Ablation Of Postinfarction Ventricular Tachycardia Research Articles

Magnetic Resonance Mapping of Catheter Ablation Lesions After Post-Infarction Ventricular Tachycardia Ablation

ObjectivesThis study sought to describe cardiac magnetic resonance (CMR) characteristics of ablation lesions within post-infarction scar. BackgroundChronic ablation lesions created during radiofrequency ablation of ventricular tachycardia (VT) in the setting of prior myocardial infarction have not been described in humans. MethodsSeventeen patients (15 men, ejection fraction 25 ± 8%, 66 ± 6 years of age) with CMR imaging prior to repeat ablation procedures for VT were studied. Electroanatomic maps from first-time procedures and subsequent CMR images were merged and retrospectively compared with electroanatomic maps from repeat procedures. ResultsThe delay between the index ablation procedure and the CMR study was 30 ± 29 months. Late gadolinium–enhanced CMR revealed a confluent nonenhancing subendocardial dark core within the infarct-related scar tissue in all patients. Intracardiac thrombi were ruled out by transthoracic and intracardiac echocardiography. These core lesions matched the distribution of prior ablation lesions, and corresponded to unexcitable areas at repeat procedures. ConclusionsAblation lesions can be detected by CMR after VT ablation in post-infarction patients and have a different appearance than scar tissue. These lesions can be observed many months after an initial ablation.

Arrhythmia exacerbation after post-infarction ventricular tachycardia ablation: prevalence and prognostic significance.

Catheter ablation is an effective treatment for post-infarction ventricular tachycardia (VT). However, some patients may experience a worsened arrhythmia phenotype after ablation. We aimed to determine the prevalence and prognostic impact of arrhythmia exacerbation (AE) after post-infarction VT ablation. A total of 1187 consecutive patients (93% men, median age 68 years, median ejection fraction 30%) who underwent post-infarction VT ablation at six centres were included. Arrhythmia exacerbation was defined as post-ablation VT storm or incessant VT in patients without prior similar events. During follow-up (median 717 days), 426 (36%) patients experienced VT recurrence. Events qualifying as AE occurred in 67 patients (6%). Median times to VT recurrence with and without AE were 238 [interquartile range (IQR) 35-640] days and 135 (IQR 22-521) days, respectively (P = 0.25). Almost half of the patients (46%) who experienced AE experienced it within 6 months of the index procedure. Patients with AE had had longer ablation times during the ablation procedures compared to the rest of the patients (median 42 vs. 34 min, P = 0.02). Among patients with VT recurrence, the risk of death or heart transplantation was significantly higher in patients with than without AE (hazard ratio 1.99, 95% CI 1.28-3.10; P = 0.002) after adjusting for age, gender, ejection fraction, cardiac resynchronization therapy, post-ablation non-inducibility, and post-ablation amiodarone use. Arrhythmia exacerbation after ablation of infarct-related VT is infrequent but is independently associated with an adverse long-term outcome among patients who experience a VT recurrence. The mechanisms and mitigation strategies of AE after catheter ablation require further investigation.

(Retraction Request) Efficacy of Intensive Radiofrequency Energy Delivery to the Localized Dense Scar Area in Post-Infarction Ventricular Tachycardia Ablation - A Comparative Study With Standard Strategy Targeting the Infarcted Border Zone.

(Retraction Request) Efficacy of Intensive Radiofrequency Energy Delivery to the Localized Dense Scar Area in Post-Infarction Ventricular Tachycardia Ablation - A Comparative Study With Standard Strategy Targeting the Infarcted Border Zone.

Targeting Noninducible Clinical Ventricular Tachycardias in Patients With Prior Myocardial Infarctions Based on Stored Electrograms.

Ablation of postinfarction ventricular tachycardia (VT) has been shown to reduce VT recurrence and decrease mortality. However, VT recurrence can occur despite extensive ablation procedures. The lack of inducibility of clinical VTs during ablation procedures remains problematic and may be in part responsible for VT recurrences. In this prospective study, we targeted documented but noninducible clinical VTs based on stored implantable cardioverter-defibrillator (ICD) electrograms. Radiofrequency ablation was performed in a consecutive group of 66 postinfarction patients (mean age, 67.5±9.2 years; men, 61; mean left ventricular ejection fraction, 25.1±10.8%) in whom clinical VTs were not inducible during an ablation procedure. In the first 33 patients (control group), only inducible VTs were targeted, and in the second 33 patients, noninducible clinical VTs were also targeted by pace-mapping based on stored ICD-electrograms (ICD-electrogram-guided ablation group). Procedural and clinical outcomes were compared at 24 months post-ablation. VT recurred in 5 patients (15%) in whom the ICD-electrogram-guided approach was performed and in 13 patients (39%) in the control group. Freedom from recurrent VT was higher (log-rank P=0.04) in the ICD-electrogram-guided group, but there was no difference in ventricular fibrillation or in total mortality between both groups. Ablation guided by pace-mapping of noninducible postinfarction clinical VTs based on ICD-electrograms is feasible and reduces the risk of recurrent VT.

Catheter ablation of postinfarction ventricular tachycardia: ten-year trends in utilization, in-hospital complications, and in-hospital mortality in the United States.

There is a paucity of data regarding the complications and in-hospital mortality after catheter ablation for ventricular tachycardia (VT) in patients with ischemic heart disease. The purpose of this study was to determine the temporal trends in utilization, in-hospital mortality, and complications of catheter ablation of postinfarction VT in the United States. We used the 2002-2011 Nationwide Inpatient Sample (NIS) database to identify all patients ≥18 years of age with a primary diagnosis of VT (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] code 427.1) and who also had a secondary diagnosis of prior history of myocardial infarction (ICD-9-CM 412). Patients with supraventricular arrhythmias were excluded. Patients who underwent catheter ablation were identified using ICD-9-CM procedure code 37.34. Temporal trends in catheter ablation, in-hospital complications, and in-hospital mortality were analyzed. Of 81,539 patients with postinfarct VT, 4653 (5.7%) underwent catheter ablation. Utilization of catheter ablation increased significantly from 2.8% in 2002 to 10.8% in 2011 (Ptrend < .001). The overall rate of any in-hospital complication was 11.2% (523/4653), with vascular complications in 6.9%, cardiac in 4.3%, and neurologic in 0.5%. In-hospital mortality was 1.6% (75/4653). From 2002 to 2011, there was no significant change in the overall complication rates (8.4% to 10.2%, Ptrend = .101; adjusted odds ratio [per year] 1.02, 95% confidence interval 0.98-1.06) or in-hospital mortality (1.3% to 1.8%, Ptrend = .266; adjusted odds ratio [per year] 1.03, 95% confidence interval 0.92-1.15). The utilization rate of catheter ablation as therapy for postinfarct VT has steadily increased over the past decade. However, procedural complication rates and in-hospital mortality have not changed significantly during this period.

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 …

Role of repeat procedures for catheter ablation of postinfarction ventricular tachycardia

In patients with ischemic heart disease, ventricular tachycardia (VT) is associated with increased mortality and morbidity. Catheter ablation is useful for reducing VT therapies but remains challenging, and recurrences are common. The purpose of this study was to assess the prognosis and safety of repeat catheter ablation procedures for postinfarct VT and to determine clinical and procedural predictors of outcomes. From a total of 280 patients undergoing catheter ablation of postinfarct VT at one center, 107 consecutive patients having a repeat procedure after one or more prior failed catheter ablation procedures (PFCA group) were compared to 173 patients who underwent a single catheter ablation (SCA group) in the same study period. Of the PFCA group, 75 (70.1%) had one procedure and 32 (29.9%) had two or more prior ablations. Ventricular function and age were similar between groups. Periprocedural complications occurred in 11.2% of patients in the PFCA group and 8.7% of patients in the SCA group (P = .484). The 1-year VT recurrence rate was higher in the PFCA group compared to the SCA group (32.6% vs 16.6%, P = .001). On multivariable analysis, prior ablation (hazard ratio [HR] 1.84, P = .018), left ventricular ejection fraction (HR 1.04, P = .019), and mean number of induced VTs (HR 1.17, P = .043) were independent predictors of VT recurrence. Failure of initial ablation does not preclude subsequent successful ablation for postinfarct VT. Whether healing of prior lesions, change in arrhythmic substrate, or changes in antiarrhythmic therapy are factors that influence recurrence warrants further study.

Abstract 4088: Isolated Potentials and Pace-Mapping to Guide Ablation for Ventricular Tachycardia in Patients with Non-Ischemic Cardiomyopathy

Background : Isolated potentials (IPs) during sinus rhythm are indicators of fixed scar in patients with prior infarcts. IPs in conjunction with pace-mapping (PM) have been helpful to guide ablation of post-infarction ventricular tachycardia (VT). The purpose of this study was to determine the value of IPs in conjunction with PM to guide VT ablation in patients with non-ischemic cardiomyopathy. Methods : 32 consecutive patients (23 male, age 56±13 years, ejection fraction 0.30±0.14) with VT and non-ischemic cardiomyopathy were analyzed. Thirty/32 patients had an implanted cardioverter defibrillator (ICD). Electroanatomic maps of the left (n=21) and right ventricle (n=13), the coronary sinus (n=3), and the epicardium (n=4) were obtained during baseline rhythm. PM was performed at sites with low voltage (&lt;1.5mV). Radiofrequency energy was delivered at sites with concealed entrainment or matching pace-maps. Mean follow-up time was 10±9 months. Results : 173 VTs (cycle length 359±86 ms) were induced. Appropriate ablation sites with IPs during sinus rhythm were recorded in 19/32 patients (59%) (group A). In these patients, a total of 195 appropriate target sites were identified for 56/100 induced VTs (56%); 136/195 sites (70%) displayed IPs. In the remaining 13 patients, no target sites with IPs were identified (group B) despite combined endocardial and transcutaneous epicardial mapping in 3/13 patients. In these 13 patients, a total of 96 appropriate target sites were identified for 25/73 induced VTs (34%). Fifteen/19 patients (79%) in group A were non-inducible at the end of the procedure compared to 2/13 patients (15%) in group B. During a mean follow-up of 10±9 months, 15/19 patients (79%) in group A compared to 1/13 patients (8%) in group B remained arrhythmia free (p=0.0002). Conclusion : IPs in conjunction with PM are helpful in identifying critical isthmus areas for ablation of VT in patients with non-ischemic cardiomyopathy. Differences in the extent of fixed scar tissue may be the reason for differences in the prevalence of IPs, and this might explain better ablation results in some patients with non-ischemic cardiomyopathy.

Epicardial ablation of postinfarction ventricular tachycardia with an externally irrigated catheter in a patient with mechanical aortic and mitral valves

Epicardial ablation of postinfarction ventricular tachycardia with an externally irrigated catheter in a patient with mechanical aortic and mitral valves

Isolated Potentials During Sinus Rhythm and Pace-Mapping Within Scars as Guides for Ablation of Post-Infarction Ventricular Tachycardia

The purpose of this study was to identify ventricular tachycardia (VT) isthmus sites by pace-mapping within scar tissue and to identify electrogram characteristics that are helpful in identifying VT isthmus sites during sinus rhythm (SR). Pace-mapping has been used in the scar border zone to identify the exit site of post-infarction VT. In 19 consecutive patients (18 men, mean age 66 +/- 9 years, mean ejection fraction 0.24 +/- 0.12) with post-infarction VT, a left ventricular voltage map was generated during SR. Pace-mapping was performed at sites with abnormal electrograms or isolated potentials. Radiofrequency ablation was performed at isthmus sites as defined by pace-mapping (perfect pace-map = 12/12 matching electrocardiogram leads; good pace-map = 10/12 to 11/12 matching electrocardiogram leads) and/or entrainment mapping. A total of 81 VTs (mean cycle length 396 +/- 124 ms) were inducible. In 16 of the 19 patients, a total of 41 distinct isthmus areas of 41 distinct VTs were identified and successfully ablated. All but one displayed isolated potentials during SR. Furthermore, 22 of the 81 VTs (27%) for which no isthmus was identified became noninducible after ablation of a targeted VT. The 16 patients in whom > or =1 isthmus was identified and ablated were free of arrhythmic events during a mean follow-up of 10 months. During SR, excellent or good pace-maps at sites of isolated potentials within areas of scar identify areas of fixed block that are protected and part of the critical isthmus of post-infarction VT. Shared common pathways might explain why non-targeted VTs might become noninducible after ablation of other VTs.

Surgical ablation of post-infarction ventricular tachycardia guided by mapping in sinus rhythm: long term results.

Some patients after myocardial infarction have an increased risk of malignant ventricular tachyarrhythmias (VTA) or sudden cardiac death. The aim of the study was to evaluate long-term results of surgical ablation of an arrhythmogenic substrate guided by simplified intraoperative mapping of pathological ventricular electrograms during sinus rhythm. The study population consisted of 77 patients (9 women; mean age 62.4+/-8.5 years) with previous Q-wave myocardial infarction and at least one documented episode of sustained VT/VF more than one month after the last infarction. The left ventricular ejection fraction was 31.3+/-8.8%. All but eight patients had clinical indication for concomitant coronary artery bypass surgery. All underwent preoperative electrophysiologic study. Intraoperative epicardial and endocardial mapping during sinus rhythm was performed using a multielectrode with 16 bipolar electrodes in combination with a multichannel recording system. Myocardial regions revealing fractionated, low amplitude signals lasting > or =130 ms were surgically excised or cryoablated. All surviving patients were restudied within one to two weeks after surgery using identical programmed electrical stimulation protocol. Five (6.5%) patients died in the perioperative (30-days) period. In the remaining cohort, inducibility of any sustained VTA after surgical procedure was observed in 21 subjects (29.2%). An implantable cardioverter-defibrillator (ICD) was implanted in these patients. Recurrence of sustained VTA was documented during follow-up period in two patients who were noninducible after the surgery (at the month 10 and 22, respectively), and both received ICD as well. No patient died of sudden cardiac death. In 14 ICD patients, no significant VTA was documented during the mean follow-up of 37.3+/-23.2 months. Altogether, 61 from the 72 patients surviving the surgery (84.7%) remained free of spontaneous recurrences of VTA during the follow-up. Surgical ablation of an arrhythmogenic substrate guided by simplified intraoperative mapping in normothermic heart during sinus rhythm appears to be both safe and efficacious procedure that prevents recurrences of VTA in a substantial proportion of patients.

Catheter ablation of ventricular tachycardia following myocardial infarction using three-dimensional electroanatomical mapping.

One challenge encountered during catheter ablation of postinfarction ventricular tachycardia (VT) is the inducibility of multiple VT morphologies associated with variable hemodynamic instability. The clinical usefulness and safety of a three-dimensional electroanatomical mapping in guiding radiofrequency (RF) catheter ablation of VT, used in parallel with a multichannel recording system, was studied in 28 men (mean age = 63.8 +/- 10.6 years, mean left ventricular ejection fraction = 28% +/- 9%). Three-dimensional voltage maps of the left ventricle were obtained in sinus rhythm with annotation of areas of fractionated or late potentials, zones of slow conduction and/or dense scar with no pacing capture at 10 mA. RF lesions were created either in sinus rhythm or during hemodynamically stable VT within reconstructed critical zones of the circuit. A total of 82 VTs were induced (mean = 2.9 +/- 1.0/patient). Hemodynamically unstable clinical VTs were induced in 5 patients, and clinical or nonclinical unstable VT in 14. Clinical VT was rendered noninducible in 24/28 (85.7%) patients, and monomorphic VT was eliminated in 16/28 (57.1%) patients. The mean procedural time was 258 +/- 82 minutes, and fluoroscopic exposure 13.5 +/- 8.8 minutes. During a mean follow-up period of 10.6 +/- 6.4 months, catheter ablation was repeated in 6 patients for VT recurrences. No significant complications occurred except for a transient cerebral ischemic attack in one patient. In conclusion, electroanatomical mapping assisted the successful and safe catheter ablation of both mappable and nonmappable VTs in a significant proportion of patients after myocardial infarction.

Standardized stimulation protocol to predict the long-term success of radiofrequency ablation of postinfarction ventricular tachycardia.

The ability to predict the success of radiofrequency ablation (RFA) is an essential step in the management of ventricular tachycardia (VT) in patients with ischemic heart disease. This study tested a standardized programmed stimulation protocol and pre-specified definitions of procedural outcome. Consecutive patients referred for RFA of delayed post infarction VT were enrolled. Programmed stimulation was performed at the beginning and the end of an RFA procedure, and consisted of an 8 beat drive followed by up to 5 extrastimuli. Immediate success was defined as no inducible monomorphic VT, and a modified result was defined as the inducibility of VT with > 2 extrastimuli beyond those required at baseline. Procedural failure was defined when these criteria were not met. Recurrences of sustained VT and arrhythmic deaths were monitored during long-term follow-up. The study enrolled 112 patients. Immediate procedural success was achieved in 38%, a modified result in 34%, and procedural failure in 28% of patients. During a mean follow-up of 78 +/- 16 months, recurrent sustained VT was observed in 25 patients. VT recurrence was 3% (3/79) in patients with a successful or modified result, compared with 67% (22/33) in those who had undergone unsuccessful procedures (P < 0.001). This standardized stimulation protocol and definitions of procedural success, enabled us to predict with high accuracy a VT recurrence-free long-term follow-up. This may have implications in recommending devices or other treatments after RFA for postinfarction VT.

Pace mapping of postinfarction scar to detect ventricular tachycardia exit sites and zones of slow conduction.

The exit site and central common pathway of slow conduction are preferred sites to guide radiofrequency ablation of postinfarction ventricular tachycardia (VT). Both require inducibility of VT. In addition, their low amplitude hampers direct recording of potentials generated by activation in pathways of slow conduction. We hypothesized that pace mapping during sinus rhythm would help to detect the VT exit site and potentials generated by activation in pathways of slow activation. In 13 patients suffering from VT late after anterior (n = 10) or inferior (n = 3) myocardial infarction, stimulation was performed in scarred endocardium at 23.5 (range 13 to 36) sites per patient during arrhythmia surgery. Multielectrode recordings (64 sites) during stimulation at a fixed cycle length of 500 msec were obtained. Endocardial breakthrough sites distant (>2 cm) from the pacing site were found at 4.3 (range 3 to 19) pacing sites per patient. Low-amplitude discrete potentials (LADPs) could be detected between the pacing site and the breakthrough site in 2.3 (range 0 to 13) of 4.3 stimulation sequences. In these patients, 19 VTs were induced and the exit site determined. In 6 patients, the distant pacing breakthrough site was identical to the VT exit site; in 7 patients, no similar exit sites were found. LADPs during VT were found at a median 2.0 (range 0 to 14) sites per patient. Pace mapping of the postinfarction endocardial scar during sinus rhythm revealed 50% of the endocardial exit sites of VT and the same number of LADPs observed during VT.

Radiofrequency Catheter Ablation of Postinfarction Ventricular Tachycardia from the Proximal Coronary Sinus

Optimum strategy for radiofrequency (RF) catheter ablation of ventricular tachycardia (VT) after inferior wall myocardial infarction (MI) that originates from the posteroseptal process of the left ventricle is not known. We describe a case report of a 57-year-old man who developed recurrent post-MI VT with ECG morphology consistent with this type of VT (i.e., left bundle branch block pattern with predominant R waves from V2 to V6 and left-axis deviation). Endocardial mapping and entrainment during VT demonstrated a critical isthmus of the reentrant circuit in the proximal coronary sinus. RF application terminated VT and rendered it noninducible.

Slow intramural heating with diffused laser light: A unique method for deep myocardial coagulation.

Catheter ablation of postinfarction ventricular tachycardia (VT) may be limited by insufficient myocardial coagulation or excessive endocardial or epicardial damage. We propose that volumetric heating restricted to intramural sites may improve the outcome and safety of this procedure, especially if delivered at rates that enhance heat conduction and forestall adverse tissue changes. A novel optical fiber with a diffusing tip for direct intramural, volumetric laser heating was tested via thoracotomy and percutaneously in normal dogs. Low-power (2.0- to 4.5-W) diode laser light (805 nm) diffused within tissue induced large lesions but no visible surface damage, mural thrombi, or transmural perforation. Mean lesion depth approximated tip length (10 mm). Mean lesion widths in the thoracotomy and percutaneous groups were 5.8+/-0.5 to 9.1+/-0.84 mm and 5.2+/-0.85 to 7.9+/-1.1 mm, respectively, depending on the light dose. Mean volumes in the percutaneous group were 1006+/-245 to 2471+/-934 mm. ST-segment depression, appearing in unfiltered bipolar electrograms recorded from the guiding catheter, was specific for lesion induction. All dogs survived the protocol, which included a 1-hour observation period. In cross section, lesions were elliptical to spherical and characterized by extensive contraction-band necrosis abruptly bordering viable tissue. No platelets or fibrin adhered to the endocardium. Slow, volumetric, and direct intramyocardial heating induces large, deep lesions without hazardous tissue damage. Such heating might cure postinfarction VT more successfully and safely than present techniques. Further testing and development of this method seem warranted.

Atlas of paced body surface QRS integral maps for localization of the site of origin of postinfarction ventricular tachycardia

Current mapping during radiofrequency (RF) catheter ablation of postinfarction ventricular tachycardia (VT) is based primarily on the use of single-site mapping techniques. Although such techniques are highly suitable for distinguishing the ultimate site where RF energy is delivered by enabling detailed localization of the exit site or critical component of the VT reentrant circuit, they are time-consuming and inefficient for initial rapid identification of the arrhythmogenic target area. This study features the design and preliminary clinical application of a new noninvasive method that is aimed at speeding up the initial phase of the VT mapping procedure. This method is based on the use of an atlas of 62-lead body surface QRS integral map patterns that was previously developed using left ventricular pace mapping in patients with remote anterior or inferior myocardial infarction. The atlas contains 18 and 22 different paced QRS integral map patterns obtained in patients with previous anterior or inferior myocardial infarction, respectively. Each specific QRS pattern in the atlas provides a unique infarct-specific spatial electrocardiographic representation of the onset of ectopic ventricular activation in a circumscribed endocardial segment of the left ventricle. Localization of the segment of VT origin is obtained by visually or mathematically comparing the QRS integral map recorded during VT with one of the two sets of paced QRS integral maps contained within the atlas with the purpose of selecting the best matching paced QRS integral map pattern. During RF catheter ablation of postinfarction VT, body surface QRS integral mapping offers an efficient clinical tool that can be used as a first-step localization procedure that may guide subsequent catheter pace mapping or activation mapping quickly to the arrhythmogenic target area.