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How to Use Pace Mapping to Identify the Critical Isthmus

Athanasios Kordalis, MD; Jean-Marc Sellal, MD; Isabelle Magnin-Poull, MD; Christian de Chillou, MD, PhD

Introduction

Ventricular tachycardia (VT) is one of the most devastating complications of structural heart disease and especially of ischemic cardiomyopathy, even years after an acute myocardial infarction. Macroreentry is the most prevalent arrhythmogenic mechanism in scar-related VTs, as scar provides the anatomical and electrophysiological conditions required for reentry.^1–3 Zones of surviving myocytes surrounded by a certain amount of fibrous tissue can result in slow conduction, while conduction barriers, either consisting of a line of conduction block, a scar area, or an anatomical obstacle, such as the mitral annulus, can create an isthmus. The so-called “protected isthmus” of the reentrant circuit becomes the target of ablation by being the critical element for the maintenance of these VTs.⁴

In well-tolerated mappable VTs, the identification of isthmus may be performed either by using entrainment techniques or by constructing activation maps during VT in 3D electroanatomic systems.^4–6 Complete activation maps during VT demonstrate an endocardial macroreentrant circuit, usually with 2 loops rotating around a protected isthmus, in above 90% of mappable postinfarct VTs.⁶ Anatomically these critical isthmuses are about 31 mm long and 16 mm wide on average, while their main electrophysiological finding is the presence of diastolic electrograms. However, in cases of poorly tolerated, unmappable VTs, the above techniques cannot be used to define the protected isthmus. Substrate-based approaches, relying on scar definition using either bipolar voltage mapping during sinus rhythm or pacing have been proposed.^7–11 In this approach, ablation aims to create linear lesions or to target abnormal electrograms (EGM) showing late potentials or fractionation. We recently demonstrated pace mapping in sinus rhythm to be a very powerful technique to unmask the isthmuses of postinfarct VT circuits.¹²

Technical Aspects of Pace Mapping

The use of pace mapping during sinus rhythm has been well described and established as an efficacious technique to localize the origin of focal VTs in patients with “healthy” hearts, as in those presenting with right ventricular (RV) or left ventricular (LV) outflow tract VTs. Most studies report high success rates with ablation at sites with identical or near identical matches in all 12-surface ECG leads.^13–16 Historically, the comparison between QRS complexes in 12-lead ECG recorded during VT and ventricular pacing at different sites has been carried out visually and expressed as the ratio of closely matching ECG leads out of the total of 12 (Figure 55.1). This method reflects a qualitative analysis without estimation of its reproducibility (both inter- and intraobserver variability) and without evaluation of the clinical significance of this variability on the outcome. Nowadays, with the help of technology, quantitative techniques have been developed and incorporated in electrophysiology recording systems or even 3D electroanatomical mapping systems. Computerized algorithms, comparing paced and tachycardia QRS morphologies, extract a lead-to-lead and overall percentage of correlation, remarkably improving the precision of pace mapping (Figure 55.1). Moreover, these quantitative data can be used from 3D electroanatomical mapping systems to generate “pace mapping maps.” Regarding focal VTs in patients without structural heart disease (like outflow tract VTs), these maps can be considered an analogue of activation maps, taking into consideration that the percentage of correlation of paced QRS as a function of the distance of the pacing site from the site of origin of the VT (e.g., site of earliest ventricular activation or exit), since the activation time of this point during VT is a function of the distance of this point from the site of origin of the VT. Smaller distances give better paced QRS matching and earlier activation times and vice versa for longer distances.¹⁷ However, distance is not the only parameter to affect the paced QRS morphology. Several factors, physiological and technical, have been proposed to alter the spatial resolution of pace mapping maps. Specifically, rapid myocardial conduction velocity, high pacing outputs, bipolar pacing, and large inter-electrode distances have been shown to decrease the precision of pace mapping. Based on the above elements, we suggest checking the pacing threshold at each pacing site and pacing at only twice the threshold output to diminish the likelihood of far-field capture. In our experience, the pacing mode (i.e., bipolar or unipolar) at a given ventricular site does not significantly affect the QRS morphology, so for convenience we pace in bipolar mode, which is the default mode when pacing channel is routed through a 3D electroanatomic system. Regarding catheter tip size, it is reasonable to consider that smaller tips lead to more focal myocardial capture and therefore to higher spatial resolution of pace maps. Nevertheless, since data comparing the effect of catheter tip size on the quality of obtained pace maps are lacking, we still use the standard ablation catheter (3.5- to 4.0-mm tip electrode) for pace mapping in everyday clinical practice. Finally, another factor to be addressed is the pacing rate. It has been suggested to pace at rates similar to VT cycle length, as the variation of coupling interval may alter the paced QRS morphology.¹⁸ However, our unpublished data, based on numerous pacing sites and on pacing rates varying from 600 to 300 ms, show only a minimal and inconsistent QRS mismatch, which is insufficient to alter the reliability of the pace mapping map.

Characteristics of Pace Mapping Along Postinfarct VT Isthmuses

The classical interpretation, regarding the topographic correlation of pacing site with the isthmus anatomy in postinfarct patients, is based on the concept that pacing at the exit site of the VT isthmus will generate a perfectly matched morphology of paced and VT QRS with a short stimulus-to-QRS (S-QRS) interval. This physiological background promoted the use of pace mapping as a technique to reveal the exit site of scar-related macroreentrant VTs.19,20 Theoretically, the stepwise displacement of the pacing site from the isthmus exit to the central isthmus, and then to the isthmus entrance, should lead to a gradual prolongation of S-QRS interval with maintenance of perfect QRS matching. On the contrary, our systematic analysis of patients with endocardial macroreentrant VT circuits revealed an abrupt transition from an area of perfectly matching paced and VT QRS to an area of poor matching. The superimposition of high-density 3D pace maps on 3D activation maps documenting a critical isthmus showed that the closely matching area corresponded to the exit of the isthmus, while the poorly matching area to the entrance of the isthmus. The virtual transition line corresponded to the core of the isthmus.¹²

The pathophysiological explanation for this observation is based on the slow conduction along the central isthmus and on the conduction barriers of its lateral limits. An excitation produced by stimulation within an isthmus can propagate to the ventricle either through its entrance or exit zone. At first, the excitation spreads concentrically around the pacing site and then is blocked laterally by the isthmus conduction barriers. Whether the nonrefractory ventricle will be excited from the entrance or exit site of the isthmus depends on the relative distance of the pacing site from the gates of the isthmus (entrance vs. exit) and the conduction velocity along the isthmus. As a consequence, when pacing at the exit zone of the isthmus, excitation reaches the exit site faster, leading to an activation wavefront of the ventricle that generates a QRS perfectly matching the VT QRS (Figure 55.2). On the contrary, when pacing at the entrance zone of the isthmus, excitation reaches the entrance site faster, leading to an activation wavefront of the ventricles that generates a QRS poorly matching the VT QRS (Figure 55.2). Given that the average length of an isthmus is only 31 mm, slight displacement of the pacing catheter along the isthmus can produce major differences on paced QRS morphology.

At first sight, this finding looks in contrast with the principles of entrainment mapping, where concealed fusion with perfectly matched paced and tachycardia QRS morphology are observed irrespective of the exact site of pacing along the critical isthmus, i.e. entrance or exit zone. The 2 zones are differentiated only by the S-QRS interval, which is short at isthmus exit and gradually prolongs as pacing closer to the isthmus entrance (Figure 55.3). This prolongation of S-QRS is an aftereffect of slow longitudinal conduction along the critical isthmus. S-QRS interval reflects conduction through the isthmus, while onset of QRS is coincident with the beginning of the excitation of the ventricle at the exit site of the isthmus and explains why S-QRS interval does not contribute to QRS morphology. The maintenance of concealed fusion, irrespective of the pacing site within the critical isthmus during entrainment, is due to the refractoriness of the ventricular myocardium adjacent to the entrance of the isthmus, which is not the case during pace mapping in sinus rhythm. The refractoriness is the result of the collision between 2 opposite, with respect to the VT activation sequence, wavefronts; the antidromic (N) paced wavefront and the previous (N-1) orthodromic wavefront (Figure 55.4).

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