TY - JOUR
AU - Anter,, Elad
AB - Abstract Aims Multielectrode mapping catheters can be advantageous for identifying surviving myocardial bundles in scar. This study aimed to evaluate the utility of a new multielectrode catheter with increased number of small and closely spaced electrodes for mapping ventricles with healed infarction. Methods and results In 12 swine (four healthy and eight with infarction), the left ventricle was mapped with investigational (OctarayTM) and standard (PentarayTM) multielectrode mapping catheters. The investigational catheter has more electrodes (48 vs. 20), each with a smaller surface area (0.9 vs. 2.0 mm2) and spacing is fixed at 2 mm (vs. 2–6–2 mm). Electrogram (EGM) characteristics, mapping efficiency and scar description were compared between the catheters and late gadolinium enhancement (LGE). Electrogram acquisition rate was faster with the investigational catheter (814 ± 126 vs. 148 ± 58 EGM/min, P = 0.02) resulting in higher density maps (38 ± 10.3 vs. 10.1 ± 10.4 EGM/cm2, P = 0.02). Bipolar voltage amplitude was similar between the catheters in normal and infarcted myocardium (P = 0.265 and P = 0.44) and the infarct surface area was similar between the catheters (P = 0.12) and corresponded to subendocardial LGE. The investigational catheter identified a higher proportion of near-field local abnormal ventricular activities within the low-voltage area (53 ± 16% vs. 34 ± 16%, P = 0.03) that were considered far-field EGMs by the standard catheter. The investigational catheter was also advantageous for mapping haemodymically non-tolerated ventricular tachycardias due to its higher acquisition rate (P < 0.001). Conclusion A novel multielectrode mapping catheter with higher number of small, and closely spaced electrodes increases the mapping speed, EGM density and the ability to recognize low amplitude near-field EGMs in ventricles with healed infarction. Mapping, Catheters, Electrodes, Ventricular tachycardia, Scar, Substrate mapping, High-density mapping What’s new? A new multielectrode mapping catheters with higher number of small and closely spaced electrodes can increase the mapping speed and electrogram density during substrate mapping and ventricular tachycardia. It improved the ability to recognize low amplitude near-field potentials within the peri-infarct area. Introduction Over the last decades, ventricular tachycardia (VT) ablation has evolved into an important therapeutic modality, particularly for patients with structural heart disease. This procedure is often guided by electroanatomical mapping (EAM) during sinus rhythm (or pacing) in effort to identify the arrhythmogenic substrate responsible for the tachycardia.1–4 Advances in mapping technologies include introduction of multielectrode mapping catheters, designed to acquire a larger number of electrograms (EGMs) per beat, producing higher density maps with shorter mapping times.5–7 In addition, electrodes have become progressively smaller and more closely spaced in effort to reduce the sampled tissue size and increase the mapping resolution (the tissue area represented by each bipolar EGM). The use of multielectrode mapping catheters allows identification of small surviving myocardial bundles that may be critical for re-entry and have been instrumental in the study of arrhythmia mechanisms. Nevertheless, the optimal number of electrodes, their surface area, spacing, and geometrical arrangement have not been well evaluated. In this respect, the fine balance between technological innovations that produce new meaningful information and those that produce an abundance of non-contributory data are unknown. In this study, we evaluated a new mapping catheter (Octaray™, ‘Investigational’) in a swine model of VT. In comparison to a standard multielectrode mapping catheter (Pentaray™, ‘Standard’), the investigational catheter contains an increased number of splines (8 vs. 5), increased total number of electrodes (48 vs. 20), and reduced surface area of each electrode (0.9 vs. 2.0 mm2). The specific aims of this study were to (i) characterize the EGM amplitude, duration, and configuration in normal and infarcted ventricles recorded by the investigational catheter and (ii) to compare its utility and limitation in comparison to the standard catheter for mapping post-infarction ventricular scar. Methods This study included 12 Yorkshire swine (70–90 kg): four healthy and eight with chronic anterior wall infarction. Anterior wall infarction was induced in 35–40 kg swine of either sex by balloon occlusion of the left anterior descending artery as previously described.8 A survival period of 10–12 weeks resulted in a large heterogeneous scar with surviving subendocardial bundles approximating infarction in humans. This infarction model often produces spontaneous and induced sustained re-entrant monomorphic VTs. Following the survival period, animals underwent in vivo cardiac magnetic resonance (CMR) imaging, followed by a terminal mapping procedure.9 All experiments were performed under general anaesthesia with isoflurane inhalation and mechanical ventilation. The research protocol was approved by the Institutional Animal Care and Use Committee and conformed to the Position of the American Heart Association on Research Animal Use. The study was performed at the Beth Israel Deaconess Medical Center Experimental Electrophysiology Laboratory and Cardiac MR Center in Boston, MA, USA. Investigational multielectrode mapping catheter The investigational multielectrode mapping catheter (OctarayTM, Biosense Webster, Irvine, CA, USA) is an advanced version of the standard multielectrode mapping catheter (PentarayTM, Biosense Webster, Irvine, CA, USA).10 As shown in Figure 1, it contains an increased number of splines from 5 to 8 and increased total number of electrodes from 20 to 48. Each spline contains six electrodes, and the surface area of each electrode is smaller in comparison with the standard catheter (0.9 vs. 2.0 mm2). The interelectrode spacing is 2-mm centre-to-centre. In comparison with the standard catheter, which has a variable interelectrode spacing alternating between 2 and 6 mm, the uniform electrode spacing in the investigational catheter allows recording of overlapping bipolar leads (i.e. 1–2, 2–3, 3–4) such that the overall number of bipolar EGMs recorded at each beat is increased from 10 in standard catheter to 40 in investigational catheter. The area coverage diameter of the investigational catheter is similar to the standard catheter (7.1 cm2); however, as the number of electrodes is larger the mapping density is higher (7 vs. 2.5 electrode/cm2). Furthermore, the new design favours a more homogenous dispersion of the splines as well as contact of both the proximal and distal electrodes with tissue. Figure 1 Open in new tabDownload slide Catheter configuration and electrode characteristics. The upper panels show a close-up view of the catheters and schematics of a single spline, highlighting the electrode size and inter-electrode spacing (in mm). The standard catheter has five splines, each incorporating four 2 mm2 electrodes with alternating interelectrode spacing of 2 and 6 mm. The investigational catheter has eight splines, each equipped with six 0.9 mm2 electrodes and a uniform interelectrode spacing of 2 mm. The lower panels illustrate the apposition of both catheters in ventricular tissue using a similar counterweight of 10 g. Adopted with permission from Ref.12 Figure 1 Open in new tabDownload slide Catheter configuration and electrode characteristics. The upper panels show a close-up view of the catheters and schematics of a single spline, highlighting the electrode size and inter-electrode spacing (in mm). The standard catheter has five splines, each incorporating four 2 mm2 electrodes with alternating interelectrode spacing of 2 and 6 mm. The investigational catheter has eight splines, each equipped with six 0.9 mm2 electrodes and a uniform interelectrode spacing of 2 mm. The lower panels illustrate the apposition of both catheters in ventricular tissue using a similar counterweight of 10 g. Adopted with permission from Ref.12 Cardiac magnetic resonance In vivo CMR imaging was performed in animals with healed infarction ≤1 week before the terminal mapping study using a 3T MRI scanner (Siemens Vida, Erlangen, Germany) with an 18-channel body coil. Three-dimensional late gadolinium enhancement (LGE) images were acquired 15–25 min after infusion of a bolus (2 mL/s) of 0.2 mmol/kg Gadobenate Gimeglumine (Gadavist; Bayer, Leverkusen, Germany). A respiratory navigator placed on the dome of the right hemi-diaphragm was used for prospective real-time correction. A gradient echo sequence was imaged in short-axis plane covering the entire heart with the following typical parameters: TR/TE= 2.7/1.3 ms, field of view = 360 × 324 mm2, flip angle = 20°, spatial resolution = 1.5 × 1.5 × 1.5 mm3, and GRAPPA factor = 2. Endocardial and epicardial contours were manually delineated in all slices, and LGE was defined using a 6-SD threshold.12 Endocardial mesh was generated using a Poisson surface reconstruction from endocardial contours. Late gadolinium enhancement maps of the endocardium and subendocardium were defined by projecting LGE of endocardial region (2-mm inner layer) onto the mesh when all voxels along the region were defined as LGE positive. Late gadolinium enhancement of midmyocardium to epicardium was defined by projecting LGE of mid to epicardial region (2 mm to epicardium outer layer) onto the mesh. Mesh processing was performed using MeshLab. The cut-off of 2 mm was chosen based on our previous study showing that maximal correlation between LGE and endocardial voltage is limited to 2 mm depth.6 Mapping protocol and electrogram acquisition Following a 10–12-week post-infarction survival period and ≤1 week after the CMR, animals underwent a terminal mapping procedure. Catheters were advanced to the left ventricle (LV) via the retrograde transaortic approach. An anatomical shell of the LV was built with either the investigational or standard catheters. Subsequently, an electroanatomical map of the LV was created with the investigational and standard catheters during right ventricular (RV) septal pacing at a cycle length of 450–550 ms. To minimize the potential for a mapping bias, the order of mapping was alternated such that in half the animals mapping was first performed with investigational catheter, while in the other half mapping was first performed with the standard catheter. A map was considered complete when the fill threshold had reached 5 mm for the entire surface area, such that interpolation between points was limited to ≤5 mm. The high-pass filter was 0.5 Hz for unipolar and 30 Hz for bipolar EGMs. The low-pass filter was 500 Hz both unipolar and bipolar EGMs and these settings were similar between the catheters. Data acquisition was automated using the following inclusion criteria: (i) QRS morphology stability defined as ≥95% morphology stability compared with the paced QRS configuration; (ii) activation time stability ≤5 ms between two consecutive beats; and (iii) maximal distance from the premade anatomical shell ≤3 mm. Collected data included the following: (i) number of EGMs per map, (ii) EGM acquisition rate, measured as the acquired number of points per minute of mapping, (iii) EGM acquisition density, measured as the acquired number of EGMs per cm2 of LV, (iv) number of EGMs acquired per beat, and (v) catheter-induced ectopy rate. The latter was measured by counting all unique ventricular activation events that were dyssynchronous with pacing (arose between pacing spikes) per minute of mapping. More sustained ventricular ectopy (e.g. a three-beat catheter-induced run of VT) counted as a single ectopic event for the purposes of our analysis. Electrogram analysis Electrogram analysis was performed offline at a sweep speed of 200–400 mm/s on either Carto 3 (Biosense Webster, Irvine, CA, USA) or LabSystem Pro EP recording system (Bard; Boston Scientific, Lowell, MA, USA). The minimum bipolar voltage amplitude of collected EGMs was 30 µV which is twice the noise level in our lab. All EGMs were manually reviewed to exclude ectopic beats and artefact. Activation time was annotated to the near-field potential. This was determined by presence of high-frequency potentials exhibiting spatiotemporal propagation across multiple electrodes at a similar acquired beat.11 Electrogram acquisition rate was defined as the average number of useable (i.e. annotated) EGMs obtained per minute of total mapping time. All EGMs data were exported from Carto 3 into MATLAB Version X (Mathworks, Natick MA, USA). Electrograms were analysed for amplitude, duration, and morphology. The surface area of the infarction for each animal was defined by the outer circumference of abnormal EGMs: bipolar voltage amplitude <1.5 mV and/or fractionated/split potentials as determined by the standard catheter. Local abnormal ventricular activity (LAVAs) were defined as high-frequency potentials, possibly of low amplitude, distinct from a far-field ventricular EGM occurring anytime during or after the far-field ventricular EGM.13 Classification of EGMs was performed by two independent reviewers (M.B. and H.Y.). In the case of discrepancy, EGM was reviewed by both reviewers and in the case of non-agreement, the EGM was not classified. Ventricular tachycardia mapping The aim of this step was to evaluate the utility of the investigational catheter for mapping VT in regard to speed, EGMs quality and manoeuvrability. The latter was evaluated qualitatively in three aspects: (i) ability to introduce the catheter into the LV retrogradely through the aortic valve; (ii) ability to manoeuvre the catheter in the mitral valve apparatus including under the papillary muscles; and (iii) the ability to cover the entire chamber. After completion of the maps during RV pacing, programmed stimulation was performed from the RV at a paced cycle length of 400–600 ms and with 1–5 extra stimuli down to ventricular effective refractory period. If pacing from the RV failed to induce sustained monomorphic VT, stimulation was repeated from the LV. In order to maximize the VT mapping time, the investigational catheter was pre-emptively placed in the region of the infarct during stimulation. Non-tolerated VTs were defined as those resulting in mean arterial pressure <40 mmHg. These were terminated with pacing or cardioversion within 1 min of non-tolerability. Statistical analysis Descriptive statistics are reported as mean ± SD for continuous variables (median values were added in cases of skewed distribution of continuous data) and as absolute frequencies or percentages for categorical variables. Distribution of EGMs voltage amplitude with either catheter was evaluated using violin type plots, histograms and reported as median, 5 and 95th percentiles. Comparison between the catheters was performed using the two-sample t-test with unequal variances and the Wilcoxon rank-sum test, as appropriate. Proportion of abnormal EGMs in scar tissue was compared using Fisher’s exact test. Inter-observer and intra-observer variability in EGM classification were quantified using the kappa statistic, which measures agreement between observers while accounting for chance. A P-value of <0.05 was considered statistically significant. Statistical analyses were performed with Stata/MP, version 15 (StataCorp, College Station, TX, USA). Results Mapping performance Mapping performance was compared separately for normal (n = 4) and infarcted (n = 8) ventricles. The number of EGMs acquired per beat was higher with investigational catheter compared with standard catheter in both normal ventricles (12.8 ± 1.1 vs. 4.5 ± 1.7 EGM/beat; P < 0.001) and ventricles with healed infarction (10.6 ± 2.1 vs. 3.8 ± 0.3 EGM/beat; P = 0.001). Electrogram acquisition rate was faster with the investigational catheter (normal: 814 ± 126 vs. 148 ± 58 EGM/min, P = 0.015; infarct: 355 ± 198 vs. 174 ± 84; P = 0.005). The overall mapping time required to achieve a complete map was shorter with the investigational catheter (normal: 5.3±0.9 vs. 12.1 ± 2.3 min, P = 0.015; infarct: 14.8 ± 7.5 vs. 20.4 ± 11.0 min, P = 0.29). The number of EGMs per map was higher with the investigational catheter (normal LV: 4202 ± 962 vs. 2255 ± 898, P = 0.024; infarcted LV: 4941 ± 1915 vs. 3297 ± 1232; P = 0.001). Electrogram density was also higher (normal LV: 38 ± 10.3 vs. 20.9 ± 10.4 EGM/cm2, P = 0.02; infarcted LV: 29.1 ± 11.3 vs. 19.6 ± 7.7 EGM/cm2; P = 0.005). Table 1 details the difference in mapping performance between the catheters in healthy and infarcted myocardium. Figure 2 shows violin plots comparison of EGM acquisition data for each catheter. Figure 2 Open in new tabDownload slide Electrogram acquisition properties in normal ventricle. Comparison of electrogram acquisition performance with the investigational and the standard in normal ventricles. Data are shown in violin plots for visualizing the distribution of data. The blue box represents the 25–75th percentiles, and the white dot represents the median and the extending line representing the 10–90th percentiles. Figure 2 Open in new tabDownload slide Electrogram acquisition properties in normal ventricle. Comparison of electrogram acquisition performance with the investigational and the standard in normal ventricles. Data are shown in violin plots for visualizing the distribution of data. The blue box represents the 25–75th percentiles, and the white dot represents the median and the extending line representing the 10–90th percentiles. Table 1 Electrogram acquisition properties . Normal LV . Post-infarct LV . Surface area (cm2) 111.9 ± 11.4 161.7 ± 34.2 Investigational Standard P-value Investigational Standard P-value EGMs per map 4202 ± 962 2255 ± 898 0.024 4941 ± 1915 3297 ± 1232 0.001 Mapping time (min) 5.3 ± 1.0 12.05 ± 2.2 0.015 14.82 ± 7.53 20.37 ± 10.95 0.29 Acquisition rate (EGM/min) 814 ± 126 148 ± 58 0.015 355 ± 198 174 ± 84 0.03 Acquisition density (EGM/cm2) 38 ± 10.3 20.9 ± 10.4 0.02 29.1 ± 11.3 19.6 ± 7.7 0.005 Single-beat acquisition (EGM/beat) 12.8 ± 1.1 4.5 ± 1.7 >0.001 10.6 ± 2.1 3.8 ± 0.3 0.001 Catheter-induced ectopy rate (b.p.m.) 13.4 ± 2.3 12.4 ± 0.7 0.537 – – – . Normal LV . Post-infarct LV . Surface area (cm2) 111.9 ± 11.4 161.7 ± 34.2 Investigational Standard P-value Investigational Standard P-value EGMs per map 4202 ± 962 2255 ± 898 0.024 4941 ± 1915 3297 ± 1232 0.001 Mapping time (min) 5.3 ± 1.0 12.05 ± 2.2 0.015 14.82 ± 7.53 20.37 ± 10.95 0.29 Acquisition rate (EGM/min) 814 ± 126 148 ± 58 0.015 355 ± 198 174 ± 84 0.03 Acquisition density (EGM/cm2) 38 ± 10.3 20.9 ± 10.4 0.02 29.1 ± 11.3 19.6 ± 7.7 0.005 Single-beat acquisition (EGM/beat) 12.8 ± 1.1 4.5 ± 1.7 >0.001 10.6 ± 2.1 3.8 ± 0.3 0.001 Catheter-induced ectopy rate (b.p.m.) 13.4 ± 2.3 12.4 ± 0.7 0.537 – – – EGM, electrogram; LV, left ventricle. Open in new tab Table 1 Electrogram acquisition properties . Normal LV . Post-infarct LV . Surface area (cm2) 111.9 ± 11.4 161.7 ± 34.2 Investigational Standard P-value Investigational Standard P-value EGMs per map 4202 ± 962 2255 ± 898 0.024 4941 ± 1915 3297 ± 1232 0.001 Mapping time (min) 5.3 ± 1.0 12.05 ± 2.2 0.015 14.82 ± 7.53 20.37 ± 10.95 0.29 Acquisition rate (EGM/min) 814 ± 126 148 ± 58 0.015 355 ± 198 174 ± 84 0.03 Acquisition density (EGM/cm2) 38 ± 10.3 20.9 ± 10.4 0.02 29.1 ± 11.3 19.6 ± 7.7 0.005 Single-beat acquisition (EGM/beat) 12.8 ± 1.1 4.5 ± 1.7 >0.001 10.6 ± 2.1 3.8 ± 0.3 0.001 Catheter-induced ectopy rate (b.p.m.) 13.4 ± 2.3 12.4 ± 0.7 0.537 – – – . Normal LV . Post-infarct LV . Surface area (cm2) 111.9 ± 11.4 161.7 ± 34.2 Investigational Standard P-value Investigational Standard P-value EGMs per map 4202 ± 962 2255 ± 898 0.024 4941 ± 1915 3297 ± 1232 0.001 Mapping time (min) 5.3 ± 1.0 12.05 ± 2.2 0.015 14.82 ± 7.53 20.37 ± 10.95 0.29 Acquisition rate (EGM/min) 814 ± 126 148 ± 58 0.015 355 ± 198 174 ± 84 0.03 Acquisition density (EGM/cm2) 38 ± 10.3 20.9 ± 10.4 0.02 29.1 ± 11.3 19.6 ± 7.7 0.005 Single-beat acquisition (EGM/beat) 12.8 ± 1.1 4.5 ± 1.7 >0.001 10.6 ± 2.1 3.8 ± 0.3 0.001 Catheter-induced ectopy rate (b.p.m.) 13.4 ± 2.3 12.4 ± 0.7 0.537 – – – EGM, electrogram; LV, left ventricle. Open in new tab Ectopy rate was similar between the investigational and standard catheters (13.4 ± 2.3 vs. 12.4 ± 0.7 ectopic events per minute, P = 0.537). In addition, catheter manoeuvrability in the ventricle, through the aortic valve, and in the mitral apparatus including the papillary muscles appeared to be similar to the standard catheter. The intra-observer and inter-observer variability was good with kappa values of 0.76 and 0.72, respectively. Electrogram characteristics in the healthy ventricle A total of 13 676 and 6268 EGMs were acquired in four normal LVs with investigational and standard catheters, respectively. Supplementary material online, Table S1 details the unipolar and bipolar EGM characteristics. Unipolar voltage amplitude was fundamentally similar, but statistically slightly lower with the investigational catheter [9.1 ± 3.9 mV (median, 8.7) vs. 10.5 ± 3.9 mV (median, 10.1); P < 0.001]. Bipolar voltage amplitude was similar between the investigational and the standard catheter [4.3 ± 2.6 mV (median, 3.66) vs. 4.5 ± 3.2 mV (median, 3.68); P = 0.265, respectively]. The 5th percentile of the bipolar voltage distribution was also comparable between the catheters (investigational: 1.34 mV; standard: 1.31 mV). Based on these results, the established definition for normal ventricular endocardial bipolar voltage amplitude at ≥1.5 mV was preserved.14 Bipolar EGM duration was shorter with the investigational catheter [33.1 ± 11 ms (median, 33) vs. 39.6 ± 12 ms (median, 40); P < 0.001]. Electrogram shape was similar between the catheters exhibiting a predominantly tri-phasic pattern in both unipolar and bipolar configurations. Figure 3 shows comparison of unipolar voltage amplitude and bipolar voltage amplitude with EGM examples. Figure 3 Open in new tabDownload slide EGM amplitude distribution in normal ventricle. The unipolar voltage amplitude (left) and bipolar voltage amplitude (right) were similar in the healthy left ventricle. Data are shown in violin plots for visualizing the distribution of EGM amplitudes. Representative EGMs are shown in the corresponding lower panels at similar gain and with scale. Note that EGM duration recorded with the investigational catheter is shorter. EGM, electrogram; LV, left ventricle. Figure 3 Open in new tabDownload slide EGM amplitude distribution in normal ventricle. The unipolar voltage amplitude (left) and bipolar voltage amplitude (right) were similar in the healthy left ventricle. Data are shown in violin plots for visualizing the distribution of EGM amplitudes. Representative EGMs are shown in the corresponding lower panels at similar gain and with scale. Note that EGM duration recorded with the investigational catheter is shorter. EGM, electrogram; LV, left ventricle. Electrogram characteristics in ventricles with healed infarction The endocardial surface area of the infarction was similar between the investigational and standard catheters (25.7 ± 9.7 vs. 23.7 ± 7.3 cm2, respectively, P = 0.12). Moreover, the surface area of very low bipolar voltage amplitude (<0.5 mV, considered ‘confluent scar’) was also similar between the investigational and standard catheters (13.8 ± 11.5 vs. 11.7 ± 7.0 cm2, P = 0.42). Similar to the observation in normal ventricles, unipolar voltage amplitude was fundamentally similar; however, statistically slightly lower with the investigational catheter [5.2 ± 1.9 (median 5.2) vs. 5.6 ± 2.1 mV (median 5.5), P = 0.04]. Bipolar voltage amplitude was similar between the investigational and standard catheters [1.0 ± 0.9 (median, 0.7) vs. 0.9 ± 0.8 mV (median, 0.7), P = 0.44]. Figure 4 shows the unipolar and bipolar voltage distributions within the infarct with both catheters. Supplementary material online, Table S1 compares the voltage distribution between the catheters. Figure 4 Open in new tabDownload slide Electrogram amplitude distribution in left ventricular scar. Unipolar and bipolar voltage amplitude distributions in the left ventricular infarct region. The upper panels show the data distribution in violin plots. Histograms are shown in lower panels. Figure 4 Open in new tabDownload slide Electrogram amplitude distribution in left ventricular scar. Unipolar and bipolar voltage amplitude distributions in the left ventricular infarct region. The upper panels show the data distribution in violin plots. Histograms are shown in lower panels. While voltage distribution within the infarct was similar between the catheters, the absolute and relative number of EGMs displaying local abnormal ventricular electrogram was greater with the investigational catheter [53 ± 16% (2931/5428 scar EGMs) vs. 34 ± 16% (810/2382 scar EGMs), P = 0.03]. Figure 5 shows a representative example of anterior wall infarction and EGMs mapped with both catheters. Supplementary material online, Figure S1 shows comparison of voltage maps created with both catheters for all swine with LV infarction. Figure 5 Open in new tabDownload slide Local characteristics in left ventricular scar. The left and right panels show voltage map of a left ventricle with healed anterior wall infarction in a left anterior oblique view. The bipolar voltage colour scale ranges from 0.1 (red) to 1.5 mV (purple). The highlighted rectangles show a higher magnification of a similar region recorded with the investigational (left) and the standard (right) catheters. Each dot in the higher magnification window represents a single electrogram. From each region, 16 representative electrograms are shown in the lower panels. Each electrogram (red tracing) is accompanies by a surface V1 ECG lead (blue tracing). Rectangles filled in pink colour represent electrograms with a high-frequency LAVA. Note the larger proportion of LAVAs observed with the investigational in comparison to the standard catheter. Electrograms have similar gain. ECG, electrocardiogram; LAVA, local abnormal ventricular electrogram. Figure 5 Open in new tabDownload slide Local characteristics in left ventricular scar. The left and right panels show voltage map of a left ventricle with healed anterior wall infarction in a left anterior oblique view. The bipolar voltage colour scale ranges from 0.1 (red) to 1.5 mV (purple). The highlighted rectangles show a higher magnification of a similar region recorded with the investigational (left) and the standard (right) catheters. Each dot in the higher magnification window represents a single electrogram. From each region, 16 representative electrograms are shown in the lower panels. Each electrogram (red tracing) is accompanies by a surface V1 ECG lead (blue tracing). Rectangles filled in pink colour represent electrograms with a high-frequency LAVA. Note the larger proportion of LAVAs observed with the investigational in comparison to the standard catheter. Electrograms have similar gain. ECG, electrocardiogram; LAVA, local abnormal ventricular electrogram. Correlation between voltage map and late gadolinium enhancement Four animals with chronic anterior infarction underwent in vivo CMR before the electrophysiological mapping procedure. The mean endocardial surface area of LGE was 24.8 ± 7.5 cm2, consistent with the surface area of low voltage (<1.5 mV) as measured with both catheters. While the sample size precluded meaningful correlation analysis, voltage distribution appeared to compare well with subendocardial LGE distribution. Figure 6 shows two examples: first, an LV with a confluent area of endocardial low voltage (upper panel) and second, an LV with heterogenous area of low voltage interspersed with areas of higher voltage amplitude (lower panel). The LGE maps of the endocardium and subendocardium (2-mm inner layer) corresponded to the bipolar voltage maps obtained with either catheters. These data suggest that both catheters produce maps with fair representation of subendocardial scar distribution. Figure 6 Open in new tabDownload slide Correlation between bipolar voltage and LGE. Upper panel: in confluent subendocardial scar, mapping with both catheters showed a homogenous low-voltage area (A and B). These areas correlated with subendocardial LGE (C). The colour coding in C is binary where yellow represents LGE and blue represents absence of LGE. (D) The LGE imaging data are shown. (E) The LGE maps of midmyocardium and the epicardium are shown. The lower panel shows an example of heterogenous scar. Note the similar voltage distribution between the catheters and a good correspondence to subendocardial LGE. However, the LGE map of the midmyocardial to epicardial layer shows a more extensive scar that was not depicted by voltage mapping. LGE, late gadolinium enhancement; LV, left ventricular. Figure 6 Open in new tabDownload slide Correlation between bipolar voltage and LGE. Upper panel: in confluent subendocardial scar, mapping with both catheters showed a homogenous low-voltage area (A and B). These areas correlated with subendocardial LGE (C). The colour coding in C is binary where yellow represents LGE and blue represents absence of LGE. (D) The LGE imaging data are shown. (E) The LGE maps of midmyocardium and the epicardium are shown. The lower panel shows an example of heterogenous scar. Note the similar voltage distribution between the catheters and a good correspondence to subendocardial LGE. However, the LGE map of the midmyocardial to epicardial layer shows a more extensive scar that was not depicted by voltage mapping. LGE, late gadolinium enhancement; LV, left ventricular. However, the voltage maps did not compare well with LGE maps rendering the volume between the midmyocardium to epicardium (2 mm to outermost layer). This highlights the relatively shallow depth of view of endocardial mapping that is a weakness of all current day mapping systems and multielectrode catheters. Ventricular tachycardia mapping A total of 17 sustained monomorphic VTs were induced in seven swine with healed myocardial infarction (in one swine VT could not be induced). The number of VT configurations per heart was 2.1 ± 1.7 (median, 1.5) and the CL was 261 ± 15 ms. Of the 17 VTs, 13 (77%) were not haemodynamically stable and terminated by pacing or cardioversion. Twelve VTs were mapped (four haemodynamically tolerated and eight not tolerated). The mapping time of tolerated VTs was 18.2 ± 6.4 min (median, 19.75 min) and the mapping time of the non-tolerated VTs was 0.9 ± 0.3 min (median, 0.73 min). The EGM acquisition rate was similar between tolerated and non-tolerated VTs [29.2 ± 12.3 EGM/beat (median, 35.6 EGM/beat) vs. 21.0 ± 10.4 EGM/beat (median, 21.3 EGM/beat); P = 0.456, respectively]. Figure 7 shows examples of haemodynamically stable and unstable VT. Note that even in an unstable VT, 18 s of mapping time (from first to last recorded EGM) were sufficient to collect large number of EGMs and to identify the diastolic pathway. This partially related to pre-emptive placement of the catheter in the area of interest before induction. Since mapping time during VT is often limited due to haemodynamic instability, only the investigational catheter was using for VT mapping. Figure 7 Open in new tabDownload slide Activation mapping in stable and unstable VT. Two representative examples of VT activation maps created with the investigational catheter. Upper panel: The left pane shows activation map of a stable VT with a mapping time of 21:31 min. A shadow of the investigational catheter is shown over the isthmus with its corresponding diastolic EGMs (arrow). The middle and left panels show the activation and voltage maps, respectively during RV pacing. Lower panel: example of an unstable VT that required early termination by cardioversion. Note that even with 18 s of mapping time, 1975 EGMs were collected. The investigational catheter is shown over the isthmus with its corresponding diastolic EGMs (arrow). Note that the VT isthmuses colocalized with area of discontinuous activation as identified during RV pacing. This knowledge facilitated positioning of the catheter at these locations before induction of arrhythmia, allowing high-yield data acquisition. EGM, electrogram; RV, right ventricular; VT, ventricular tachycardia. Figure 7 Open in new tabDownload slide Activation mapping in stable and unstable VT. Two representative examples of VT activation maps created with the investigational catheter. Upper panel: The left pane shows activation map of a stable VT with a mapping time of 21:31 min. A shadow of the investigational catheter is shown over the isthmus with its corresponding diastolic EGMs (arrow). The middle and left panels show the activation and voltage maps, respectively during RV pacing. Lower panel: example of an unstable VT that required early termination by cardioversion. Note that even with 18 s of mapping time, 1975 EGMs were collected. The investigational catheter is shown over the isthmus with its corresponding diastolic EGMs (arrow). Note that the VT isthmuses colocalized with area of discontinuous activation as identified during RV pacing. This knowledge facilitated positioning of the catheter at these locations before induction of arrhythmia, allowing high-yield data acquisition. EGM, electrogram; RV, right ventricular; VT, ventricular tachycardia. Discussion This study examined a new multielectrode mapping catheter with an increased number of splines, increased total number of electrodes, and reduced electrode surface area in comparison to a standard multielectrode catheter. We evaluated the utility and limitations of this catheter for mapping ventricles with scar in a swine model of healed infarction. The investigational catheter increased the mapping speed and EGM density in comparison to the standard multielectrode catheter. This expected finding results from the higher number EGMs acquired at each beat. The higher mapping speed was particularly helpful for mapping haemodynamically unstable VTs. The apparent mapping resolution was similar between the investigational and the standard catheter. Infarcts exhibited similar voltage amplitude distribution that corresponded well with subendocardial scar identified by LGE. This finding suggests that endocardial mapping resolution may plateau at electrode size ≤1 mm. Previous studies that compared multielectrode mapping catheters with linear ablation catheters in a similar model of healed infarction found that multielectrode catheters were able to identify surviving myocardial bundles that were not recognized by ablation catheters.5,14 These data were also validated in humans with atrial and ventricular arrhythmias15,16 and have led to the emergence of high-resolution mapping technologies and development of new catheters with progressively smaller electrodes and shorter interelectrode spacing. However, multiple other factors including catheter orientation, contact angle, conduction velocity, and catheter design also have a significant influence on EGM morphology and amplitude. One significant factor in mapping resolution is the design and location of the electrodes in respect to one another. In a bipolar catheter, two electrodes lie at a certain distance from each other, which inevitably causes the electrodes to sense the activation wave at different times depending on the catheter orientation and on the interelectrode spacing, with a greater spacing leading to a greater difference between the times at which the activation wave arrives at each electrode. Moreover, at contact angles greater than 0° (where 0° is parallel to the tissue and 90° is perpendicular to the tissue), the signal intensity is stronger at the distal electrode than at the proximal electrode and the difference in timing between the electrodes diminishes, which results in a lower voltage amplitude and an EGM shape resembling a unipolar potential (which is also less dependent on wavefront direction). In the case of reduced conduction velocity (including in scar), the difference between the times at which the wave arrives at the electrodes increases; however, at the same time, the magnitude of signal overlap between them also increases, which conversely results in a larger degree of cancellation and an even further reduced voltage amplitude.17–19 These observations underscore the complex relationship between catheter design and voltage amplitude and may explain why reducing the electrode size in a similar catheter design may have limited effect on mapping resolution. In this regard, a difference in mapping resolution may be explained by the design of the multielectrodes. For example, the difference in mapping resolution between the Thermocool and Pentaray catheters may largely be related to the difference in catheter design, and particularly to the relationship between the proximal and distal electrodes. In comparison to the Thermocool catheter, the proximal electrode of the Pentaray is more likely to have a lower angle (parallel to the tissue) and thus be in better contact with the tissue. This results in higher voltage amplitude and increased ability to identify low amplitude potentials. In contrast, the standard Pentaray and the investigational Octaray have a similar mapping resolution. The similar design between these two catheters may explain the similar mapping resolution between them, despite the smaller electrodes of the latter. Lastly, while both the standard and the investigational catheters had similar sensitivity to identify endocardial and subendocardial scar compared with CMR, neither was adequately sensitive to describe transmural scar distribution. In this respect, Rottmann20 have shown that in a computer model roughly 90% of the voltage amplitude derives from the closest 1 mm layer, highlighting the limitations of EAM to define the intramural substrate. Limitations In this study, we used an established human-like model of subendocardial infarction and VT. Previous studies have shown good correlation between scar distribution in swine and humans with healed infarction; however, this data require further validation in humans with infarction at different territories. The findings of this study are specific for this particular catheter design. In this regard, this new catheter shares similar challenges in catheter manoeuvrability as the Pentaray. Conclusions The rapid emergence of high-resolution mapping technologies including multielectrode catheters has derived from both an intellectual necessity to gain better insights into mechanisms and a clinical need to expedite mapping time. This new multielectrode mapping catheter increases the number of EGMs that can be acquired at each beat from 20 to 48. It produces higher density maps that can be made faster and improve the ability to identify near-field abnormal potentials that may be useful for guiding ablation. Funding This study was funded by Biosense Webster. However, the funding entity was not involved in the data analysis and in the writing of this manuscript. Conflict of interest: E.A. has received research grants from Biosense Webster, Boston Scientific, Itamar Medical, and Affera Inc. All other authors have no conflicts of interest relevant to this study. References 1 Marchlinski FE , Callans DJ , Gottlieb CD , Zado E. 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TI - A novel multielectrode catheter for high-density ventricular mapping: electrogram characterization and utility for scar mapping
JF - EP Europace
DO - 10.1093/europace/euz364
DA - 2020-03-01
UR - https://www.deepdyve.com/lp/oxford-university-press/a-novel-multielectrode-catheter-for-high-density-ventricular-mapping-1BzW0l5Zt2
SP - 440
VL - 22
IS - 3
DP - DeepDyve
ER -