++
The ECG inverse solution can be applied to aid catheter ablation of scar-related VT, which is still one of the most challenging procedures in clinical electrophysiology. The majority of these tachycardias are poorly tolerated or difficult to induce, and they frequently transform to other tachycardia morphologies.24 Successful ablation of scar-related VT requires an understanding of its mechanism and of the underlying electroanatomic substrate. Such insight can be partly achieved by percutaneous endocardial or epicardial mapping with a single catheter, which is steered to multiple sites to define the substrate for arrhythmia during sinus rhythm.25-27 However, this alone is often not sufficient for predicting successful ablation sites; some tachycardias are "unmappable" with point-by-point mapping, and alternative methods for identifying exit sites for these tachycardias have to be sought.28 One of the frequently used methods is pace mapping in the peri-infarct zone.29 Our objective here was to investigate how BSPM and the ECG inverse solution, in conjunction with pace mapping, can be used to facilitate radiofrequency ablation of scar-related VT.
+++
Three-Dimensional Electroanatomic Mapping
++
Catheter mapping and ablation were revolutionized by electroanatomic mapping. The CARTO electroanatomic mapping system (Biosense Webster, Inc., Diamond Bar, CA) employed in this study uses a magnetic sensor in the catheter tip to detect its location in the magnetic field created by magnets placed beneath the patient, and a triangulated ventricular surface is displayed by a system (see Fig. 12–8), allowing visualization of various electrical measurements in real time.24,30 This system can be used to perform sinus rhythm voltage mapping, which involves sampling of the endocardial or epicardial bipolar electrograms recorded from an electrode catheter at multiple locations.25 Low-amplitude bipolar electrograms have been shown to correspond to infarcted myocardium, with amplitudes typically less than 0.5 mV over the dense scar.27 The CARTO system can also perform activation mapping, which annotates the anatomic construct with local activation times.25
++
The limitations of point-by-point mapping of activation sequences have led to the development of pace mapping methods for assessing the location of the mapping catheter relative to the reentry circuit.31-33 The procedure involves successive stimulation at various sites and comparing the paced QRS patterns with the template pattern of the clinical VT. Distinct patterns of BSPM distributions were observed for ectopic ventricular activation sequences initiated at various endocardial pacing sites for patients with idiopathic VT,34 as well as for patients who have had a prior myocardial infarction.33,35
++
Propagation of electrical activation in the diseased myocardium is discontinuous, and small differences in the pacing site can induce different propagation patterns and resulting QRS complexes.31,33 Nevertheless, the pacing from a catheter located near the exit of a reentry circuit of VT usually produces a QRS morphology similar to that of VT, with a short stimulus-to-QRS delay.36 Pacing that produces a QRS matching VT after a delay (stimulus-to-QRS interval >40 ms) has been shown to mark a site in a reentry channel within an infarct scar that is considered a good candidate for ablation.36 Trying to approach the exit site using sequential pace mapping can be challenging and requires an intuitive interpretation of the 12-lead ECG. We hypothesized that this process could be aided by BSPM and ECG imaging.
++
Some intraoperative studies involving endocardial and epicardial mapping have shown that scar-related VT does not always arise in the subendocardium.37-40 This evidence was further supported by studies using hearts explanted from patients who have had a myocardial infarction.41 VTs in which epicardial breakthrough preceded the earliest endocardial activity were reported,39 and some were successfully terminated by an epicardially directed procedure.38,42,43 Sosa et al44 described subxiphoid access to the pericardial space for mapping and ablation; this approach was used in the study reported here.
++
The case presented here was referred for ablation of scar-related VT to the Cardiac Electrophysiology Laboratory of the Queen Elizabeth II Health Sciences Centre in Halifax. The patient (age, 64 years) had a history of severe ischemic cardiomyopathy. Previous VT storms were resistant to drug therapy and were treated with VT ablation in 2003 and 2005. Several morphologies of VT from the patient's study in 2005 suggested an epicardial origin of arrhythmia. In 2007, the patient presented with incessant slow VT (with two distinctly different morphologies, denoted VT A and VT B). A cardiac resynchronization therapy defibrillator (CONTAK RENEWAL 3 RF; Boston Scientific, Natick, MA) had been implanted, and the patient was chronically paced. After written informed consent and detailed explanation of the procedure, the patient underwent a successful ablation of both VTs in June 2007.
++
The detections on the implantable cardioverter defibrillator (ICD) were deactivated prior to the ablation procedure, which was performed under general anesthesia. The groins were infiltrated with 2% lidocaine without epinephrine; 5- and 6-French sheaths were inserted percutaneously into the right femoral vein, and an 8-French sheath was inserted percutaneously into the right femoral artery. To gain access to the pericardial space, a Weiss needle was advanced below the xiphoid process to the pericardium under fluoroscopic guidance. A wire was then inserted into the pericardial space, a tract was progressively dilated with 6- and 8-French dilators, and an 8.5-French convoy sheath was advanced to the pericardial space. A 6-French hexapolar catheter was advanced to the right ventricular apex. A Navistar Thermocool F-curve catheter (Biosense Webster) was introduced into the pericardial space via the convoy sheath and used for epicardial mapping. The same catheter was later introduced into the left ventricle via the retrograde aortic approach and used for endocardial mapping and ablation.
++
BSPM data were collected during sinus rhythm, ICD pacing, roving catheter pacing, and VT. Multipoint catheter mapping and pacing were performed by the CARTO electroanatomic mapping system (Biosense Webster) using the Navistar Thermocool catheter. Bipolar and unipolar electrograms were recorded both by the CARTO system and by the GE Cardiolab system (GE Healthcare, Piscataway, NJ). The time delay was determined from the 12-lead ECG on the GE Cardiolab system; a stimulus-QRS interval >40 ms was referred to as delay.45
++
ECGs were processed as described earlier in the "Body Surface Potential Mapping" section. The patient-specific geometry of the torso and epicardial surface was extracted from the CT data, the transfer matrix, A, was calculated, and the inverse solution was obtained by means of a second-order Tikhonov regularization with the L-curve method used to determine the regularization parameter as described earlier in the "Forward and Inverse Problems of ECG" section and in Appendices A and B. MAP3D visualization software46 was used to display potential distributions on epicardial and torso surfaces.
++
The gold standard for assessing the accuracy of the inverse solution was the information collected by the CARTO electroanatomic mapping system during the ablation procedure. The patient-specific CARTO geometry was registered manually and fused with the CT data, as illustrated in Fig. 12–7. The locations of the CARTO sites where pacing was delivered and the estimated locations of these sites obtained by the inverse solution were compared to determine localization accuracy. CARTO voltage mapping was performed to delineate the scar and scar margin.
++
+++
Reference Maps Delineating Scar Region
++
Figure 12–8 shows the epicardial voltage substrate maps obtained with the CARTO system. These maps delineate electroanatomic substrate by using color mapping to annotate bipolar signal amplitude (30-400 Hz) that distinguishes between normal myocardium, infarct scar, and border zone around scarred tissue. Regions of low-amplitude signal appear on the anterolateral left ventricle and over the lateral right ventricular wall. Moderate-size patches of confluent scar cover the midsection of the lateral left ventricle.
++
+++
Localization of Epicardial Pacing Sites by Inverse Solution
++
Pacing on the epicardial surface initially produces epicardial potential distributions with an area of negative potentials surrounding the pacing site, along with two areas of low-level positive potentials due to conduction anisotropy at the stimulation site, as demonstrated in vivo using dense electrode arrays.47 By using BSPM recordings obtained during epicardial pace mapping (n = 22), we tested the accuracy of the inverse solution in localizing the epicardial stimulation site by comparing the calculated location of the potential minimum with the known location of epicardial pacing determined by the CARTO system. Figure 12–9 shows, for an epicardial pacing site at the basal inferior left ventricle, computed epicardial potential maps at four instants of time, with corresponding input data (recorded body surface potential maps, also shown for both the anterior and posterior torso in Fig. 12–3). The initial minimum on the epicardial surface (of –0.96 mV, near the pacing site) with an area of negative potentials that surround it is discernible after a long delay at 124 ms after pacing stimulus. At peak depolarization, the potential minimum drifts far from the pacing site. During early repolarization, at 275 ms, a low-amplitude maximum (0.347 mV) of epicardial potentials appears again in close proximity to the pacing site. With the insight provided by epicardial maps, measured BSPM distributions (see both Fig. 12–3 and top of Fig. 12–9) seem to be compatible with epicardial-to-endocardial direction of activation initiated on the inferior wall of the left ventricle (as evidenced by the equivalent dipole pointing straight up at 124 ms).
++
++
The results for pacing site localization by means of the inverse solution for all (n = 22) epicardial pacing sites of this patient are summarized in Fig. 12–10, which shows, in four views (corresponding to electroanatomic substrate maps in Fig. 12–8), the actual pacing sites, plotted from coordinates provided by the CARTO system, and the estimates of the location of these sites obtained by the inverse solution. The electroanatomic substrate around each pacing site was characterized by the bipolar voltage detected by the CARTO system and by the delay in response to pacing.
++
++
We found, not surprisingly, that the electroanatomic substrate around the pacing site affected localization accuracy. For the group of pacing sites in structurally normal myocardium with no delay (n = 7), the median Euclidean distance between the actual and estimated pacing site was just 11 mm, and the potential minimum appeared after a mean interval of 29 ms following the pacing spike. For pacing in scar and scar margin—which implied involvement of the scar substrate in modifying early activation sequence—the discrepancy was larger, but it did not exceed 35 mm.
+++
Localization of ICD Pacing Site by Inverse Solution
++
Localizing the paced activation initiated from the leads of the ICD device provides another approach to testing the localization accuracy of the inverse solution because the tip of the ICD lead can be accurately determined from the CT images. The BSPM recording was done during pacing from an ICD device implanted in another patient, also recruited under scar-related VT study, who had an ICD pacing electrode in the endocardial right ventricular apex.
++
The epicardial potential maps obtained for early activation by the inverse solution (Fig. 12–11) provided a clue for estimating the site of pacing. Because the ICD pacing site was on the right ventricular endocardial surface, the activation wave front propagated first across the right ventricular wall before it broke through on the epicardial surface. Thus, an area of positive potentials appeared initially near the pacing site, reflecting propagation of the wave front toward the epicardial surface, and then, after the breakthrough, an area of negative potentials emerged and intensified throughout depolarization and was replaced by a distribution with opposite polarity during repolarization. The Euclidean distance between the actual location of an endocardial pacing electrode and the location of the early minimum on the epicardial surface was 12 mm. This small discrepancy can be attributed either to the involvement of right ventricular conduction system or to the anisotropic intramural propagation, or to both.
++
+++
Activation Times Obtained by Inverse Solution
++
To assess the inverse solution's ability to preserve timing information, the activation time was determined by the CARTO system from bipolar electrograms at multiple points on the epicardial surface by the roving catheter, whereas the ICD device paced at the endocardial site near the right ventricular apex. The epicardial surface reconstructed from measurements made by the CARTO system was aligned with the epicardial surface reconstructed from the CT scan, and CARTO points were projected onto the nearest nodes of this patient-specific epicardial surface. Figure 12–12 shows the activation times at all nodes of this surface as estimated by three-dimensional interpolation from data provided by the CARTO system. The activation time obtained via the inverse solution was determined in each calculated epicardial electrogram by the steepest-descent criterion during depolarization; the isochronal maps obtained by this method are shown in Fig. 12–13.
++
++
++
The activation times yielded by the CARTO system show early depolarization of the right ventricular apex (red) and the activation wave spreading over the right ventricular anterior wall in approximately 100 ms (see Fig. 12–12, left); the latest area to activate (purple) is the basal region of the posterior left ventricle (see Fig. 12–12, right). The inverse-solution isochrones in Fig. 12–13 show a qualitatively similar spread of activation; the early activation of the right ventricular apical region, the progression of the activation wave over the right ventricular anterior wall and then the left ventricular posterior wall, and the latest activation of the posterobasal wall are all correctly estimated by the inverse solution. However, there is some discrepancy in the time scale, which reflects inability of the steepest-descent criterion to detect the activation wave front from low-amplitude electrograms in the region with depressed conduction.
+++
Localization of the Reentrant Circuit's Exit Site by Inverse Solution
++
The earliest region to depolarize during scar-related VT is the site where the reentry circuit exits the scar to reexcite normal myocardium and sustain the arrhythmia. Localizing these exit sites is essential during the ablation procedure to guide delivery of radiofrequency energy that interrupts the reentrant pathway. To evaluate the potential usefulness of inverse ECG in aiding radiofrequency ablation, we applied the methodology tested during paced activation to BSPM data recorded during VT.
++
The onset of reentrant activation can usually be determined from body surface ECGs (see Fig. 12–2), and the BSPM distribution observed during this phase can be used to estimate the locus of exit site from calculated epicardial potential distributions or activation isochrones.
++
Two separate morphologies of VT (denoted VT A and VT B) were recorded for this patient, and both tachycardias were successfully ablated. Figure 12–14 shows (in 20-ms increments) a sequence of body surface potential maps for VT A. Initial distributions (during the first 10 ms) have very low amplitudes; the first discernible pattern of body surface potentials with a maximum near precordial site of lead V4 develops at 11 ms, and this distribution remains stationary until nearly 70 ms; subsequently, the maximum migrates toward the right chest. The repolarization minimum near the site of V2 appears at approximately 250 ms and remains stationary until approximately 410 ms.
++
++
Epicardial potential distributions obtained by the inverse solution for VT A (Fig. 12–15A) show early negative potentials on the high basal inferior region (at 69 ms) near scar border zone; this area of negative potentials remains stationary during the depolarization phase (106 ms). A map of the isochrones of activation (Fig. 12–15B) shows earliest activation starting at the high inferobasal left ventricle in the region where the earliest potential minimum appeared. The isochronal map shows activation spreading in a counterclockwise direction around the area of block on the inferior epicardial surface, starting at the inferior left ventricular base and ending on the basal inferior and inferolateral right ventricle while the superior view of the isochronal map shows activation spreading globally from apex to base. The ablation site was endocardial; its projection on the epicardial surface (marked by asterisk) was located near the early potential minimum and the region of early activation.
++
++
Figure 12–16 shows (in 20-ms increments) a sequence of body surface potential maps for pacing from the endocardial site that can help to locate the site of successful ablation of VT A.
++