tachycardias are referred to as idiopathic; those with a clear region of scar, such as that prior myocardial infarction (MI); and patients with nonischemic cardiomyopathies, including valvular heart disease.

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