Author + information
- Received October 27, 2016
- Revision received January 9, 2017
- Accepted January 12, 2017
- Published online July 17, 2017.
- Daniele Muser, MD,
- Jackson J. Liang, DO,
- Rajeev K. Pathak, MD, PhD,
- Silvia Magnani, MD,
- Simon A. Castro, MD,
- Tatsuya Hayashi, MD,
- Fermin C. Garcia, MD,
- Gregory E. Supple, MD,
- Michael P. Riley, MD, PhD,
- David Lin, MD,
- Sanjay Dixit, MD,
- Erica S. Zado, PA-C,
- David S. Frankel, MD,
- David J. Callans, MD,
- Francis E. Marchlinski, MD and
- Pasquale Santangeli, MD, PhD∗ ()
- Cardiac Electrophysiology Section, Cardiovascular Division, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania
- ↵∗Address for correspondence:
Dr. Pasquale Santangeli, Cardiovascular Division, Hospital of the University of Pennsylvania, 9 Founders Pavilion–Cardiology, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.
Objectives The goal of this study was to determine the long-term outcomes of catheter ablation (CA) of electrical storm in patients with nonischemic dilated cardiomyopathy (NIDCM) compared with patients with ischemic cardiomyopathy (ICM).
Background CA of ventricular tachycardia (VT) electrical storm has been shown to improve VT-free survival in patients with ICM. Data on the outcomes of CA of electrical storm in patients with NIDCM are insufficient.
Methods The study included 267 consecutive patients with NIDCM (n = 71; ejection fraction 32 ± 14%) and ICM (n = 196; ejection fraction 28 ± 12%). Endo-epicardial CA was performed in 59 (22%) patients. CA was guided by activation and entrainment mapping for tolerated VT and pacemapping/targeting of abnormal substrate for unmappable VT.
Results After a median follow-up of 45 (25th to 75th percentile: 9 to 71) months and 1 (25th to 75th percentile: 1 to 8) procedures, 76 (29%) patients died, 25 (9%) underwent heart transplantation, 87 (33%) experienced VT recurrence, and 13 (5%) had recurrence of electrical storm. Overall VT-free survival was 54% at 60 months (48% in NIDCM and 54% in ICM; p = 0.128). Patients with VT recurrence experienced a median of 2 (1 to 10) VT episodes in the 5 (1 to 14) months after the procedure. Death/transplantation-free survival was 62% at 60 months (53% in NIDCM and 64% in ICM; p = 0.067). Persistent inducibility of any VT with cycle length ≥250 ms at programmed stimulation at the end of the procedure was the only independent predictor of VT recurrence. Low ejection fraction, New York Heart Association functional class, and VT recurrence over follow-up independently predicted death/transplantation.
Conclusions CA of electrical storm was similarly effective in patients with NIDCM compared with patients with ICM, with elimination of electrical storm in 95% of cases and achievement of complete VT control at long-term follow-up in most patients.
In patients with structural heart disease, the occurrence of ventricular tachycardia (VT) electrical storm, defined according to multiple episodes of VT leading to appropriate implantable cardioverter-defibrillator (ICD) therapies within a short period of time, represents a major prognostic event with a striking independent association with adverse outcomes (1–3). Catheter ablation (CA) has been shown to effectively achieve VT control in the short- and mid-term follow-up of patients with ischemic cardiomyopathy (ICM) presenting with electrical storm (4–6). Thus far, data on the outcomes of CA of electrical storm in patients with nonischemic dilated cardiomyopathy (NIDCM) are insufficient and limited to small observational series (4–8). The goal of the present study was to assess the long-term outcomes of CA of electrical storm in patients with NIDCM compared with patients with ICM.
The study population consisted of 267 consecutive patients (196 with ICM and 71 with NIDCM) with drug-refractory electrical storm referred for CA between January 2005 and December 2014. Electrical storm was defined as the occurrence of ≥3 episodes of VT/ventricular fibrillation separated by >5 min during a 24-h period resulting in an appropriate ICD therapy (9). Patients with either idiopathic ventricular fibrillation or ventricular fibrillation triggers from Purkinje tissue at the border zone of myocardial infarction were excluded from this series.
The distinction between ICM and NIDCM was based on the presence of clinical coronary artery disease and/or previous myocardial infarction. In particular, NIDCM was defined according to evidence of dilation and left ventricular (LV) systolic impairment (left ventricular ejection fraction [LVEF] <50%) in the absence of significant coronary artery disease (>50% stenosis, assessed by using coronary angiography or coronary artery computed tomography scanning). Patients with congenital heart disease, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, LV noncompaction, restrictive cardiomyopathy, myocarditis, cardiac sarcoidosis, toxic cardiomyopathy, tachycardia-induced cardiomyopathy, and primary valvular abnormalities were excluded. All patients provided written informed consent to participate.
All patients underwent the procedure in the fasting state, and it was performed under conscious sedation whenever possible. General anesthesia was used when necessary at the discretion of the operator or anesthesiologist involved in the procedure for ventilation, oxygenation, or patient comfort and during epicardial mapping and ablation procedures. Catheters were placed in position in the heart with the use of fluoroscopic guidance. A standard transvenous 6-F quadripolar catheter with 5-mm interelectrode distance (Bard Inc., Delran, New Jersey) was placed at the right ventricular apex. An 8-F, 64-element phased-array intracardiac echocardiography catheter (AcuNav, Acuson, Mountain View, California) was used to assist catheter manipulation, to assess tissue–catheter contact, and to monitor for complications. A deflectable 3.5-mm open irrigated tip catheter (NaviStar ThermoCool, Biosense Webster, Diamond Bar, California) was used for mapping and ablation. The mapping/ablation catheter was advanced to the right ventricle (transvenous approach) or left ventricle (retrograde aortic or transseptal approach) according to the presumed site of origin of the VT or the underlying substrate. The programmed ventricular stimulation protocol to induce VT included up to triple extrastimuli from at least 2 right ventricular or LV sites with at least 2 drive cycle lengths (CLs). The 12-lead electrocardiography morphology of all spontaneous VTs (when available) and the intracardiac near-field and far-field electrograms of the ICD were collected and compared with the inducible VTs during the procedure. Induced VTs were identified as clinical if they matched the CL and morphology of stored ICD electrograms (near-field and far-field) and the 12-lead electrocardiography when available.
A high-density three-dimensional electroanatomic map (CARTO, Biosense Webster, Inc.) was created during sinus or paced rhythm maintaining a color and surface fill threshold ≤15 mm to ensure adequate sampling; the goal was to identify low-voltage areas and abnormal electrograms consistent with scar. The bipolar signals were filtered at 30 to 400 Hz (CARTO V.9 and V.7 systems, Biosense Webster, Inc.) or 16 to 500 Hz (CARTO-3 system, Biosense Webster, Inc.) and were displayed at a speed of 100 mm/s. The peak-to-peak signal amplitude of the bipolar electrogram was measured automatically and confirmed during manual review. The electrogram signals were displayed as color gradients on a three-dimensional computerized bipolar voltage map. Reference values for identifying abnormal endocardial bipolar and unipolar and epicardial bipolar electrogram signal amplitudes in the right and left ventricles were defined according to previously established criteria (10–12). An endocardial bipolar signal amplitude >1.5 mV either in the right or left ventricle, and an endocardial unipolar signal amplitude >8.3 mV in the left ventricle and >5.5 mV in the right ventricle, were categorized as normal and represented in the electroanatomic map by the color purple. Abnormal voltage areas were represented by a non-purple range of colors, with the most abnormal signal amplitude (arbitrary defined as <0.5 mV) represented by the color red. The decision for an epicardial approach was made when: 1) the 12-lead electrocardiography of the VT suggested an epicardial origin; 2) there was evidence of epicardial substrate on imaging studies (e.g., magnetic resonance, intracardiac echocardiography); 3) a unipolar electrogram abnormality (<8.3 mV) occurred in the presence of no or minimal bipolar (<1.5 mV) electrogram abnormality; and 4) the endocardial ablation procedure (either early VT recurrence or persistent inducibility of VT) failed.
Access to the pericardial space and epicardium was obtained by using the percutaneous subxiphoid approach described by Sosa et al. (13). The reference value for defining abnormal electrograms in the epicardium was <1.0 mV, as reported previously (14). To further limit the influence of epicardial fat and small-vessel coronary vasculature (i.e., vessels that cannot be directly appreciated by using coronary angiogram) on the low-voltage region, the contiguous low-voltage electrograms had to demonstrate not only a low amplitude but also signals with discrete late potentials (recorded after the QRS of the surface electrocardiography). They also had to demonstrate broad multicomponent or split signals within the boundary of the defined contiguous low-voltage area. Signals >1.0 mV that also exhibited abnormal, multicomponent, split, or late potentials were tagged and noted if they were adjacent to confluent low-voltage areas typically included in substrate-based ablation targets.
The main target of CA was to eliminate the clinical VTs and all mappable nonclinical VTs. All induced VTs with a CL ≥250 ms were considered potentially relevant and routinely targeted for ablation. For hemodynamically tolerated VTs, entrainment mapping was performed within the low-voltage area at sites exhibiting diastolic activity to identify critical sites of the VT re-entrant circuit. A critical site that was an appropriate target for ablation was defined as a site exhibiting entrainment with concealed QRS fusion and return cycle within 30 ms of the VT CL with matching stimulus-to-QRS and electrogram-to-QRS intervals or where VT terminated during pacing without global capture (15,16). Radiofrequency energy was delivered at these sites. If delivery of radiofrequency energy failed to terminate VT within 60 s, the ablation catheter was moved to an alternative site meeting the same criteria. For hemodynamically unstable VTs, substrate modification was performed with linear or cluster lesions targeting sites identified by pace mapping; it included signals with discrete split or late potentials recorded during sinus rhythm or with right ventricular apical pacing, as previously described (11). The site of origin was approximated by using pacemapping to reproduce the VT QRS complex and to identify sites with a long stimulus-to-QRS interval. Limited activation and entrainment information was used to corroborate the pacemap information whenever possible. Substrate ablation was typically extended to target markedly abnormal fractionated split and late potentials; there was a specific emphasis on abnormal potentials recorded within a 2- to 3-cm radius of the site of origin, defined by entrainment mapping or the best pacemap with clusters of radiofrequency lesions targeting abnormal potentials with the endpoint of signal modification or elimination. Epicardial radiofrequency lesions always avoided large coronary vessels by at least 1 cm based on cine angiography. If monomorphic VT inducibility persisted after targeting all spontaneous and initially inducible VT, residual VT morphologies were remapped by using the aforementioned techniques. The amount of fluid in the epicardial space associated with the open irrigated catheter was monitored with intracardiac echocardiography and continuous arterial blood pressure monitoring for evidence of hypotension, and it was drained intermittently or continuously to preclude hemodynamic compromise. At the end of the ablation procedure, 2 to 3 mg/kg of triamcinolone was routinely administered intrapericardially to reduce inflammation. A pigtail catheter was typically left in place in the pericardial sac and removed within 24 h after the absence of continued pericardial drainage or fluid accumulation was confirmed on transthoracic echocardiography. Data on minor access-related pericardial bleeding episodes (i.e., not requiring any intervention) were not systematically collected, and only data on major bleeding episodes (i.e., requiring intervention) were reported.
Radiofrequency energy application targeted a maximum temperature of 42°C and a maximum impedance drop of 12 to 15 Ohms with an output of 20 to 50 W. Lesion duration was typically set for 60 to 90 s. It was further increased to ≥3 min in duration at sites associated with transient suppression of VT with monitoring to confirm stable impedance drop or when intramural substrate was suspected in nonischemic cardiomyopathy; these assessments were based on normal bipolar voltage with abnormal unipolar signal or by pacing the right ventricular base and assessing transmyocardial conduction time (17,18). Hemodynamic support devices (percutaneous mechanical hemodynamic support with the Impella device [Abiomed, Danvers, Massachusetts] or intra-aortic balloon pump) were used at the discretion of the operator in cases of periprocedural hemodynamic instability.
Long-term outcomes included the following: 1) survival free of any VT (defined as any symptomatic VT or sustained VT on ICD interrogation or 12-lead electrocardiography) after single or multiple procedures; 2) survival free of electrical storm; and 3) survival free of the composite endpoint of death or cardiac transplantation.
Acute procedural outcomes consisted of noninducibility of the clinical VT and of any inducible VT (excluding nonclinical VTs with a CL <250 ms). Acute efficacy was assessed on the basis of inducibility of VT at the end of the ablation procedure with a uniform stimulation protocol (up to 3 extrastimuli from up to 2 ventricular sites with at least 2 drive CLs) and at the time of repeat programmed stimulation before hospital discharge; this simulation was performed noninvasively from a single right ventricular site via the ICD system (noninvasive programmed stimulation [NIPS]). Post-procedural device programming was consistent throughout the years and typically included a VT zone able to detect (and treat if still inducible) the slowest clinical and/or induced VT. The effect of additional antiarrhythmic drug therapy on CL slowing was also taken into account to avoid underdetection of VT.
Patients were routinely evaluated at 4 to 8 weeks after ablation and then at 3- to 6-month intervals. For patients not followed up at our institution, the referring cardiologists were contacted, and ICD interrogations were reviewed to determine VT recurrence. Telephone interviews were performed at 6- and 12-month intervals with patients or family members to confirm the absence of arrhythmia symptoms. The Social Security Death Index database was also searched for mortality information.
Continuous variables were expressed as mean ± SD if normally distributed or median (interquartile range: 25th to 75th percentile) if not normally distributed. All continuous variables were tested for normal distribution by using the 1-sample Kolmogorov-Smirnov test. Categorical data are expressed as counts and percentages. Continuous variables were compared by using independent-sample parametric (unpaired Student t) or nonparametric (Mann-Whitney U) tests. Paired variables among the same patients were compared by using paired-sample parametric (paired Student t) or nonparametric (paired Wilcoxon signed rank) tests for continuous variables and McNemar’s test for binary variables. Categorical variables were compared by using the chi-square test or the Fisher exact test when appropriate. Survival curves were generated by using the Kaplan-Meier method and compared by using the log-rank test. Univariate and multivariable Cox proportional hazards analyses were used to test the association between the outcome events and baseline covariates.
All potential confounders were initially entered into the model on the basis of known clinical relevance; a model reduction was then performed by excluding variables with a p value >0.20 based on the log-likelihood test. Models predicting mortality/transplantation used VT recurrence over follow-up as a time-dependent covariate. Even if clinically relevant, the result of NIPS was not included in the multivariable model because NIPS was performed in only one-half of the study sample, and this method would have reduced the power of the analysis by reducing the total number of patients included. The proportional hazards assumption was assessed by using Schoenfeld’s residuals test. Two-tailed tests were considered statistically significant at the 0.05 level. All analyses were performed by using IBM SPSS version 23.0 (IBM SPSS Statistics, IBM Corporation, Armonk, New York).
The baseline features of the study population are summarized in Table 1. Compared with patients with ICM, patients with NIDCM were significantly younger (60 ± 15 years vs. 67 ± 11 years; p < 0.001), with fewer comorbidities, including hypertension (44% vs. 75%; p < 0.001), diabetes (14% vs. 31%; p = 0.007), hyperlipidemia (30% vs. 77%; p < 0.001), and atrial fibrillation/flutter (34% vs. 49%; p = 0.028); they also had a higher LVEF (32 ± 14% vs. 28 ± 12%; p = 0.026). Before the CA procedure, patients failed a median of 2 (1 to 2) antiarrhythmic drugs, with no difference between the NIDCM and ICM groups (p = 0.080). No differences were observed in the proportion of patients undergoing amiodarone treatment.
CA and acute procedural outcomes
The main procedural data are summarized in Table 2. Over the study period, 374 procedures were performed in the 267 patients included, with a mean number of procedures per patient of 1.2 ± 0.5 (range 1 to 4) in the ICM group and 1.8 ± 1.2 (range 1 to 8) in the NIDCM group (p = 0.001 for comparison). Epicardial mapping was performed in 59 (22%) patients (12 [6%] in the ICM group vs. 47 [66%] in the NIDCM group; p < 0.001), and 47 (80%) of them underwent epicardial ablation (9 [75%] in the ICM group vs. 38 [81%] in the NIDCM group). A mechanical hemodynamic support device was used in 30 (15%) cases in the ICM group and 8 (11%) cases in the NIDCM group (p = 0.404). Hemodynamic LV support was placed at the beginning of the procedure in 31 (82%) patients (26 [87%] of 30 in the ICM group vs. 5 [63%] of 8 in the NIDCM group; p = 0.146 for comparison). In the remaining 7 (18%) patients (4 [13%] of 30 in the ICM group vs. 3 [38%] of 8 in the NIDCM group; p = 0.146), hemodynamic support devices were placed during the procedure because of hemodynamic instability. An antegrade transseptal approach for LV mapping and ablation was more frequently used among patients with ICM (23% vs. 9%; p = 0.012).
At least 1 hemodynamically nontolerated VT was present in 195 (73%) patients. The mean CL of the clinical tachycardia was 401 ± 95 ms, and patients with ICM tended to have slower CL compared with patients with NIDCM (409 ± 96 ms vs. 380 ± 92 ms, respectively; p = 0.032). Ten (4%) patients presented with multiple morphologies of VT in addition to a history of polymorphic VT/ventricular fibrillation. In all of these patients, sustained VT was uniformly induced at the time of the procedure, and they underwent VT ablation and substrate modification. A predominant substrate-based approach without or with only limited entrainment/activation mapping was performed in 214 (80%) patients. At the end of the last procedure, 240 (90%) patients underwent programmed ventricular stimulation; in 27 cases, this procedure was not performed because of unstable patient conditions. No significant differences were observed in terms of acute procedure outcomes between the 2 groups. At the end of the last procedure, at least 1 VT with CL ≥250 ms was inducible in 45 (26%) patients with ICM and in 21 (32%) patients with NIDCM (p = 0.393). A total of 139 (52%) patients underwent NIPS a median of 3 (2 to 4) days after the procedure. Noninducibility of any VT with CL ≥250 ms at NIPS was achieved in 36 (33%) of 109 patients in the ICM group and in 10 (33%) of 30 patients in the NIDCM group (p = 0.975).
A total of 11 (3%) major complications occurred during 374 procedures (Table 2). Two patients with ICM had pericardial effusion requiring surgery. In 1 case, a lateral mitral annular laceration occurred during mapping; in the other case, there was a perforation of the LV wall during radiofrequency ablation. A pericardial effusion occurred in 4 patients and was successfully drained percutaneously without consequence (3 patients in the ICM group in whom the effusion occurred during endocardial LV ablation, and 1 patient in the NIDCM group with accidental perforation of the right ventricular free wall during pericardial access). In 2 patients with NIDCM, an occlusion of a small coronary artery branch occurred during epicardial ablation. Transient phrenic nerve injury occurred in 1 patient during epicardial ablation. In 1 patient, complete atrioventricular block occurred with ablation at the basal septum, and in 1 case a retroperitoneal bleed occurred that required urgent surgical repair.
After a median follow-up of 45 (9 to 71) months, 25 patients underwent heart transplantation, and 76 died (Table 3). Overall death/transplantation-free survival was 62% at the 60-month follow-up with a trend toward worse outcomes in the NIDCM group (53%) compared with the ICM group (64%; log-rank test, p = 0.067) (Figure 1); this outcome was driven by a higher rate of heart transplantations in patients with NIDCM (18% vs. 6%; p = 0.041). Cumulative VT-free survival after the last procedure was 54% at 60 months (54% in ICM and 48% in NIDCM, respectively; log-rank test, p = 0.128). Electrical storm recurred in 9 (5%) patients with ICM and in 4 (6%) patients with NIDCM within 16 (1.5 to 51) months after the procedure (p = 0.727). Cumulative electrical storm recurrence-free survival was 93% at the 60-month follow-up (Figures 1 and 2). Although VT recurred in 87 (33%) patients after the ablation, a substantial reduction in the 6-month VT burden was observed in most of these cases (i.e., including patients with recurrent VT post-procedure); there was a median of 32 (15 to 55) VT episodes during the 6 months before the procedure and a median of 0 (0 to 1) VT episodes during the 6 months after the procedure (p < 0.001 for comparison). In particular, among the 87 patients with VT recurrences, 60 (69%) of 87 patients had only isolated (i.e., ≤3) VT episodes during the 6 months after the procedure.
At the last follow-up, 120 (45%) patients were taking only β-blockers, 57 (21%) were taking sotalol or class I antiarrhythmic drugs (15 also/mainly for atrial arrhythmias), and 90 (34%) were taking amiodarone (24 also/mainly for atrial arrhythmias) (Figure 3). The number of patients taking amiodarone (90 [34%] vs. 213 [80%]; p < 0.001) at the last follow-up was significantly lower compared with before the ablation.
Predictors of long-term outcomes
The results of the univariate and multivariable Cox proportional hazards analyses to determine the association between baseline covariates and outcome events are reported in Tables 4 and 5⇓⇓. On multivariable analysis, inducibility of any VT with CL ≥250 ms at the end of the procedure (hazard ratio [HR]: 2.63; 95% confidence interval [CI]: 1.60 to 4.36; p < 0.001) was the only variable independently associated with VT recurrence during follow-up. Independent predictors of death and/or transplantation at follow-up were LVEF (HR: 0.96; 95% CI: 0.94 to 0.98; p < 0.001), New York Heart Association functional class (HR: 1.59; 95% CI: 1.21 to 2.10; p = 0.001), and VT recurrence at follow-up (HR: 5.48; 95% CI: 3.49 to 8.62; p < 0.001).
The present study documents the long-term outcomes of CA of drug-refractory electrical storm in the largest cohort of patients with the longest follow-up to date (median >3 years) and specifically compares the outcomes in NIDCM versus ICM. The major findings are as follows: 1) CA of electrical storm in patients with NIDCM is effective and safe to achieve long-term VT control in most patients, with abolition of electrical storm recurrence in >90% of cases and overall results comparable to those in patients with ICM; 2) inducibility of VT at the end of the procedure was the only variable independently related to VT recurrence post-ablation; and 3) VT recurrence together with LV systolic dysfunction and advanced New York Heart Association functional class were independent predictors of death or transplantation long term.
Previous studies have uniformly reported a strong negative prognostic impact of electrical storm in patients with structural heart disease and ICD, with a substantial increase in mortality (1,2,19). The adverse prognosis could be related to progressive deterioration of cardiac function resulting from frequent shocks, prolonged exposure to a low-output state due to high VT burden (which compromises cardiac contractility and the function of other end-organs such as the kidney), and systemic toxicity from high-dose antiarrhythmic drug therapy (20,21). The role of CA in the management of electrical storm is well defined in the setting of ICM. Observational studies have reported good short- and mid-term VT control in patients with ICM and electrical storm (4–6), although long-term (>1 year) outcome data are scarce. Furthermore, in the setting of NIDCM, there is insufficient information on the role of CA for electrical storm, with few data from small subgroups including <15 patients (Table 6) (7). The cumulative available evidence would suggest a higher risk of VT recurrence and mortality in patients with NIDCM compared with those with ICM (4,5,7). Our findings are in contrast with this concept; we found no significant differences in VT-free survival after CA of electrical storm in this population of patients with NIDCM compared with ICM. Overall, 93% of patients were free from recurrent electrical storm at the 60-month follow-up, with 54% having complete VT elimination with no recurrent episodes. Furthermore, these results were obtained with a reduction in the use of antiarrhythmic medications compared with preablation (Figure 3). Of note, similar to previous reports on endo-epicardial ablation in NIDCM, two-thirds of patients with NIDCM needed a combined endocardial/epicardial procedure to achieve long-term outcomes comparable to those in patients with ICM (22).
A recent important study by Kumar et al. (23) compared the long-term outcomes after VT ablation in patients with ischemic and nonischemic heart disease and in patients without overt structural heart disease. Similar to our study, Kumar et al. (23) reported that patients with ICM are typically older, have a lower ejection fraction, and are affected by more comorbidities compared with patients with NIDCM or with patients without structural heart diseases. However, at variance with our study, patients with ICM in the study by Kumar et al. (23) had better long-term VT-free survival compared with patients with NICM. This difference may be related to the fact that we included only a very select group of patients presenting with electrical storm in whom, owing to the high baseline arrhythmic burden, an accurate characterization of the regions of the substrate that are responsible for the clinical VT events may be easier compared with other populations of patients with NICM and VT (but no VT storm). Overall, this outcome may favorably affect long-term outcomes of CA.
The overall death/transplantation-free survival in the present study was 62% at 60 months. It was also not significantly different in patients with ICM compared with those with NIDCM; this finding is true even if rates of death cannot be fully compared given the fact that patients with NIDCM were overall healthier with less advanced heart failure status. Independent predictors of mortality included low LVEF and advanced heart failure status (i.e., New York Heart Association functional class), which is consistent with prior reports (4).
Of note, persistent VT inducibility at the end of the procedure was the only independent predictor of long-term VT recurrence, and the latter was strongly associated with subsequent mortality. The result of NIPS was not included in the multivariable model to avoid a significant reduction in the total number of patients included in the analysis (it was performed in only 52% of the study population). However, persistent inducibility of VT at NIPS was significantly related to VT recurrence at univariable analysis. These findings confirm our initial experience with NIPS in which both VT inducibility at the end of the procedure and VT inducibility at NIPS was significantly associated with VT recurrence over follow-up at multivariable analysis (24).
This observational study summarized the experience of a tertiary referral center that specializes in CA of VT. As such, the characteristics of the patient population and outcomes of CA may be affected by selection/referral bias. Due to the observational nature of the study and the lack of a control group undergoing different treatment strategies (e.g., escalation/combination of antiarrhythmic drugs, sympathetic denervation), we cannot prove that CA is superior to other therapies in electrical storm management (25). Moreover, the choice to perform post-procedure NIPS was left to the discretion of the operator, and it might have been influenced by other unmeasured factors such as overall clinical status of the patient, duration of the procedure, and acute procedural success. Typically, nonischemic patients exhibited a predominant basal and/or septal substrate involving the perivalvular regions, whereas in ischemic patients, the substrate involved the previous infarction scar. Unfortunately, detailed information regarding the precise sites of clinical/inducible VT termination was not systematically collected. Moreover, information on the hemodynamic tolerability of the clinical VT episodes was not collected.
Seventy-four (28%) of 267 patients had a follow-up <12 months, but this time frame was typically due to occurrence of other competing events such as death or heart transplantation within 12 months rather than an insufficient follow-up duration. Finally, data on specific ICD programming and type of therapies (i.e., antitachycardia pacing vs. shocks) before and after the ablation procedure were not available for all patients. However, as noted earlier, post-procedure device programming was uniform and included a VT zone able to detect (and treat if still inducible) the slowest clinical and/or induced VT; the effect of additional antiarrhythmic drug therapy on CL slowing was also taken into account to avoid underdetection of VT. Because any sustained VT episode was counted as a recurrence in this study, we believe that our relatively conservative device programming (to detect and potentially also treat slow VTs) further strengthens the value of ablative therapy in these patients in terms of important outcomes such as electrical storm recurrence and any VT recurrence.
This study is the largest with the longest follow-up to date evaluating the role of CA for the treatment of electrical storm in patients with NIDCM compared with those with ICM. These data indicate that CA of electrical storm in NIDCM provided good long-term arrhythmia-free survival, comparable to patients with ICM. The majority of patients had elimination of electrical storm, and complete VT suppression was achieved in most subjects with a reduction in the concomitant use of antiarrhythmic medications.
COMPETENCY IN MEDICAL KNOWLEGE: Electrical storm is a life-threatening condition for which CA represents an effective treatment strategy. It eliminated electrical storm in most subjects and provided good long-term arrhythmia-free survival regardless of the etiology of the underlying structural heart disease.
TRANSLATIONAL OUTLOOK: Large randomized clinical trials would be needed to further assess the best treatment strategy of electrical storm.
Funded in part by the Richard T. and Angela Clark Innovation Fund and the Mark S. Marchlinski Research Fund in Cardiac Electrophysiology. Dr. Supple has received honoraria for lectures from St. Jude Medical, Biotronik, Biosense Webster, and Medtronic. Dr. Calans has served as a consultant to Biosense Webster and St. Jude Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Abbreviations and Acronyms
- catheter ablation
- confidence interval
- cycle length
- hazard ratio
- implantable cardioverter-defibrillator
- ischemic cardiomyopathy
- left ventricular
- left ventricular ejection fraction
- nonischemic dilated cardiomyopathy
- noninvasive programmed stimulation
- ventricular tachycardia
- Received October 27, 2016.
- Revision received January 9, 2017.
- Accepted January 12, 2017.
- 2017 American College of Cardiology Foundation
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