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BBRVT occurs due to reentry within a well-defined circuit involving the right and left bundle, connected proximally by the His bundle and distally by the septal myocardium. BBRVT typically occurs in patients with structural heart disease, especially dilated cardiomyopathy, where a longer circuit and/or HPS disease provide sufficient delay to sustain reentry.1 It is crucial to rule out this diagnosis by EP testing in any patient with cardiomyopathy presenting with VT, especially those demonstrating LBBB or a nonspecific intraventricular conduction delay on baseline ECG. BBRVT is characterized by a typical BB pattern (similar to sinus rhythm) with rapid rates of 180 to 300/min, often causing hemodynamic instability. A LBBB pattern during VT is more common, and a normal or left axis can be encountered.² In contrast to most other VTs, a short intrinsicoid deflection is typical of BBRVT, consistent with the initial activation of the HPS and not myocardial cell-to-cell propagation.

Ventricular Tachycardia in Patients with Coronary Artery Disease

Post-infarct VT is typically based on a reentrant mechanism and relies on a circuit incorporating a region of slow conduction in or near the infarct (scar) zone; hence, the resultant ECG represents the activation spreading from the exit site of the circuit. In general, the QRS patterns in these patients are less accurate in localizing the target zone compared to patients with focal VTs. This is related to altered conduction in areas damaged by prior infarct; nevertheless, the ECG offers the capacity to regionalize the exit site to an area of 10 to 15 cm².³ Several algorithms have been proposed for noninvasive localization of the VT circuit’s exit; however, starting with the following basic principles is invaluable:

1. Post-MI VTs almost always arise in the left ventricle or IVS. In this respect, knowledge of the location of the prior infarct facilitates the localization process: VTs associated with inferior MI arise from the inferobasal septum or free wall, and those associated with anterior MI arise from the antero-apical or infero-apical septum or free wall.

2. Overall, VTs arising from the IVS have narrower QRS durations compared to free wall VTs.

3. LBBB VTs almost always localize to the septum, (or within 1 cm of the septum) while RBBB VTs can arise anywhere in the left ventricle, posing a greater challenge for localization.

4. The presence of positive or negative concordance in the precordial leads strongly suggests a basal or apical exit site, respectively.

5. A superior axis in general points to an IVT exit location (thus many inferior MI VTs have a superior axis) or apical locations (in anterior MI), while an inferior axis generally implies an antero-basal location.

Using these simple principles, an adequate localization of the VT exit site can be inferred in most cases encountered in daily practice. More sophisticated algorithms have been suggested by Miller et al.³ and Kuchar et al.,⁴ and more recently by Segal et al.,⁵ and will be summarized in the following discussion.

In the algorithm described by Miller et al.,³ VTs were analyzed based on the location of the prior infarct, BBB pattern, QRS axis, and R-wave progression. Eight patterns of R-wave progression were described and are illustrated in Figure 32.1. In patients with prior inferior MI, large R waves were usually observed in leads V₂ to V₄. Decreasing or reversing R-wave amplitude is seen when the exit site moves more laterally or posteriorly. A left axis was usually seen in VTs arising near the septum; the more the VT moves laterally, the more “right” or superior the axis will become. In patients with anterior MI, the accuracy of the ECG localization is lower than in patients with inferior MI, probably due to the more extensive myocardial damage. In these patients, most LBBB VTs arise from the apical septum, and an anterior vs. inferior location is dependent on the axis (inferior vs. superior axis, respectively). Most RBBB VTs in these patients have a right-superior axis and arise from the antero-apical septum but are usually the most difficult to localize, probably due to variation in extent of infarction and residual myocardium that contributes to the ECG.

An algorithm proposed by Kuchar et al.⁴ (Figure 32.2) was based on results of pace mapping in patients with prior infarction. The left ventricle in this study was divided into 3 parts in each of 3 axes (apical/middle/basal; septal/central/lateral; and anterior/middle/inferior zones); this is of somewhat limited utility because of the variability of propagation from scarred regions (nonspecific results).

In the algorithm of Segal et al.,⁵ VTs were studied based on the BBB pattern and polarity in the limb leads (Figure 32.3). The studied population was not limited to patients with anterior or inferior infarcts but included any MI location. Although R-wave progression was studied, it had no specific bearing on the localization of the VT exit site representing an important variation compared to the Miller et al.³ algorithm. The left ventricle was divided similarly to the study by Kuchar et al.⁴ All LBBB VTs studied were mapped to the septum; a superior axis correlated with basal- and mid-septal locations. LBBB VTs with an inferior axis were mostly localized to the mid-septum. All RBBB VTs were mapped away from the septum: a positive lead I polarity and superior axis pointed to a mid- or basal-posterior location, while a negative lead I and superior axis mapped to an apical-posterior location. Inferior axis RBBB VTs were mapped to the anterior wall, with localization to the mid-anterior wall if lead I is negative vs. basal location if it is positive. This algorithm had an overall ≥ 70% positive predictive value when validated prospectively.⁵

Note that in these studies, 15% to 20% of all VTs couldn’t be localized using these algorithms. For this reason, they should be used as regionalizing tools to help guide mapping. It is our practice to construct a comprehensive activation map of the whole ventricle with dense mapping focused on the suspected culprit area of the exit, especially in patients with sustained, hemodynamically stable VTs.

Less information is available regarding ECG regionalization of VT in patients with various forms of NICM, except that in most cases, circuits and their respective exit sites are more likely to be in the basal third of either left or right ventricles.6,7 In addition, epicardial circuits and exits are more common in myopathies than in post-MI substrates,⁷ and BBRVT is far more common in these cases.

In ARVC, right ventricular basal sites (peritricuspid annulus, outflow tract) predominate and epicardial ablation is often necessary for complete effect.⁸ Sarcoidosis-related VT tends to affect the RV more than the LV, but in most cardiomyopathic hearts, the LV is the source of VT.⁹ VTs uniformly have an LBBB pattern, generally with gradually increasing R-wave amplitude from right to left in precordial leads; frontal plane axis is typically a reliable indicator of exit region (i.e., leftward superior axis suggests exit on the inferolateral RV free wall, strongly inferior axis suggests outflow tract exit, etc).

Of note, these algorithms for scar-based VT regionalize the exit site of the VT, rather than the more optimal ablation site (within a mid-diastolic corridor). Most evidence suggests that the exit site and diastolic corridor are within 2 cm of each other, however. In addition, many patients with VT episodes in the setting of structural heart disease already have an ICD, which generally treats VT episodes quickly and precludes obtaining a 12-lead ECG in order to use its features to plan mapping and ablation studies.

Idiopathic Ventricular Tachycardias

Idiopathic VTs constitute around 10% of clinically encountered VTs and occur, by definition, without identifiable associated structural heart disease. Several classifications have been proposed for these VTs including their site of origin as well as their response to pharmacologic intervention: 2 categories have been widely recognized, including verapamil-sensitive VTs and adenosine-sensitive VTs.

Verapamil-Sensitive, Purkinje-Associated Ventricular Tachycardias

These VTs—previously known as fascicular VTs—are now identified as Purkinje-associated VTs pertaining to their inclusion of Purkinje fibers in a moderately large circuit on the left ventricular aspect of the septum. These are the major type of idiopathic VTs based on reentry (others being focal in origin); the exit site (a sharp Purkinje potential) had served as the target for ablation, but more recent evidence suggests targeting sites with smaller diastolic potentials on the septum.¹⁰ These VTs have a classical ECG appearance of RBBB and left-anterior or less commonly left-posterior fascicular block pattern (Figure 32.4). A relatively narrow QRS (140 ms) is the rule corresponding to a septal exit site of the VT. A left superior axis is usually associated with more posterior exit site along the septum (towards the posteromedial papillary muscle) while a more apical exit site has a right-superior axis. Often, there is a “shelf” or “step” in the upstroke of the inferior leads. Because these VTs have a relatively narrow QRS, occur in younger patients, are usually hemodynamically stable, and terminate in response to verapamil (but not adenosine), they are often mistaken for SVT.

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