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Prophylactic catheter ablation for induced monomorphic ventricular tachycardia in patients with implantable cardioverter defibrillators as primary prevention

Takekuni Hayashi, Seiji Fukamizu, Rintaro Hojo, Kota Komiyama, Yasuhiro Tanabe, Tamotsu Tejima, Kyoko Soejima, Mitsuhiro Nishizaki, Masayasu Hiraoka, Junya Ako, Shin-ichi Momomura, Harumizu Sakurada
DOI: http://dx.doi.org/10.1093/europace/eut050 1507-1515 First published online: 19 April 2013

Abstract

Aims Prophylactic catheter ablation (CA) has been established to reduce the incidence of appropriate implantable cardioverter-defibrillator (ICD) therapy (anti-tachycardia pacing or shock) in secondary prevention patients. The aim of this study was to determine whether prophylactic CA for induced ventricular tachycardia (VT) reduces the incidence of appropriate ICD therapy in primary prevention patients.

Methods and results We retrospectively investigated 66 consecutive patients with structural heart disease who had undergone ICD implantation as primary prevention and electrophysiological study. Patients with hypertrophic cardiomyopathy or no inducible monomorphic VT had been excluded, and the remaining 38 patients were divided into two groups; those who had undergone prophylactic CA for induced monomorphic VT (the CA group, n = 18), and those who had not undergone CA (the non-CA group, n = 20). During a mean follow-up of 50 ± 38 months, 1 patient (5%) received appropriate ICD therapy in the CA group and 13 (65%) in the non-CA group. Kaplan–Meier survival analysis revealed a significantly higher event-free survival rates for appropriate ICD therapy in the CA group compared with the non-CA group (P = 0.003). Among the patients, one patient (5%) in the CA group and nine patients (45%) in the non-CA group suffered appropriate shock (P = 0.018).

Conclusions Prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy including shock in primary prevention patients. These results indicate that prophylactic CA may be considered for structural heart disease patients who are candidates for ICD implantation as primary prevention.

  • Catheter ablation
  • Implantable cardioverter-defibrillator
  • Primary prevention
  • Ventricular tachycardia

What's new?

  • Prophylactic catheter ablation (CA) has been found to reduce the incidence of appropriate implantable cardioverter-defibrillator (ICD) therapy in secondary prevention patients. However, it is unknown whether prophylactic CA for induced ventricular tachycardia (VT) can reduce the incidence of appropriate ICD therapy in primary prevention patients. This study aimed to fill this research gap by examining whether prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy and improves survival in patients who had undergone ICD implantation as a primary prevention. In the present study, Kaplan–Meier survival analysis revealed significantly higher event-free survival rates for appropriate ICD therapy in the CA group compared with the non-CA group (P = 0.003). Our study showed that prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy including shock in primary prevention patients.

Introduction

Implantation of an implantable cardioverter-defibrillator (ICD) is currently the standard therapy for prevention of sudden cardiac death in patients with low left ventricular ejection fraction (LVEF). Appropriate ICD therapy [anti-tachycardia pacing (ATP) or shock] is effective presumably because termination potentially life-threatening ventricular tachycardia/fibrillation (VT/VF) before they cause haemodynamic compromise or result in hypotension, syncope, progressive heart failure, ischaemia, or multiorgan system failure related to prolonged tachyarrhythmia. However, ICD implantation is not a cure for VT/VF and poses several risks, including decreased quality of life; increased mortality among patients who suffer ICD shock compared with patients who do not; and clinically significant anxiety and depression as a result of recurrent ICD shock, which has been found to occur in more than 50% of patients.15 Furthermore, ICD implantation has been found not to protect against sudden cardiac death in 3–7% of patients.6

The Substrate Mapping and Ablation in Sinus Rhythm to Halt Ventricular Tachycardia (SMASH-VT) and the Ventricular Tachycardia Ablation in Coronary Heart Disease (VTACH) found that prophylactic catheter ablation (CA) reduces the incidence of appropriate ICD therapy in patients who had undergone ICD implantation as a means of secondary prevention and had a history of myocardial infarction (MI).7,8 However, it remains unknown whether prophylactic CA for induced VT reduces the incidence of appropriate ICD therapy for primary prevention patients. This study aimed to fill this research gap by examining whether prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy and improves survival in patients who have undergone ICD implantation as a means of primary prevention.

Methods

Patient selection

We performed cardiac electrophysiological study (EPS) for indication of ICD implantation as a means of primary prevention in patients with structural heart disease. In ischaemic cardiomyopathy patients, those with an LVEF ≤ 40% or those with syncope suspected to have been caused by VT/VF, had undergone EPS. In non-ischaemic cardiomyopathy patients, those with significant LV dysfunction or unexplained syncope had undergone EPS. Between March 1997 and April 2011, a total of 66 consecutive patients with structural heart disease who had undergone ICD implantation as a means of primary prevention and EPS prior to or after ICD implantation in our institution, were enrolled retrospectively. Of these patients, 36 of whom had been diagnosed with ischaemic cardiomyopathy and 30 with non-ischaemic cardiomyopathy. Eleven patients with hypertrophic cardiomyopathy were excluded in consideration of the preservation of LVEF and the low inducibility of sustained monomorphic VT in many cases. After an additional 17 patients without inducible monomorphic VT (no inducible VT/VF in 4 patients, inducible only polymorphic VT in 6 patients, inducible only VF in 7 patients) had been excluded from consideration, 38 patients, 28 of whom had been diagnosed with ischaemic cardiomyopathy and 10 with non-ischaemic cardiomyopathy, remained in the study. These 38 patients were divided into two groups: those who had undergone prophylactic CA for induced monomorphic VT, termed the CA group (n = 18) and those who had not undergone CA, termed the non-CA group (n = 20). Before undergoing CA, informed consent was obtained from each patient according to the protocol approved by the Hospital Human Research Committee.

Procedures and device programming

Electrophysiological study had included the delivery of 1–3 extrastimuli during pacing at two basic cycle lengths (400 and 600 ms) from two right ventricular (RV) sites [the RV apex (RVA) and the RV outflow tract] and burst pacing. The minimum coupling interval had been 180 ms in the 1–2 extrastimuli and 200 ms during that of three extrastimuli. The positive endpoint of EPS was induction of monomorphic VT for duration >30 s or requiring termination for haemodynamically intolerance. In cases of induced monomorphic VT, programmed ventricular stimulation had been continued to confirm reproducible inducibility of identical monomorphic VT. Prophylactic CA had been performed for patients with reproducible monomorphic VT but not for patients over 80 years of age or who had been referred for ICD implantation at our institute after undergoing EPS at another hospital. Target VT was defined as reproducibly induced monomorphic VT. Catheter ablation was performed using a non-irrigated or irrigated ablation catheter (NaviStar or NaviStar ThermoCool; Biosense Webster) via a transvenous or retrograde transaortic approach.

For patients with inducible haemodynamically tolerated monomorphic VT, CA was performed at sites with mid-diastolic potential, where pacing entrained the VT with concealed fusion, a post-pacing interval within 30 ms of the VT cycle length (VTCL), and a stimulus-to-QRS interval of <70% of the VTCL with or without the use of a three-dimensional (3D) electroanatomical (EA) mapping system (Carto, Biosense Webster). The use of this 3D EA mapping system had become possible in our institute from May 2002. In cases in which the 3D EA mapping system had been used, bipolar endocardial voltage mapping of the RV and/or LV was performed during sinus or RV pacing rhythm. The electrical scar was defined by voltage criteria, i.e. the electrogram amplitudes ≤0.5 mV were defined as dense scar, and voltages >0.5 mV and ≤1.5 mV as scar border zones.912

For patients with inducible haemodynamically intolerated monomorphic VT, exit sites had been identified and targeted on the basis of pace mapping during sinus rhythm with a paced QRS morphology similar to that of the VT QRS morphology. Pacing had been performed at the scar border zone and at sites with fragmented potential, double potential, and delayed potential. Substrate modification had been performed by linear ablation lines along the scar border by extending lesions at exit sites or through an identified isthmus.9,13,14 Prophylactic CA had not been performed for haemodynamically intolerated monomorphic VT in cases in which the voltage map appeared normal.

Programmed ventricular stimulation was repeated after VT ablation. Successful ablation was defined as non-inducibility of the monomorphic VT at the end of the procedure and partially successful ablation as non-inducibility of the target monomorphic VT.

In principle, device programming had consisted of a VF zone with a cut-off rate of 188–220 b.p.m. and a VT zone with a cut-off cycle length of 40 ms above the induced maximum VTCL and ATP followed by shock therapy. In the cases of inducible monomorphic VT that had been disorganized to the VF or that had accelerated to rapid VT by overdrive pacing from RVA during EPS, device programming had been configured to the VF zone only. For the VT and VF therapy zones, the number of beats to detection was set at 8–16 beats. Program parameters, including those for the supraventricular tachycardia (SVT) discriminators, had not been specified in the protocol, and had been left to the individual physician's discretion.

Routine follow-up

Patients were followed up every 3 months at the ICD clinic. Data collection included number of VT/VF and SVT episodes, type of treatment required, medical justifications for device programming changes, cardiovascular medications prescribed, and the number of cardiovascular events. The device-detected VT/VF and SVT episodes were classified by two electrophysiologists. Additional clinical data were collected and transthoracic echocardiography was performed every subsequent 1 or 2 years. Coronary intervention was performed in cases of confirmed active and ongoing myocardial ischaemia. During follow-up, CA including epicardial approach was performed for recurrent appropriate ICD therapy.

Statistical analysis

Continuous variables were compared using the independent sample student's t-test and expressed as mean ± standard deviation. Categorical variables were compared using the χ2 or Fisher's exact test, as applicable. Probability of freedom from appropriate ICD therapy was examined using Kaplan–Meier analysis with the log-rank test. All statistical analyses were performed using SPSS software version 19.0 (SPSS Inc.) and all results reaching a P value of <0.05 were considered statistically significant.

Results

Baseline characteristics

Figure 1 graphically shows the procedure for patient selection. Thirty-eight patients (mean age, 64 ± 10 years; 34 men; mean LVEF 32 ± 10%) were followed for a mean of 50 ± 42 months. Of these 38 patients, 20 had not undergone CA, 6 because endocardial EA mapping had shown normal voltage, 6 because the EA mapping system had not been available before May 2002, 2 because they had been over 80 years of age, 3 because they had undergone EPS at another hospital, and 6 due to inaccessibility on account of thrombus in the LV or the presence of combined aortic and mitral valve replacement. Comparison of the baseline characteristics of the CA group and the non-CA group indicated no significant differences between the groups except for gender regarding the variables of age, ischaemic aetiology, LVEF, estimated glomerular filtration rate, abnormalities on signal-averaged electrocardiograms (i.e. two of the following three criteria had been met: duration of the filtered QRS complex ≥114 ms, duration of the terminal low-amplitude signal >38 ms, and the root mean square of the terminal 40 ms of the QRS complex <20 µV), presence of non-sustained VT, the number of induced monomorphic VTs, minimum or maximum-induced VTCL, and type of ICD (Table 1). Among both groups, eight patients had been administered amiodarone, six for paroxysmal atrial fibrillation, and two for frequent ventricular premature contraction.

View this table:
Table 1

Patient baseline characteristics

CA group (n=18)Non-CA group (n=20)P value
Age, years65 ± 1065 ± 120.94
Male gender, no. (%)14 (78)20 (100)0.04
Ischaemic cardiomyopathy, no. (%)15 (83)13 (65)0.28
LVEF (%)32 ± 1132 ± 100.97
eGFR (mL/min)55 ± 2657 ± 270.81
Abnormalities on SAECG, no. (%)15 (83)16 (80)1.00
NSVT, no. (%)13 (72)16 (80)0.70
Unexplained syncope, no. (%)3 (16)6 (30)0.45
Induced monomorphic VT
 Number1.9 ± 1.12.3 ± 1.60.35
 Minimum VTCL (ms)264 ± 60259 ± 590.81
 Maximum VTCL (ms)287 ± 57306 ± 770.40
Medication, no. (%)
 Amiodarone3 (17)5 (25)0.41
 β-Blocker11 (61)14 (70)0.73
 ACE inhibitor or ARB11 (61)13 (65)1.00
Type of ICD, no. (%)
 Single-chamber6 (25)7 (35)1.00
 Dual-chamber12 (75)13 (65)1.00
 Mean follow-up period, months48 ± 3951 ± 460.84
  • Data are given as mean ± SD.

  • LVEF, left ventricular ejection fraction; NYHA, New York Heart Association; eGFR, estimated glomerular filtration rate; SAECG, signal-averaged electrocardiograms; NSVT, non-sustained ventricular tachycardia; VT, ventricular tachycardia; VTCL, ventricular tachycardia cycle length; ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker.

Figure 1

Trial profile. HCM, hypertrophic cardiomyopathy; VT, ventricular tachycardia; VF, ventricular fibrillation; CA, catheter ablation; EAM, electroanatomical mapping; EPS, electrophysiological study.

Results of prophylactic ventricular tachycardia ablation

A total of 34 incidences of monomorphic VT had been induced in the CA group. Of these 34 incidences, 30 incidences of haemodynamically intolerated monomorphic VT had been induced in 15 patients for whom endocardial substrate CA had been performed using the EA mapping system (Table 2 and Figure 2), and 4 incidences of haemodynamically tolerated monomorphic VT had been induced in 4 patients (1 patient had also inducible 1 haemodynamically intolerated monomorphic VT) for whom endocardial CA had been performed using conventional mapping with or without the EA mapping system. Endocardial CA was performed using a non-irrigated ablation catheter in 16 patients (89%) and an irrigated ablation catheter in 2 patients (11%). The acute success (non-VT inducibility after ablation) rate of CA was 83% (including induced only VF after VT ablation in one patient) and the partial success (induced non-target VT after ablation) rate was 17%. A significant CA-related complication, specifically, thromboembolic occlusion of the right coronary artery requiring coronary intervention, had occurred in one patient (6%).

View this table:
Table 2

Ablation characteristics and outcome

PtAge/sexSubstrateLVEF (%)VTs (n)VT typeVTCL rangeRF typeInducible VT after ablationOutcome
144/MMI(A)392S+U240–280StdNTMMVTPartial
269/MMI(I)304U470–480StdNTMMVTPartial
363/MMI(I)291U255IrrigatedVFSuccess
454/MMI(IL)194U240–280StdNoneSuccess
559/MMI(I)291S350StdNoneSuccess
680/MMI(A)222U200–300StdNTMMVTPartial
772/MMI(A)214U240–270StdNoneSuccess
877/MMI(I)301U240StdNoneSuccess
965/MMI(A)281U300StdNoneSuccess
1050/MMI(A)382U265–285StdNoneSuccess
1156/MMI(I)272U240–250IrrigatedNoneSuccess
1266/MMI(A)302U265StdNoneSuccess
1367/MMI(I)351S450StdNoneSuccess
1471/FMI(I)191U230StdNoneSuccess
1580/MMI(A)431U270StdNoneSuccess
1663/FSarcoidosis403U200–300StdNoneSuccess
1763/MDCM393U230–250StdNoneSuccess
1875/FSarcoidosis651S240StdNoneSuccess
  • Pt, patient; LVEF, left ventricular ejection fraction; VT, ventricular tachycardia; VTCL, ventricular tachycardia cycle length; RF, radiofrequency; MI(A), previous anterior myocardial infarction; MI(I), previous inferior MI; MI(IL), previous infero-lateral MI; DCM, dilated cardiomyopathy; S, haemodynamically tolerated monomorphic VT; U, haemodynamically intolerated monomorphic VT; Std, non-irrigated 4 mm-electrode RF; NTMMVT, non-target monomorphic VT; VF, ventricular fibrillation.

Figure 2

Example of VT ablation. (A) Electroanatomical voltage mapping during sinus rhythm shows extending the low-voltage area and the scar in patient with prior inferior MI. (B) Induced VT was haemodynamically intolerated. Paced QRS morphology at site with fragmented potential during sinus rhythm was similar to the VT QRS morphology. The intracardiac electrogram of the ablation catheter positioned at this area showed mid-diastolic potential during the induced haemodynamically intolerated VT. Substrate ablation was performed around this area. No monomorphic VT was induced after substrate ablation.

Follow-up and outcomes

During a mean follow-up of 50 ± 42 months, three patients (8%) died due to cardiovascular events (one patient in the CA group and two patients in the non-CA group, Figure 3). One patient in each group died of progressive heart failure, remaining one patient died of VF storm. And three patients (8%) died due to non-cardiac reasons (two patients in the CA group and one patient in the non-CA group, Figure 4).

Figure 3

Kaplan–Meier curve estimate of survival free from cardiovascular death.

Figure 4

Kaplan–Meier curve estimate of survival free from all-cause death.

Regarding ICD therapy during follow-up, 14 patients (37%) received appropriate ICD therapy (1 patient in the CA group and 13 patients in the non-CA group), of whom 10 (26%) suffered appropriate ICD shock excluding ATP (1 patient in the CA group and 9 in the non-CA group). Among these 10 patients, 1 patient (in the CA group) suffered ICD shock for VF and 9 patients for VT. The mean VTCL of the first documented episode of clinical VT had been of longer duration than the maximum VTCL of induced VT (355 ± 49 vs. 297 ± 68 ms). Among the nine patients who had suffered ICD shock for VT, the VT episode had been disorganized to VF or accelerated to rapid VT by ATP therapy in six patients, while device programming had been configured to the VF zone only in three patients because inducible VT had been disorganized to VF or had accelerated to rapid VT by overdrive pacing from RVA during EPS. Additionally, the mean VTCL of the first documented episode of clinical VT was relatively long. One of the reasons for this is that a slow conduction zone may become extended in patients who have received appropriate ICD therapy for VT because of the high presence of signal-averaged electrocardiogram abnormalities (12/13, 92%) and taking of amiodarone (5/13, 38%). During sample selection, 17 patients (12 males and 5 females; mean age, 59 ± 10 years; mean LVEF 36 ± 12%) without inducible monomorphic VT had been excluded. Of these patients, five patients (29%) had suffered appropriate ICD shock for monomorphic VT during a mean follow-up of 47 ± 41 months. In these patients, defibrillator device programming consisted of VF 1 zone because of no inducible monomorphic VT. As for inappropriate ICD therapy during follow-up, seven patients (18%) received inappropriate ICD shock (three patients in the CA group and four patients in the non-CA group).

Survival free from appropriate ICD therapy in the CA group vs. non-CA group was 100 vs. 70% at 12 months. Kaplan–Meier survival analysis revealed a significantly higher event-free survival rate for appropriate ICD therapy and ICD shock in the CA group compared with the non-CA group (P = 0.003 and 0.018, respectively; Figures 5 and 6).

Figure 5

Kaplan–Meier curve estimate of survival free from appropriate ICD therapy. ICD, implantable cardioverter-defibrillator.

Figure 6

Kaplan–Meier curve estimate of survival free from appropriate ICD shock. ICD, implantable cardioverter-defibrillator.

During the course of follow-up, nine patients (one patient in the CA group and eight patients in the non-CA group) had undergone VT ablation for recurrent appropriate ICD therapy. Of these patients, one patient with prior MI in the CA group had undergone endocardial VT ablation three times for recurrent ICD shock. Of the remaining eight patients, one patient with prior MI had required combination endocardial and epicardial CA and four patients with prior MI had undergone only endocardial CA for recurrent VT. Two patients with dilated cardiomyopathy (DCM) and mitochondrial cardiomyopathy (MTCM) who had undergone endocardial and epicardial CA but whose VT had remained uncontrolled. Therefore, they had undergone additional trans-coronary ethanol ablation (TCEA) for deep intramural VT. When the voltage map showed normal voltage for one patient who had undergone endocardial voltage mapping after aortic valve replacement, non-surgical subxiphoid epicardial puncture had been attempted to treat this patient, but had ultimately been unsuccessful due to adhesion of the epicardium.

Discussion

Previous studies showed that experiencing ICD shock leads to a decrease in quality of life and an increase in mortality.3,5,15 The results of the present study indicate that the incidence of appropriate ICD therapy, including that of appropriate shock, is significantly lower in patients who have undergone prophylactic CA for induced monomorphic VT compared with patients who have not undergone prophylactic CA. This finding is clinically significant, as reducing the incidence of appropriate ICD therapy may not only reduce the incidence of device discharge, an unpleasant experience for the patient, but also decrease the risk of subsequent adverse cardiovascular events. A sub-analysis conducted by the Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II) indicated that (i) patients with inducible sustained monomorphic VT received appropriate ICD therapy at a significantly higher rate than the patients with no inducible VT/VF during 4-year follow-up period (60 vs. 36%, P = 0.038) and that (ii) induction of VT with a CL ≥ 240 ms is associated with a high incidence of VT events.16 In the present study, sustained monomorphic VT had been induced in all patients, and the minimum and maximum inducible VTCL were 261 ± 58 and 297 ± 68 ms, respectively. Among the patients in the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), a multicentre clinical trial in which patients with New York Heart Association class II or III heart failure and an LVEF of 35% or less but no previous sustained VT/VF (i.e. primary prevention patients) were randomly given ICD implantation, amiodarone therapy, or placebo treatment, the cause of structural heart disease had been ischaemic cardiomyopathy in 52% and non-ischaemic cardiomyopathy in 48%.17 A sub-analysis of the SCD-HeFT study showed that 182 patients (22%) had received at least one appropriate ICD therapy and 128 (16%) had suffered appropriate ICD shocks during a mean follow-up of 45 months.3 The Multicenter UnSustained Tachycardia Trial (MUSTT) also showed that the incidence of spontaneous sustained VT/VF during a 5-year follow-up period was between 20 and 21%. In the present study, a total of 14 (37%) of the 38 patients, especially 13 (65%) of the 20 patients in the non-CA group, had received at least one appropriate ICD therapy during a mean follow-up of 50 ± 42 months. This rate is approximately double the rate of the incidence of spontaneous VT during the follow-up periods in the MUSTT and SCD-HeFT. One explanation for this discrepancy is that the patient selection differs; EPS was not performed in the SCD-HeFT, and only 161 (23%) of 704 patients had undergone ICD implantation in the MUSTT. In the present study, all patients had inducible sustained monomorphic VT and the incidence of VT/VF was similar to that in the MADIT-II. These results support that our patient selection of ICD implant as primary prevention is proper.

In Japan, ICD implantation has been used as a primary prevention strategy for patients with syncope and inducible monomorphic VT/VF.18 In contrast, in Europe and the USA, patients with cardiac conditions associated with a high risk of sudden death, who have unexplained syncope that is likely to be due to VT/VF are considered for secondary prevention.19 In the present study, nine patients (24%) with syncope and inducible monomorphic VT were enrolled to receive ICD implantation as a means of primary prevention according to the Japanese guidelines for ICD.

We performed prophylactic CA in every patient with reproducibly induced monomorphic VT. In addition, we did not exclude patients according to the underlying heart disease. However, in the present study, 20 patients did not undergo prophylactic CA for several reasons (35% had non-ischaemic cardiomyopathy). Finally, the majority of patients with ischaemic cardiomyopathy were included (74% overall; 83% in the CA group). Although this patient selection bias may influence the results, patients with non-ischaemic cardiomyopathy in the CA group (three patients) who had endocardial low-voltage areas did not receive appropriate ICD therapy during the follow-up period. The results of our study may apply to patients with endocardial low-voltage areas.

In the CA group, endocardial ventricular scars had been detected by EA mapping and CA had been performed using only an endocardial approach. Of the six patients in the non-CA group who had undergone endocardial mapping, no endocardial ventricular scar had been detected. For such patients, the substrate for VT may have extended intramurally or epicardially. Of these six patients, four had undergone CA for recurrent appropriate ICD therapy during a follow-up visit. Of these four patients, one had undergone unsuccessful non-surgical subxiphoid epicardial puncture for recurrent VT after aortic valve replacement; one had presented with prior MI and a normal endocardial voltage map but with VT that could only be suppressed by endocardial CA for VT exit sites using pace mapping; and two patients, one with DCM and one with MTCM, had undergone additional TCEA for VT suppression after unsuccessful endocardial and epicardial for deep intramural VT had been performed. Prophylactic epicardial CA and TCEA for induced monomorphic VT had not been performed for primary prevention patients because these procedures pose a higher risk of complications compared with endocardial CA.

Interestingly, the CA group had the lowest incidence of appropriate ICD therapy (5%, 1 out of 18) during follow-up, whereas the patients without inducible monomorphic VT (excluded group from the present study) had an intermediate incidence (29%, 5 out of 17) and the non-CA group had the highest incidence (65%, 13 out of 20). As it is well known, inducible monomorphic VT thought to be associated with an increased likelihood of clinical VT events;16,20 however, prophylactic CA for patients without inducible monomorphic VT may reduce the incidence of appropriate ICD therapy. As the SMASH-VT study included patients who had undergone prophylactic substrate ablation for VF, its results indicate that prophylactic substrate ablation for patients without inducible monomorphic VT (i.e. inducible VF, polymorphic VT, and no inducible VT/VF) reduce the incidence of appropriate ICD therapy. Prophylactic CA for such patients was not performed in the present study. Further study is warranted to determine whether prophylactic CA for patients without inducible VT improves clinical outcomes.

In the present study, CA-related thromboembolic occlusion of the right coronary artery occurred in one patient (with a non-irrigated ablation catheter), and coronary intervention was performed. Cerebral or systemic embolism occurred in 2.7% of patients in a previous study that used a close irrigation system for radiofrequency ablation.21 An irrigation ablation catheter was used in only two patients in our study. Better surface cooling and the flow provided by open irrigation compared with closed irrigation have been suggested to reduce coagulum formation on the ablation catheter and tissue surface. We did not observe any CA-related fatal complications. Prophylactic CA was found to be feasible and safe for primary prevention patients.

The VTACH study reported that prophylactic CA reduces the incidence of appropriate ICD therapy in patients with stable spontaneous VT and prior MI. While the SMASH-VT study reported similar results, it had examined a differed patient population; 89% of the patients who had prior spontaneous VT/VF and 11% had been syncope with inducible VT (no prior spontaneous VT/VF). On the basis of these studies, prophylactic CA should be considered for patients with prior MI, reduced LVEF, and ICD implantation as secondary prevention. In the present study, to the best of our knowledge, our present study was the first report to identify that prophylactic CA reduces the incidence of appropriate ICD therapy in primary prevention patients.

In the present study, device programming consisted of a VF and VT zone according to EPS results. However, the mean VTCL of the first documented episode of clinical VT had been of longer duration than the maximum VTCL of induced VT. A total of 10 (71%) out of 14 patients who received appropriate ICD therapy suffered ICD shock. Previous studies demonstrated that programming the device for ATP of VT could potentially terminate most VT episodes and reduce the number of painful shocks for primary prevention patients.2225 Thus, appropriate device programming of ATP may help reduce the incidence of unpleasant shocks. It cannot be determined from these results whether the use of EPS-guided device programming is appropriate.

Limitations

Our study has several limitations. First, it was a non-randomized retrospective analysis and consisted of a relatively small population who were highly selected and eligible for VT ablation. Second, device programming, including SVT discriminators, had not been specified in the protocol. During follow-up, nine patients had appropriate ICD shock for VT. Among these patients, the VT episode had been disorganized to VF or had accelerated to rapid VT by ATP therapy in six patients, while device programming had been configured to only the VF zone in three patients. Appropriate device programming of ATP therapy may help reduce the incidence of unpleasant shocks.

Mostly patients with ischaemic cardiomyopathy were included in this study (74% of the total patients, 83% in the CA group). Twenty patients (35% had non-ischaemic cardiomyopathy) had not undergone CA for some reasons, including normal voltage in the endocardial voltage map. The major limitation of this study is the presence of bias owing to the nature of patient selection; that is, patients were selected to undergo EPS on the basis of certain clinical characteristics that may not be present in the entire patient population that this study aimed to investigate. A final limitation is that only endocardial CA for monomorphic VT was performed in this study, and it thus remains unknown whether the results can be applied to patients with inducible monomorphic VT originating from the epicardial or intramural myocardium.

Conclusions

The results of the present study indicate that prophylactic CA for induced monomorphic VT reduces appropriate ICD therapy including shock in primary prevention patients. To determine whether prophylactic CA had contributed to the relatively high event-free survival of the study sample, a prospective randomized clinical trial must now examine whether prophylactic CA for induced monomorphic VT improves survival in primary prevention patients. Overall, the results indicate that prophylactic CA for induced monomorphic VT may be considered for structural heart disease patients with reduced LVEF who are candidates for ICD implantation as primary prevention.

Conflicts of interest: none declared.

References

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