Postinfarction Ventricular Tachycardia Research Articles

Substrate Ablation of Post-infarction Ventricular Tachycardias

Substrate Ablation of Post-infarction Ventricular Tachycardias

Sinus Rhythm Targeting of Channels for Ablation of Postinfarction Ventricular Tachycardia

Scar-related reentry is the most common cause of sustained monomorphic ventricular tachycardia (VT) in patients with structural heart disease. These scars are comprised not only of dense fibrosis but also contain surviving myocyte bundles that support reentry. The separation of myocytes creates a circuitous path (zig-zag conduction) that slows conduction despite the presence of relatively normal action potential upstrokes.1,2 Gap junction remodeling and ion channel alterations may also contribute to slow conduction.3 After myocardial infarction, the scar evolves as part of the ventricular remodeling process, and acute reperfusion favorably influences this process. Article see p 90 Of 689 patients with acute ST elevation myocardial infarction who received acute percutaneous intervention for reperfusion reported by Zaman et al,4 only 17% had a left ventricular ejection fraction <40%, and of these, only 32 (≈5% of the total group) had inducible VT when studied early after the infarction. By 1 year, only 19% of the patients with inducible VT had spontaneous VT. Interestingly, the VTs that occurred spontaneously (a mean of 11 months after the infarct) were substantially slower as compared with those that were induced early after infarction. Thus, it seems likely that the ongoing remodeling efforts result in conduction slowing in or around the channels of surviving myocytes in the infarct that foster reentrant VT. The risk of VT may increase over years. The time between infarction and referral for VT ablation was an average of 16 years for patients who receive acute infarct reperfusion in one study.5 Once VT is clinically manifest, the reentry substrate is relatively stable, such that the risk of recurrence exceeds 40% by 2 years. An implantable defibrillator is protection against sudden death, but recurrent VT is associated with worse outcomes.6 Catheter ablation has an important role in reducing …

Primary Radiofrequency Ablation of Ventricular Tachycardia Early After Myocardial Infarction

Background— Ventricular tachycardia (VT) is a significant complication of myocardial infarction. Radiofrequency ablation for postinfarct VT is reserved for drug refractory VT or VT storms. Our hypothesis is that radiofrequency ablation in the early postinfarct period could abolish or diminish late recurrences of VT. Methods and Results— Myocardial infarct was induced by balloon occlusion of the left anterior descending artery in 35 sheep. The 25 survivors underwent programmed ventricular stimulation and electroanatomical mapping 8 days postinfarct. Animals with inducible VT (12 out of 25 animals) underwent immediate radiofrequency ablation. Further VT inductions were performed 100 and 200 days postinfarct. At day 8, 3.0±0.9 VT morphologies per animal were inducible. All were successfully ablated with 24±6 applications of radiofrequency energy. All had ablations on the left ventricular endocardium, and 67% had ablations on the right ventricular aspect of the interventricular septum. All targeted arrhythmias were successfully ablated acutely. One animal was euthanized because of hypotension from a serious pericardial effusion. The other 11 survived and remained arrhythmia free on subsequent inductions on the 100th and 200th days ( P &lt;0.001). The 13 animals without inducible VT remained noninducible at the subsequent studies. A historical control arm of 9 animals with inducible VT at day 8 remained inducible at day 100. Conclusions— Radiofrequency ablation on the eighth day after infarction abolished inducibility of VT at late induction studies ≤200 days in an ovine model. Early identification and ablation of VT after infarction may prevent or reduce late ventricular arrhythmias but needs to be validated in clinical studies.

Dissociated late potentials during sinus rhythm after radiofrequency ablation in a patient with postinfarction ventricular tachycardia

A 72-year-old man with ischemic cardiomyopathy was admitted for the treatment of ventricular tachycardia (VT). Because his VT was poorly tolerated hemodynamically, substrate mapping was performed. The map revealed the presence of low-voltage areas in the inferolateral wall of the LV. Late potentials (LPs) were recorded during sinus rhythm, and pacing at the site revealed a good pacemap for targeting the VT. Delivery of radiofrequency (RF) current to the area where LPs were recorded rendered the targeted VT noninducible. After RF delivery, dissociation of the LPs with an interval of 3140ms was documented during sinus rhythm.

Localizing the critical isthmus of postinfarct ventricular tachycardia: The value of pace-mapping during sinus rhythm

Most postinfarct ventricular tachycardias (VTs) are sustained by a reentrant mechanism. The "protected isthmus" of the reentrant circuit is critical for the maintenance of VTs and the target for catheter ablation. Various techniques based on conventional electrophysiology and/or detailed three-dimensional (3D) reconstruction of the VT circuit are used to unmask this isthmus. The purpose of this study was to assess pace-maps (PMs) to identify postinfarct VT isthmuses. We hypothesized that an abrupt change in paced QRS morphology may be used to identify a VT isthmus and be targeted for successful ablation. High-density 3D PMs were matched to the subsequent 3D endocardial reentrant VT activation mapping in 10 patients (8 men; age 70.7 ± 10.8 years) who underwent successful postinfarct VT ablation. At each pacing site in a given patient, the 12-lead ECG recorded during pacing was compared to that of VT, with the resulting matching percentage (up to 100% for perfect matches) allocated to this point to generate color-coded PMs. With respect to VT isthmuses, the best percentages of matching were found in the exit zones and isthmus exit part (89% ± 8% and 84% ± 7%, respectively) and the poorest adjacent to scar border in the outer entrance zones (23% ± 28%), in the entrance zones (39% ± 34%), and in the entrance part of the isthmus (32% ± 26%). The color-coded sequence (from the best to the poorest matching sites) on the PMs revealed figure-of-eight pictures matching the VT activation time maps and identifying VT isthmuses. Pace-mapping is useful for unmasking VT isthmuses in patients with well-tolerated postinfarct endocardial reentrant VTs.

Epicardial Ablation of Ventricular Tachycardia in Ischemic Heart Disease

Epicardial approaches have increased ablation success in nonischemic cardiomyopathy, but the use for postinfarction ventricular tachycardias (VT) is less clear. We report the findings for epicardial VT ablation in postinfarct patients. Records of 444 consecutive patients with VT because of prior infarction referred for 600 catheter ablation procedures were reviewed. Epicardial procedures were performed in the electrophysiology laboratory in 56 (13%) patients using percutaneous (43 patients) or surgical (13 patients) epicardial access. In 7 patients, epicardial ablation was performed surgically in the operating room. In the electrophysiology laboratory epicardial VT targets were identified in 38 (68%) patients and epicardial ablation abolished ≥1 VT in 27 patients (6% of the total study population); inducibility was not tested after ablation in 4, and VT remained inducible in 7 patients. No ablation was performed in 18 (32%) patients because of no accessible epicardial target or a complication. Major complications occurred in 8 (14%) of the 57 electrophysiology laboratory procedures. After the first procedure any VT recurred in 21 (54%) of 39 patients who had epicardial ablation compared with 164 (47%) of 347 endocardial-only ablation patients (P=0.35). Epicardial ablation is potentially useful in ≥6% of the postinfarction VT population, but the number could be substantially greater because more than two thirds of patients selected for epicardial mapping after failed ablation had an epicardial VT target. Successful epicardial ablation of a VT was not predictable from infarct location or other patient characteristics.

Electrophysiologic characterization of local abnormal ventricular activities in postinfarction ventricular tachycardia with respect to their anatomic location

Local abnormal ventricular activities (LAVA) in patients with scar-related ventricular tachycardia (VT) may appear at any time during or after the far-field electrogram. Although they may be separated from the far-field signal by an isoelectric line and extend beyond the end of surface QRS, they may also appear fused or buried within the QRS. The purpose of this study was to characterize LAVA in postinfarction VT patients with respect to their anatomic locations. Thirty-one patients with postinfarction VT underwent mapping/ablation during sinus rhythm with a three-dimensional electroanatomic mapping system. From a total of 18,270 electrograms reviewed in all study subjects, 1104 LAVA (endocardium 839, epicardium 265) were identified and analyzed. The interval from onset of QRS complex to ventricular electrogram (EGM onset) on the endocardium was significantly shorter than the epicardium (P < .001). EGM onset was shortest in the septal endocardium and longest in the inferior and lateral epicardium. There was a significant positive correlation between EGM onset and LAVA lateness as estimated by the interval from surface QRS onset to LAVA (r = 0.52, P < .001). LAVA were more frequently detected after the QRS complex in the epicardium (241/265 [91%]) than in the endocardium (551/839 [66%], P < .001). Only 43% of endocardial septal LAVA were detected after the QRS complex. Lateness of LAVA is affected to a large extent by their locations. The chance of detecting late LAVA increases when electrogram onset is later. Substrate-based approach targeting delayed signals relative to the QRS complex may miss critical the arrhythmogenic substrate, particularly in the septum and other early-to-activate regions.

Ablation targets in reentrant ventricular tachycardia

Introduction Magnetic resonance imaging (MRI) with late gadolinium enhancement has been used to pinpoint myocardial infarction features in animal models. In swine postinfarction, this imaging technique has been used to identify areas with slow conduction during reentrant ventricular tachycardia (VT). In this model, the reentry isthmus is composed of a small volume of viable myocardium bounded by scar tissue laterally and at depth. During reentrant VT, arcs of conduction block form where scar is present. In proximity to the infarct, the enhanced MRI scan shows a mixture of electrically conducting viable myocardium and nonviable tissue where conduction is slow during VT. The region is termed the heterogeneous zone (HZ) and appears gray in the contrast-enhanced images, as compared with the white infarct scar and dark gray or black normal myocardium. More recently, the relationship between HZ characteristics and reentrant VT inducibility was shown in swine postinfarction. The authors tested the hypothesis that by ablating the HZ in its entirety, reentrant VT would no longer be inducible, whereas when ablation was incomplete, reentrant VT would still be inducible, though possibly with a differing reentrant circuit morphology. They found that only when the HZ was entirely ablated did the reentrant VT become noninducible. In a new study on this topic, published in this issue of HeartRhythm, the feasibility of using the contrastenhanced imaging in postinfarction VT patients to target arrhythmogenic regions before electrophysiologic (EP) study and radiofrequency ablation is assessed.

Postinfarction Ventricular Tachycardia Substrate Characterization: A Comparison Between Late Enhancement Magnetic Resonance Imaging and Voltage Mapping Using an MR-Guided Electrophysiology System

Catheter ablation of ventricular tachycardia (VT) is preceded by characterization of the myocardial substrate via electroanatomical voltage mapping (EAVM). The purpose of this study was to characterize the relationship between chronic myocardial fibrotic scar detected by multicontrast late enhancement (MCLE) MRI and by EAVM obtained using an MR-guided electrophysiology system, with a final aim to better understand how these measures may improve identification of potentially arrhythmogenic substrates. Real-time MR-guided EAVM was performed in six chronically infarcted animals in a 1.5T MR system. The MCLE images were analyzed to identify the location and extent of the fibrotic infarct. Voltage maps of the left ventricle (LV) were created with an average of 231 ± 35 points per LV. Correlation analysis was conducted between bipolar voltage and three MR parameters (infarct transmurality, tissue categorization into healthy and scar classes, and normalized relaxation rate R1). In general, tissue regions classified as scar by normalized R1 values were well correlated with locations with low bipolar voltage values. Moreover, our results demonstrate that MRI information (transmurality, tissue classification, and relaxation rate) can accurately predict areas of myocardial fibrosis identified with bipolar voltage mapping, as demonstrated by ROC analysis. MCLE can help overcome limitations of bipolar voltage mapping including long durations and lower spatial discrimination and may help identify the sites within scars, which are commonly believed to trigger arrhythmic events in postinfarction patients.

Regional Myocardial Wall Thinning at Multidetector Computed Tomography Correlates to Arrhythmogenic Substrate in Postinfarction Ventricular Tachycardia

Background— A majority of patients undergoing ablation of ventricular tachycardia have implanted devices precluding substrate imaging with delayed-enhancement MRI. Contrast-enhanced multidetector computed tomography (MDCT) can depict myocardial wall thickness with submillimetric resolution. We evaluated the relationship between regional myocardial wall thinning (WT) imaged by MDCT and arrhythmogenic substrate in postinfarction ventricular tachycardia. Methods and Results— We studied 13 consecutive postinfarction patients undergoing MDCT before ablation. MDCT data were integrated with high-density 3-dimensional electroanatomic maps acquired during sinus rhythm (endocardium, 509±291 points/map; epicardium, 716±323 points/map). Low-voltage areas (&lt;1.5 mV) and local abnormal ventricular activities (LAVA) during sinus rhythm were assessed with regard to the WT. A significant correlation was found between the areas of WT &lt;5 mm and endocardial low voltage (correlation- R =0.82; P =0.001), but no such correlation was found in the epicardium. The WT &lt;5 mm area was smaller than the endocardial low-voltage area (54 cm 2 [Q1–Q3, 46–92] versus 71 cm 2 [Q1–Q3, 59–124]; P =0.001). Among a total of 13 060 electrograms reviewed in the whole study population, 538 LAVA were detected and analyzed. LAVA were located within the WT &lt;5 mm (469/538 [87%]) or at its border (100% within 23 mm). Very late LAVA (&gt;100 ms after QRS complex) were almost exclusively detected within the thinnest area (93% in the WT&lt;3 mm). Conclusions— Regional myocardial WT correlates to low-voltage regions and distribution of LAVA critical for the generation and maintenance of postinfarction ventricular tachycardia. The integration of MDCT WT with 3-dimensional electroanatomic maps can help focus mapping and ablation on the culprit regions, even when MRI is precluded by the presence of implanted devices.

A Stepwise Approach to the Management of Postinfarct Ventricular Tachycardia Using Catheter Ablation as the First-Line Treatment

Background— The occurrence of ventricular tachycardia (VT) after myocardial infarction is associated with poorer prognosis. In such patients, implantable cardioverter-defibrillators are recommended. Catheter ablation of VT is currently recommended only as an adjunctive therapy. Whether a successful VT ablation alone might be a viable strategy in some of these patients, however, remains unknown. The aim of the present study was to evaluate this strategy. Methods and Results— Between January 2002 and December 2011, 189 patients with cardiomyopathy underwent 259 VT ablations in our center. Forty-five patients (mean age, 65.2±9.6 years; 91% men) with a history of myocardial infarction and mean left ventricular ejection fraction of 39.7±9.7% matched the study criteria and were included in this analysis. Acute success was obtained in 40 of 45 patients (88.9%). During a follow-up, on the basis of our stepwise algorithm (using acute success, repeat electrophysiological study, and recurrence of VT), 19 of 45 patients (42.2%) underwent implantable cardioverter-defibrillators implantation. During a median follow-up of 4.5 (interquartile range, 2.1–7.0) years, all-cause mortality occurred in 14 of 45 patients (31.1%). Using multivariate Cox regression analysis, age (hazard ratio, 1.13; 95% confidence interval, 1.03–1.22; P =0.007) was the only independent predictor of mortality, whereas implantable cardioverter-defibrillators implantation was not (hazard ratio, 0.54; 95% confidence interval, 0.18–1.64; P =0.28) Conclusions— Our results suggest that a stepwise approach to the management of VT with ablation as a first-line treatment in postinfarct patients presenting with VT might be a reasonable option. Further studies are required to confirm these results.

Relationship Between Voltage Map “Channels” and the Location of Critical Isthmus Sites in Patients With Post-Infarction Cardiomyopathy and Ventricular Tachycardia

The goal of this study was to determine the relationship of the ventricular tachycardia (VT) isthmus to channels of preserved voltage on an electroanatomic voltage map in postinfarction cardiomyopathy. Substrate mapping in patients with postinfarction cardiomyopathy and VT may involve lowering the voltage cutoff that defines the scar (<1.5 mV) to identify "channels" of relative higher voltage within the scar. However, the prevalence of channels within the scar identified by using electroanatomic mapping and the relationship to the protected VT isthmus identified by entrainment mapping is unknown. Detailed bipolar endocardial voltage maps (398 ± 152 points) from 24 patients (mean age 69 ± 9 years) with postinfarction cardiomyopathy (ejection fraction 33 ± 9%) and tolerated VT were reviewed. Endocardial scar was defined according to voltage <1.5 mV. Isolated late potentials (ILPs) were identified and tagged on the electroanatomic voltage map. The baseline voltage cutoffs were then adjusted until all channels were identified. The VT isthmus was identified using entrainment mapping. Inferior and anterior/lateral infarction was present by voltage mapping in 18 and 6 patients, respectively (scar area 44 ± 24 cm(2)). By adjusting voltage cutoffs, 37 channels were identified in 21 (88%) of 24 patients. The presence of ILPs within a channel was seen in 11 (46%) of 24 patients and 17 (46%) of 37 channels. A VT isthmus site was contained within a channel in only 11 of 24 patients or 11 of 37 channels. No difference in voltage characteristics was identified between clinical and nonclinical channels. Voltage channels with ILPs harbored the clinical isthmus with a sensitivity and specificity of 78% and 85%, respectively. Channels were identified in 88% of patients with VT by adjusting the voltage limits of bipolar maps; however, the specificity of those channels in predicting the location of VT isthmus sites was only 30%. The presence of ILPs inside the voltage channel significantly increases the specificity for identifying the clinical VT isthmus.

Endocardial ablation of postinfarction ventricular tachycardia with nonendocardial exit sites

Most infarct-related ventricular tachycardias (VTs) have an exit site that can be targeted by endocardial ablation. However, some VT reentry circuits have an exit site that is intramural or epicardial. Even these circuits may have an endocardial component that can be endocardially ablated. To assess the prevalence of postinfarction VTs with a nonendocardial exit site that can be successfully eliminated by endocardial ablation. Twenty-eight consecutive patients with postinfarction VT (27 men, age 69 ± 8 years, ejection fraction 0.25% ± 0.15%) were referred for VT ablation. A total of 213 VTs were inducible (cycle length 378 ± 100 ms). Pace mapping was performed throughout the scar, and critical sites were identified for 137 VTs (64.5%). Critical sites identified by entrainment mapping and/or pace mapping were divided into exit and nonexit sites depending on the stimulus-QRS/VT cycle length ratio (S-QRS/VT CL ≤ 0.3 vs>0.3). Endocardial exit sites (S-QRS/VTCL ≤ 0.3) were identified for 100 of 137 VTs. Only critical nonexit sites were identified for 37 of 137 (27%) VTs. Nonexit sites were confined to a smaller area within the endocardium (1.81 ± 1.7 cm(2)) and were located within dense scar (0.28 ± 0.24 mV) further away from the border zone (2.05 ± 2.79 cm) than did the VT exit sites. Exit sites had a larger area of matching pace maps (3.86 ± 1.9 cm(2); P<.01) and were at a closer distance to the border zone (0.93 ± 1.06 cm; P<.01). A total of 133 of 137 VTs were ablated. The success rate was similar for VTs in which exit sites were targeted (n = 90 of 100) and VTs in which only nonexit sites were targeted (n = 36 of 37) (P = .83). In about one-third of postinfarction VTs for which critical sites were identified, the exit site was not endocardial. Critical nonexit sites that are effective for ablation are often within dense scar at a distance from the border zone and can be missed if only the border zone is targeted.

Local lentiviral Connexin 43 (Cx43) transduction reduces incidence of post-infarct ventricular tachycardias (VT's) in mouse

Local lentiviral Connexin 43 (Cx43) transduction reduces incidence of post-infarct ventricular tachycardias (VT's) in mouse

Myocardial Structural Associations With Local Electrograms

Background— The association of scar on late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) with local electrograms on electroanatomic mapping has been investigated. We aimed to quantify these associations to gain insights regarding LGE-CMR image characteristics of tissues and critical sites that support postinfarct ventricular tachycardia (VT). Methods and Results— LGE-CMR was performed in 23 patients with ischemic cardiomyopathy before VT ablation. Left ventricular wall thickness and postinfarct scar thickness were measured in each of 20 sectors per LGE-CMR short-axis plane. Electroanatomic mapping points were retrospectively registered to the corresponding LGE-CMR images. Multivariable regression analysis, clustered by patient, revealed significant associations among left ventricular wall thickness, postinfarct scar thickness, and intramural scar location on LGE-CMR, and local endocardial electrogram bipolar/unipolar voltage, duration, and deflections on electroanatomic mapping. Anteroposterior and septal/lateral scar localization was also associated with bipolar and unipolar voltage. Antiarrhythmic drug use was associated with electrogram duration. Critical sites of postinfarct VT were associated with &gt;25% scar transmurality, and slow conduction sites with &gt;40 ms stimulus-QRS time were associated with &gt;75% scar transmurality. Conclusions— Critical sites for maintenance of postinfarct VT are confined to areas with &gt;25% scar transmurality. Our data provide insights into the structural substrates for delayed conduction and VT and may reduce procedural time devoted to substrate mapping, overcome limitations of invasive mapping because of sampling density, and enhance magnetic resonance–based ablation by feature extraction from complex images.

Reasons for Recurrent Ventricular Tachycardia After Catheter Ablation of Post-Infarction Ventricular Tachycardia

The purpose of this study was to assess the determinants of ventricular tachycardia (VT) recurrence in patients who underwent VT ablation for post-infarction VT. The factors that predict recurrence of VT after catheter ablation in patients with prior infarctions are not well described. Catheter ablation was performed in 98 consecutive patients (88 males [90%]; mean age 67 ± 10 years; ejection fraction 27 ± 13%) with post-infarction VT. Electrograms from the implantable cardioverter-defibrillator were analyzed, and VTs were classified as clinical, nonclinical, or new clinical. A total of 725 VTs were induced during the ablation procedure. All VTs were targeted. In 76 patients, 105 clinical VTs were inducible. Critical sites were identified with entrainment mapping and pace-mapping (≥10 of 12 matching leads) for 75 of 105 clinical VTs (71%) and for 278 of 620 nonclinical VTs (45%). Post-ablation, the clinical VT was not inducible in any patient, and all VTs were rendered noninducible in 63% of the patients. Over a mean follow-up period of 35 ± 23 months, 65 of 98 patients (66%) had no recurrent VTs and 33 (34%) had VT recurrence. A new VT occurred in 26 of 33 patients (79%), and a prior clinical VT recurred in 7 patients (21%). Patients with recurrent VT had a larger scar area as assessed by electroanatomic mapping compared with patients without recurrent VTs (93 ± 40 cm(2) vs. 69 ± 30 cm(2); p = 0.002). In patients with repeat procedures, the majority of inducible VTs for which a critical area could be identified were at a distance of 6 ± 3 mm to the prior ablation lesions. Patients with recurrent VTs have a larger scar as assessed by electroanatomic mapping. Most recurrent VTs were new, and the majority of these VTs were mapped to the vicinity of prior ablation lesions in patients with repeat procedures.

Introduction to Ventricular Tachycardia

This article introduces the section devoted to ventricular tachycardia (VT), comprising a series of thought-provoking cases. Unusual cases of idiopathic VT, VT in post-infarction cardiomyopathy and VT in valvular and dilated cardiomyopathy are presented. The cases illustrate several important points regarding the use of activation, entrainment, and substrate mapping for identifying the most appropriate sites for ablation in these cases.

Showing Up Channels for Postinfarct Ventricular Tachycardia Ablation

The number of scar-related ventricular tachycardia (VT) ablation procedures is increasing worldwide. This is certainly due to the ever growing number of patients implanted with an implantable cardioverter defibrillator in whom an ablation procedure may be required to better control the ventricular arrhythmia burden, but is also likely related to our better understanding of the arrhythmias mechanisms as well as the improvement of the mapping techniques during the last 15 years. Most VTs, especially those arising after myocardial infarction, depend on a critical isthmus. Defining precisely the critical isthmus of postinfarct VT may be challenging, particularly when the arrhythmia is poorly tolerated. In the literature, there are extensive data concerning the value of conventional electrophysiological techniques, especially entrainment mapping in association with postpacing interval measurements, regarding the identification of postinfarct VT isthmuses. There are, however, other--sometimes emerging--approaches to image critical postinfarct VT channels. We have summarized these, reviewing data from the published literature as well as our own experience.

Value of right ventricular mapping in patients with postinfarction ventricular tachycardia

Postinfarction ventricular tachycardia (VT) typically involves the left ventricular endocardium. Right ventricular involvement in the arrhythmogenic substrate of postinfarction VT is considered unusual. To assess the role of right ventricular mapping and ablation in patients with prior septal myocardial infarction. From among 37 consecutive patients with recurrent postinfarction VT, 18 patients with evidence of left ventricular septal involvement of myocardial infarction were identified; these patients were the subjects of this report. In these 18 patients, 166 VTs (cycle length 372 ± 117 ms) were induced. Right ventricular voltage mapping was performed in all 18 patients with left ventricular septal myocardial infarction. Right ventricular voltage mapping showed areas of low voltage in 11 patients; pace mapping from these areas revealed matching pace maps for 17 VTs, and radiofrequency ablation from the right ventricular endocardium but not the left ventricular endocardium eliminated 14 of 17 VTs. VTs with critical components in the right ventricle had a left bundle branch block morphology that had similar characteristics as left bundle branch block VTs with critical areas involving the left ventricular septum. Patients with right ventricular VT breakthrough sites had a lower ejection fraction than did patients without VT breaking out on the right ventricular septum (18% ± 5% vs 33% ± 15%; P = .01). Right ventricular mapping and ablation may be necessary in order to eliminate all inducible VTs in patients with postinfarction VT. More than half the patients with septal myocardial infarction have right ventricular septal areas that are critical for postinfarction VT and that cannot be eliminated by left ventricular ablation alone.

Septal Involvement in Patients With Post-Infarction Ventricular Tachycardia: Implications for Mapping and Radiofrequency Ablation

The purpose of this study was to assess the prevalence of the re-entry circuit within the interventricular septum in post-infarction patients referred for ventricular tachycardia (VT) ablation. Post-infarction ventricular tachycardia can involve the endocardial myocardium, the intramural myocardium, the epicardium, or the His Purkinje system. Among 74 consecutive patients with recurrent post-infarction VT, 33 patients (45%) were identified in whom the critical part of the VT involved the interventricular septum. A total of 206 VTs were induced in these 33 patients. In 46 of the 206 VTs, a critical component was identified in the interventricular septum. The critical isthmus of the re-entry circuit was identified by entrainment mapping, activation mapping, or pace-mapping. In 32 of 46 VTs (70%), the critical component of the re-entry circuit was confined to the endocardium. In 9 of 46 VTs (20%), the critical component involved the Purkinje system, and in 5 of 46 VTs (11%), an intramural area was critical. Entrainment and/or pace-mapping helped to identify critical areas of endocardial VTs as well as VTs involving the Purkinje fibers, but neither of these mapping techniques localized intramural VTs. Electrocardiographic characteristics were specific for each of the septal locations. All VTs mapped to the interventricular septum were acutely successfully ablated. VTs recurred in 9 of 33 patients with septal VTs during a mean follow-up period of 40 ± 20 months. Post-infarction VT involving the interventricular septum can involve the endocardial muscle, Purkinje fibers, or intramural muscle fibers. Electrocardiographic characteristics differ depending on the type of tissue involved.