How to Utilize Electroanatomical Mapping to Identify Critical Channels for Ventricular Tachycardia Ablation


How to Utilize Electroanatomical Mapping to Identify Critical Channels for Ventricular Tachycardia Ablation

Henry H. Hsia, MD; Kojiro Tanimoto, MD, PhD


Catheter ablation in patients with recurrent VT requires identification of components of the reentrant circuit and is mostly limited to hemodynamically tolerated monomorphic VTs. However, most of the induced VTs are unstable, with multiple morphologies, and do not permit extensive pacing maneuvers during arrhythmias.

High-density electroanatomical mapping provides an accurate 3-dimensional (3D) characterization of the diseased myocardium and allows a substrate-based ablation strategy focuses on the identification of abnormal myocardium that participates as critical components of the reentry circuit. Pathological studies have suggested that zones of slow conduction/isthmus of the reentrant circuits are often located within myocardial scar, and EGM recordings from these sites often exhibit multi-component, delayed signals of higher voltage amplitude compared to the surrounding scar (Figure 43.1).1,2 By careful analysis of the electroanatomical substrate and local voltage profiles, VT-related conducting channels can be identified that correspond to the zone of slow conduction / isthmus site within the reentry circuit.3,4 Such channels are defined as paths demonstrating contiguous electrograms with voltage higher than that of the surrounding areas, and participate in orthodromic activation during VT (Figure 43.2). Identification of such channels helps to localize the potential reentrant VT circuit and focuses additional mapping effort.


Figure 43.1 Anatomical substrate post-myocardial infarction. The left panel shows a theoretical construct of intramural scar-mediated reentry with diastolic activity recorded in the isthmus (electrodes 1 through 5) before exiting the circuit (bold arrow) between 2 areas of collagen (blue) on trichrome staining of an experimental infarction. The right panel shows an endocardial resection of infarcted papillary muscle near the origin of the VT. Dense fibrotic connective tissue (C) is surrounded by rims of residual myocardial fibers (R). This is represented by the middle schematic drawing with dotted areas indicated viable myocardial cells and black areas indicated fibrotic connective tissue. Extracellular recordings from site A to M during stimulation, demonstrating varying degrees of fractionation and conduction delay. Slow conduction perpendicular to the fiber direction in infarcted myocardial tissue is caused by a “zigzag” course of activation at high speed. (Adapted with permission from Tung R. Circulation. 2011;123:2284; deBakker J. Circulation. 1988;77:589; deBakker J. Circulation. 1993;88;915.)


Figure 43.2 Channel identification with voltage color gradient adjustment. A reentrant VT circuit (Panel A) is depicted by the illustrative cartoon of scar and multiple pathways. The circuit resides in the low voltage scarred tissue. The baseline color gradient showed dense scar (red), normal tissue (purple) and the intermediate colored border zone (Panel B). The VT-related conducting channels represent the orthodromic activation during reentry (isthmusimageexitimageouter loop) and often corresponds to zone of slow conduction (Panel C). Such channels may be visible by adjusting the color threshold on a voltage map (Panel D). VT-related conducting channels are defined as a path demonstrating contiguous electrograms with voltage higher than that of the surrounding areas (Panel E).

Preprocedural Planning

A thorough preoperative assessment can facilitate procedural planning for efficient mapping and improves ablation outcomes. Defining patients’ underlying arrhythmogenic substrate requires careful review of patients’ history and data. In patients with coronary artery disease and prior myocardial infarction, the reentrant VTs often originate from subendocardial sites of infarcted myocardium, adjacent to the dense scar.5,6 However, nonendocardial substrates in scar-related as well as in idiopathic VTs have recently been increasingly recognized.79 In patients with dilated nonischemic cardiomyopathy, confluent areas of abnormal low-voltage scars (epicardial ≥ endocardial) are often located over the basal lateral left ventricle near the valve annulus. A prior history of open-chest coronary bypass grafting or valvular surgery is important if a percutaneous epicardial approach is being considered,10,11 whereas a history of significant peripheral vascular disease, prior mechanical aortic prostheses, or mitral valvular prostheses may preclude a retrograde aortic or transseptal approach for endocardial intervention.

The presence of Q waves on the ECG provides noninvasive clues for localization of prior myocardial infarction and the potential scar arrhythmia substrates in patients is ischemic cardiomyopathy. A useful ECG algorithm based on 12-lead ECG allows localization of “site-of-origin” for ischemic VTs with a reasonable (> 70%) predictive accuracy to guide further mapping efforts.12 In the absence of monomorphic VT, PVC morphologies during sinus rhythm can also be useful to locate the generalized regions of VT origin or ascertain the possibility of Purkinje involvement. Furthermore, various QRS morphologic criteria have been used to distinguish endocardial from possible epicardial or non-endocardial sites of origins.1315

However, the 12-lead ECGs of the spontaneous presenting VTs are often unavailable. Utilization of the stored electrograms (EGMS) from patients’ ICDs can be helpful in providing additional data. Comparison of the cycle lengths and the intracardiac “far-field” or “near-field” electrogram morphologies during induced VTs can be used to distinguish “clinical” VT from “nonclinical” arrhythmias. Although the spatial resolution of pace mapping based on ICD electrogram morphologies is inferior to that of 12-lead ECGs, they may be useful for determining whether an ablation catheter is located near the VT exit site. This may focus mapping efforts, streamline workflow, and improve ablation outcomes.16

Although ischemia does not cause recurrent monomorphic VTs, an adequate assessment of the ischemic burden is essential, particularly in elderly patients with history of ischemic heart disease and prior surgical/percutaneous interventions. From a procedural safety point of view, we have a low threshold to perform coronary angiograms to exclude potentially significant coronary arterial stenosis in this population with extensive structural heart disease.

Echocardiography is useful to identify regions of wall motion abnormalities, wall thinning, or aneurysm consistent with prior infarcts/scar, suggesting potential locations of arrhythmogenic substrate. Echocardiography also allows identification of intracardiac thrombus, which would preclude an endocardial approach. The presence of aortic or mitral valve stenosis may influence and guide retrograde aortic versus transseptal ablation approach. Patients with both mechanical aortic and mitral valves may require an epicardial or alternative approach.

Magnetic resonance imaging (MRI) with gadolinium-delayed enhancement has increasingly been utilized for localization of arrhythmogenic substrates in both patients with post-infarction VTs and those with nonischemic cardiomyopathy.1719 Regional wall motion abnormalities and wall thinning (WT) detected on multi-slice CT were also correlated to low voltage/scar regions, almost exclusively located within 3 mm of the thinnest region20 and were inside the MRI-delayed enhancement areas.21 The integration of CT/MRI imaging and electroanatomic maps can be helpful to plan the appropriate mapping and ablation strategies.


Patient Preparation

The majority of our patients who undergo VT ablation have multiple inducible ventricular tachyarrhythmias. Unique to VT mapping, ECG pattern recognition is crucial in localizing the VT exit and for pace mapping. Accurate placement of surface ECG electrodes is imperative. Erroneous ECG interpretations will lead to confusion, procedural delay, and failed outcome.

Our protocol recommends the use of the electroanatomical system for substrate mapping (CARTO, Biosense Webster, Diamond Bar, CA). Care must be taken for placement of the reference patch to compensate for the dilated, leftward rotated left ventricles in most of our patients. The reference patch should be placed lower in the middle of the ventricular silhouette in the anterior-posterior projection to ensure proper registration of the electroanatomical navigational data. Although the St. Jude Ensite NavX system (St. Jude Medical, St. Paul, MN) may also be used to construct the voltage maps, identification of VT-related conducting channels using this system has not been studied.

For the real-time ICD EGM recordings, a device-specific junction box (for example, Medtronic, Minneapolis, MN) may be obtained from the vendor that connects the programmer to the EP recording system (GE Prucka, Marlborough, MA) in the analog channels for display.

In our laboratory, the majority of our patients with left ventricular VT ablation, the arterial access is through the right femoral artery with an 8- or 8.5-Fr sheath for retrograde aortic approach. In patients with significant peripheral vascular disease, a long sheath is used for better support. A separate, redundant femoral arterial access may be considered for hemodynamic monitoring and support (such as intraaortic balloon pump) in patients with severe ventricular dysfunction. The majority of our patients also undergo intracardiac echocardiographic (ICE) imaging during either endocardial or epicardial VT ablation procedures. The right femoral vein is accessed to accommodate an 8- or 11-Fr sheath for the placement of a 10-Fr phased-array ICE catheter. Two right ventricular catheters are routinely placed at the RVA and near the HB. The RVA catheter marks the ventricular apex, and the His catheter marks the ventricular base, opposite the aortic valve.

For procedures performed using an epicardial approach, or in patients who may have VTs that originate near the mitral annulus, an additional CS catheter, inserted either from the right internal jugular vein or from the femoral vein, is used to outline the basal LV silhouette and to facilitate mapping.


Although it is not necessary, the majority of our patients with scar-based VT who undergo ablation are under general anesthesia. Multiple episodes of poorly tolerated arrhythmias are often induced and require shock terminations. Among the many advantages, general anesthesia helps to control patients’ discomfort, minimizes movement, and improves mapping accuracy. The disadvantage of general anesthesia is the abolition of the sympathetic tone for the compensatory vasoconstrictive response during rapid VTs. Nonetheless, close collaboration between the anesthesiologist and the electrophysiologist allows optimal hemodynamic management and respiratory support during the procedure.


Intravascular insertion and manipulation of catheters, creation of ablation lesions, activation of coagulation factors, and potential disruption of atherosclerotic plaques contribute to a risk of thromboembolism during and after catheter ablation. Patients with structural heart disease undergoing left heart catheterization have a risk of stroke or thromboembolism of ~1%. We recommend meticulous monitoring of the ACT every 20 minutes. The target ACT is maintained at ~300 seconds.


Most patients who undergo VT ablation have significant structural heart disease and multiple inducible ventricular tachyarrhythmias (mean 4 ± 3 VT morphologies). A hybrid approach is needed, combining both the conventional mapping techniques and the substrate mapping approaches (Table 43.1).14 A conventional mapping strategy consists of activation mapping and entrainment mapping, and both require sustained reentry and cannot be performed during poorly tolerated VT.

To optimize the result of substrate mapping during sinus/paced rhythm, areas of interest within the abnormal myocardium should be tagged, which helps to define the geometry of the circuit and its relationship to the underlying scar. Identification of conducting channels, along with other collaborative mapping strategies, helps to characterize the VT circuit (these include defining EUS, detecting LPs, and pace mapping [Figure 43.3]). Conventional mapping methods such as activation and/or entrainment/resetting response also complement the substrate mapping to confirm the functional significance of these conducting channels.


Figure 43.3 General approach to catheter mapping and ablation of VT. Identification of VT-related conducting channels is part of the overall strategy of VT ablation, particularly for substrate mapping. Careful sampling of local bipolar EGMs during sinus or paced non-VT rhythm is critical for construction of voltage maps and characterization of the electroanatomical substrate. Identification of EUS, LP/E-IDC, and pace mapping facilitates the detection of conducting channels.

In any given patient, the mapping strategy has to be individualized. Detailed, high-density EGM recording is essential. The average number of sampled points per chamber should be a minimum of 150 to 200 for adequate definition of anatomy and EP characterization of the VT substrate.

Our protocol recommends the use of the open irrigated radiofrequency ablation catheter (NaviStar THERMOCOOL, Biosense Webster, Diamond Bar, CA). By cooling the electrode-tissue interface, irrigated electrodes allow for delivery of greater power without significant rise of impedance or catheter tip temperature. This consistently produces deeper and larger lesions compared to standard solid electrodes, and is particularly important for relatively large circuits, and reentry pathways may be located deep in scarred myocardium.15,16 In addition, the smaller distal mapping electrode pair (3.5 mm with 2-mm spacing) allows better spatial resolution compared to the standard 4- or 8-mm tip.

In order to identify the potential VT-related channels, we first must perform a detailed electroanatomical voltage map to characterize the local voltage profile of the substrate. Bipolar endocardial ventricular signals are recorded and filtered at 10 to 400 Hz on the CARTO System, and the peak-to-peak signal amplitude of the bipolar EGM is measured automatically. A 3D anatomical shell of the cardiac chamber is constructed, and the EGM signals are coupled and displayed as color gradients on a voltage map. Such voltage maps may be registered onto a previously constructed anatomical shell from the ICE images using the CARTOSOUND software. Valvular locations are tagged and excluded from the voltage analysis. Valvular sites are identified by fluoroscopic catheter tip positions that demonstrate simultaneous recordings of equal atrial and ventricular signal amplitudes. The voltage maps are then edited, and intracavitary points are eliminated.

The reference value for distinguishing normal and abnormal bipolar EGM amplitude has been previously established at 1.5 mV for the right ventricle and 1.8 mV for the left ventricle. The normal signal amplitude is defined as the value above which 95% of all bipolar signal voltages from the endocardium of normal ventricles are included. “Dense scar” is arbitrarily defined as areas with signal amplitude less than 0.5 mV. The “border zone” is defined as a transition zone between dense scar and normal tissue (0.5 to 1.5/1.8 mV).17 For epicardial mapping, the “normal” epicardial signal amplitude is set at above 1.0 mV.

Isthmus sites have been shown to reside predominantly (> 80%) in the dense scar (< 0.5 mV) whereas most exit sites are located in the border zone (Table 43.2).4 Pace mapping along the border zone (0.5–1.5 mV) is performed to approximate the exit of the VT circuit, which is defined by sites with a similar paced QRS morphology compared to that during spontaneous ventricular arrhythmia with a short stimulus-QRS interval, arbitrarily defined as < 40 ms. Once the exit is identified, pace mapping and further mapping efforts should be directed progressively away from the abnormal border zone toward the center of the low-voltage dense scar (< 0.5 mV) for localizing the isthmus of the reentry circuit.

Aug 27, 2018 | Posted by in CARDIOLOGY | Comments Off on How to Utilize Electroanatomical Mapping to Identify Critical Channels for Ventricular Tachycardia Ablation
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