Ablation of ventricular tachycardia in patients with nonischemic cardiomyopathy

Nonischemic Cardiomyopathy. Mapping and ablation of ventricular tachycardia (VT) in patients with nonischemic cardiomyopathy can be challenging. In this article, we describe the approach to VT in patients with nonischemic cardiomyopathy that we use at the University of Michigan. Imaging, especially with delayed enhanced cardiac magnetic resonance imaging, plays a central role in planning a mapping and ablation procedure. During the mapping procedure, pace-mapping in conjunction with voltage maps focusing on areas with isolated potentials helps to identify scar areas that are critical for VT in these patients.     

Mapping and radiofrequency catheter ablation of the three types of sustained monomorphic ventricular tachycardia in nonischemic heart disease

INTRODUCTION: Sustained monomorphic ventricular tachycardia (VT) associated with nonischemic cardiomyopathy (CMP) is uncommon. Optimal approaches to catheter mapping and ablation are not well characterized, but they are likely to depend on the VT mechanism. The purpose of this study was to evaluate the mechanisms of sustained monomorphic VT encountered in nonischemic CMP and to assess the feasibility, safety, and efficacy of catheter radiofrequency ablation for treatment. METHODS AND RESULTS: Twenty-six consecutive patients with nonischemic CMP referred for management of recurrent VT were studied. In 16 (62%) patients, VT was related to a region of abnormal electrograms consistent with scar and the response to pacing suggested a reentrant mechanism. In 5 (19%) patients, VT was due to bundle branch or interfascicular reentry. In 7 (27%) patients, the VT mechanism was focal automaticity, 4 of whom had evidence of tachycardia-induced CMP. After catheter ablation targeting parts of reentrant circuits, VT was not inducible in 8 (53%) of 15 patients with scar-related reentry, was modified in 5 (33%) patients, and still was inducible in 2 (13%) patients. Ablation was successful in 5 of 5 patients with bundle branch reentry and in 6 of 7 patients with a focal automaticity mechanism. Overall, catheter ablation abolished clinical recurrence of VT in 20 (77%) of 26 patients during a follow-up of 15 +/- 12 months. CONCLUSION: Three different mechanisms of VT are encountered in patients with nonischemic CMP. The mapping and ablation approach varies with the type of VT. In this selected population, the overall efficacy was 77%.     

Sinus rhythm QRS amplitude and fractionation in patients with nonischemic cardiomyopathy to identify ventricular tachycardia substrate and location

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Clinical outcomes of radiofrequency catheter ablation of ventricular tachycardia in patients with hypertrophic cardiomyopathy

Background

Monomorphic ventricular tachycardia (VT) is rare in patients with hypertrophic cardiomyopathy (HCM), management of which is challenging. Limited data exists on the utility of catheter ablation for the treatment of VT in this population.

Objectives

We aimed to assess clinical outcomes of catheter ablation for VT in HCM patients.

Methods

A systematic search, without language restriction, using PubMed, EMBASE, SCOPUS, Google Scholar, and ClinicalTrials.gov was performed. The meta-analysis was performed using a meta-package for R version 4.0/RStudio version 1.2 and Freeman Tukey double arcsine method to establish the variance of raw proportions. Outcomes measured included (1) acute procedure success (defined as noninducible for clinical VT), (2) freedom from VT at follow-up, (3) mortality.

Results

This systematic review of six studies (three from the United States and three from Japan) incorporated a total of 68 drug-refractory HCM patients who underwent VT radiofrequency catheter ablation (mean age 57.6 ± 13.3 years, mean LVEF 45.8 ± 15.4%, 85% men, maximum septal wall thickness 17.4 ± 4.6 mm, and 32.3% with an apical aneurysm). Acute procedural success was achieved in 84.5% patients (95% confidence interval [CI]: 70.6%–95.2%) with 27.9% patients had recurrent VT requiring multiple ablations (median 1, IQR 1–3). During the follow-up period (18.3 ± 11.7 months), the pooled incidence of freedom from recurrent VT after index procedure was 70.2% (95% CI: 51.9%–86.2%), while after the last ablation was 82.8% (95% CI: 57%–99.2%). There were two deaths during follow-up, one from heart failure and one from SCD 0.8% (95% CI: 0%–5.8%).

Conclusion

The results of our pooled analysis demonstrated that catheter ablation for VT in HCM patients was associated with high acute procedural success, and reduced VT recurrence—findings comparable to previously published reports in other disease substrates.     

Right ventricular scar‐related ventricular tachycardia in nonischemic cardiomyopathy: Electrophysiological characteristics,mapping, and ablation of underlying heart disease

1 Background

Right ventricular (RV)‐scar related ventricular tachycardia (VT) is often due to arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) or cardiac sarcoidosis (CS), but some patients whose clinical course has not been described do not fulfill diagnostic criteria for these diseases. We sought to characterize the electrophysiologic substrate and catheter ablation outcomes of such patients, termed RV cardiomyopathy of unknown source (RCUS).

2 Methods and results

Data of 100 consecutive patients who presented with RV cardiomyopathy and/or RV‐related VT for ablation were reviewed (51 ARVC/D, 22 CS; 27 RCUS). Compared to ARVC/D, RCUS patients were older (P = 0.001), less commonly had RV dilatation (P = 0.001) or dysfunction (P = 0.01) and fragmented QRS, parietal block, and T‐wave inversion. Compared to CS, R‐CUS patients had less severe LV dysfunction. Extent and distribution of endocardial/epicardial scar and inducible VTs in RCUS patients were comparable with ARVC/D and CS patients. At a median follow‐up of 23 months, RCUS patients had more favorable VT‐free survival (RCUS 71%, ARVC/D 60%, CS 41%, P = 0.03) and survival free of death or cardiac transplant (RCUS 92%, ARVC/D 92%, CS 62%, P = 0.01). No RCUS patients developed new criteria for ARVC/D or CS in follow‐up.

3 Conclusions

Up to one‐third of patients with RV scar‐related VT are not classifiable as ARVC/D or CS. These patients had a somewhat better prognosis than ARVC/D or sarcoid and did not develop evidence of these diseases during the initial 2 years of follow‐up. The extent to which this population comprises mild ARVC/D, CS, or other diseases is not clear.     

Sinus rhythm electrocardiogram identification of basal-lateral ischemic versus nonischemic substrate in patients with ventricular tachycardia

Purpose

Sinus rhythm (SR) electrocardiogram (ECG) features in patients with nonischemic cardiomyopathy (NICM) and ventricular tachycardia (VT) have been described. ECG characteristics that distinguish nonischemic VT substrate from prior myocardial infarction (MI) have yet to be determined. We aimed to identify ECG differences between patients with basal-inferolateral scar due to NICM versus prior MI.

Methods

SR/atrial-paced ECGs from patients who underwent VT ablation with endocardial/epicardial basal-inferolateral nonischemic scar (n?=?25) were compared to patients with inferior/inferolateral MI (n?=?30). Surface QRS complexes in each lead were analyzed. Patients with bundle branch block or ventricular pacing were excluded. The best diagnostic algorithm was determined by multivariate analysis then validated prospectively.

Results

The NICM group had smaller R amplitude in leads I, II, and III (p????0.05 for all), greater S amplitude in leads II, III, and V6 (p????0.001 for all) and S/R ratio in lead V6 (p?=?0.001). Inferior Q waves were uncommon in NICM (24?% vs. 87?%, p?<?0.001). Lateral QRS fragmentation was uncommon (20?%) but only found in NICM. A three-step algorithm was derived with 100?% sensitivity and 77?% specificity for NICM. In the validation cohort (n?=?51), ICM was appropriately excluded in 93?% of the cases of NICM (91?% interobserver agreement) by the algorithm.

Conclusions

Lateral lead QRS fragmentation, absence of inferior Q waves, and lead V6 S/R ratio ??0.25 on the SR ECG distinguishes patients with basal?Clateral scar due to NICM from those with prior MI. These findings demonstrate the value of the surface ECG in identifying unique scar-based VT substrate.     

Termination of polymorphic ventricular tachycardia storm by catheter ablation in a patient with cardiomyopathy induced by incessant idiopathic left ventricular tachycardia

We detail findings in a patient with incessant idiopathic left ventricular tachycardia (ILVT), induced cardiomyopathy, and an "electrical storm" consisting of recurrent polymorphic ventricular tachycardia (PVT). Catheter ablation not only eradicated the ILVT, but also additionally suppressed recurrent PVT. These findings suggest that the recurrent PVT storm in this patient related to long-standing tachycardia-induced cardiac electrical remodeling that led to QT prolongation.     

Macroreentrant ventricular tachycardia mimicking focal ventricular tachycardia in a case with arrhythmogenic right ventricular cardiomyopathy

A 67-year-old man with ventricular tachycardia (VT) due to arrhythmogenic right ventricular cardiomyopathy (ARVC) underwent electrophysiologic testing. Electroanatomic mapping during the VT seemed to reveal a focal mechanism from near the tricuspid annulus (TA). Several radiofrequency applications delivered at the presumed focus resulted in termination but re-induction of the VT. Additional electroanatomic mapping underneath the TA led to the diagnosis of macroreentrant VT. Several RF applications targeting isolated and late potentials observed there during sinus rhythm eliminated the VT. In ARVC cases, detailed mapping underneath the TA should be performed to reveal the VT mechanism, resulting in suppressing VT recurrences. There was no financial support for this study.     

Ablation of ventricular tachycardia by isolating the critical site in a patient with arrhythmogenic right ventricular cardiomyopathy

We describe a patient with arrhythmogenic right ventricular cardiomyopathy in whom ventricular tachycardia (VT) was ablated by isolating a relatively large area of the critical site using catheter ablation. Endocardial mapping showed abnormal fragmented electrograms with delayed potential (DP) from an entire area of the aneurysm. Pace mappings from the aneurysm produced a QRS morphology identical to that of clinical VT. After catheter ablation was performed at the exit site of the VT critical area, programmed stimulation inside the aneurysm captured the DP but not the QRS complexes. These data suggest that VT can be ablated successfully by isolation of the critical area.     

Mapping for ventricular tachycardia

Mapping strategies for ventricular tachycardia (VT) have evolved significantly in the past 2 decades. This review discusses mapping techniques that can help in successful VT ablation. The electrocardiogram (ECG) remains a vital component of VT mapping and can help to identify the chamber of origin of VT. The ECG morphology of VT, however, is influenced by orientation of heart and location of the scar. Activation mapping during VT is an important technique that can help in further localization. Care has to be exercised to ensure that small signals are not ignored and far-field signals are recognized. Pace-mapping to mimic the VT is another way to map exit site for scar based reentrant VT or the site of origin of triggered and automatic VT in the absence of structural heart disease. For the latter group, this technique is widely used in determining the site of ablation. It is important to ensure a complete ECG match (12 out of 12 leads) of the pace-map to the clinical arrhythmia in these patients. In patients with structural heart disease, entrainment mapping remains the gold standard for defining the protected isthmus and other components of the VT circuit. Using this technique, successful ablation of reentrant VT can be achieved in 60–90% of patients. In order to perform entrainment mapping, the VT has to be hemodynamically tolerated; this is not the case in 25% of pts with scar based reentrant VT. The development of 3-dimensional mapping systems allows for more anatomically based linear ablation in patients with poorly tolerated uniform VT. Despite these advances, there are still about 10–20% VTs that cannot be ablated successfully with the above described techniques, especially in patients with structural heart disease. Other recent advances such as percutaneous closed chest epicardial mapping technique and cooled tip ablation catheter technology have the potential to enhance mapping and successful ablation of VT.     

三维标测指导致心律失常性右心室心肌病室性心动过速的射频消融

目的介绍致心律失常性右心室心肌病（ARVC）室性心动过速（室速）的三维标测方法及其消融策略。方法21例ARVC室速患者,因1—4种抗心律失常药物治疗无效,临床上呈反复发作、无休止发作或植入型心律转复除颤器（ICD）植入后频繁放电治疗,接受导管消融治疗。其中,男性19例,女性2例,平均年龄（32±12）岁。9例患者接受电解剖（Carto）标测,12例患者接受非接触标测（EnSite—Array）。在首先明确病变基质的基础上,通过激动标测、拖带标测及起搏标测,分析心动过速的起源、可能的传导径路及其出口以及它们与病变基质的关系。通常于心动过速的出口处及其周边行局灶消融,术中病变基质周边的延迟激动电位应一并消融。结果21例患者,2例呈无休止发作,1例患者表现为频繁室性早搏及加速性室性自主心律,余18例患者消融中共诱发出34种心动过速。所有心动过速均呈左束支阻滞形,平均心动过速周长为（289±68）ms。16例患者（28种室速）消融治疗即刻成功,3例患者（7种室速）部分成功,2例患者（2种室速）消融失败,即刻消融成功率76．2％。所有患者消融术后继续服用抗心律失常药物。平均随访6～30（1d±7）个月,成功患者中2例复发,其中1例再次消融成功;未达即刻成功的5例患者,经抗心律失常药物治疗后,均无室性心律失常事件发生,其中包括1例消融后植入ICD者。结论三维标测系统可首先明确ARVC患者的病变基质,在此基础上结合激动标测和心内各种电刺激技术,可直观显示心动过速的起源、缓慢传导区出口及折返环路,以此制定消融策略可成功治疗ARVC室速。心动过速起源于心肌深部或ARVC病变进展,是消融失败和复发的常见原因。     

Heterogeneous loss of connexin43 protein in nonischemic dilated cardiomyopathy with ventricular tachycardia

INTRODUCTION: Gap junction alterations recently have been implicated in chronic heart failure, but direct evidence between gap junction manifestation in nonischemic dilated cardiomyopathy (DCM) is lacking. The current study examines whether qualitative changes or altered distribution of gap junctional connexin43 (Cx43) are related to global ventricular function and ventricular arrhythmia in DCM. METHODS AND RESULTS: We investigated 31 DCM patients (52 +/- 15 years) and 5 control subjects (55 +/- 10 years). Expression of Cx43 proteins was qualitatively and quantitatively determined using immunoconfocal microscopy in right ventricular biopsy specimens from each patient. The expression level of Cx43 protein was defined as the proportion of tissue area occupied by Cx43 (percent tissue area) in each test area. Cx43 immunoreactive signal expressed as percent tissue area was not correlated with the change in left ventricular ejection fraction (P = 0.17). Of 31 DCM patients, 23% subsequently developed sustained ventricular tachycardia (VT), which allowed retrospective division of the samples into two groups: non-VT and VT. Left ventricular ejection fraction was comparable in both groups, but the percent tissue area in the VT groups was significantly decreased compared with that of the non-VT groups (P = 0.03). Furthermore, Cx43 protein was distributed heterogeneously in the VT groups (P < 0.0001). CONCLUSION: Heterogeneous reduction of Cx43 protein may result in development of malignant ventricular arrhythmia in DCM.     

致心律失常性右心室心肌病室性心动过速的导管射频消融

目的致心律失常性右心室心肌病（ARVC）所致的多形室性心动过速（室速）具有较高的死亡风险，心内非接触式标测可提供快速而准确的标测并指导消融。方法32例患者（男性26例，女性6例），年龄（37．2±13．8）岁，其中14例有晕厥／黑矇史，2例已植入心律转复除颤器（ICD）。所有患者均经左锁骨下静脉送入EnSite多电极矩阵导管进行非接触式标测。结果全部患者共诱发出67阵室速，其心电图形态不同，但均为左束支阻滞形室速。频率130～310（210．0±32．2）次／min，其中42阵室速的频率t〉200次／min。24例（75％）患者有〉t2种形态的室速。在非接触式标测指导下对室速的起源进行了片状消融。消融的即时成功率为84，4％（27／32），15．6％（5／32）的患者经消融后室速频率明显减慢。随访9～72（28．6±16．0）个月，无一例患者发生晕厥／黑矇。术中无并发症。随访期间81．3％的患者不服药亦无室速发生，其余均获得明显改善。结论ARVC所致的室速可在非接触式标测的指引下经片状射频消融而消除或获得明显改善。本组无一例发生心脏骤停或心脏性猝死。某些患者消融后可能出现迟发效应。