Efficacy of Anti-Tachycardia Pacing for Terminating Fast Ventricular Tachycardia in Japanese Implantable Cardioverter Defibrillator Patients

– Primary Results of the SATISFACTION Study –

Abstract

Background: Anti-tachycardia pacing (ATP) delivered by implantable cardioverter defibrillators (ICD) safely avoids painful shocks with minimum risk of tachycardia acceleration. The etiology of ventricular tachycardia (VT) in those studies, however, was predominantly coronary artery disease (CAD). Patient etiology differs by geography and could affect ATP efficacy rate. The primary objective of this study was to examine how often the first ATP therapy terminates fast VT (FVT) in Japanese ICD patients with regional etiologies.

Methods and Results: Seven hundred and fifteen patients received ICD or cardiac resynchronization therapy defibrillator with the function of ATP during capacitor charging. The primary endpoint was the first ATP success rate for terminating FVT with cycle length 240–320 ms. During a mean follow-up of 11.3 months, 888 spontaneous VT episodes were detected, including 276 FVT (31.1%) in 42 patients. The first-ATP success rate for FVT in the overall group (41% CAD, 59% non-CAD including 23% idiopathic VT) was 62.1% (61.7% adjusted). Success rate was not different between non-CAD and CAD patients (61.4% adjusted and 57.5% adjusted, respectively, P=0.75). Eight FVT episodes (2.9%) accelerated after the first ATP attempt, all of which were terminated by subsequent device therapy (additional ATP or shock).

Conclusions: ATP efficacy for FVT was similar between ICD patients with and without CAD etiology. (Circ J 2014; 78: 2643–2650)

Trials have confirmed the superiority of the implantable cardioverter defibrillator (ICD) and cardiac resynchronization therapy defibrillator (CRT-D) compared with anti-arrhythmic therapy for primary or secondary prevention of sudden cardiac death and mortality.^1–11 The Multicenter Automatic Defibrillator Implantation Trial (MADIT) II trial showed that inappropriate ICD shock was common and was associated with increased risk of all-cause mortality.¹² The Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) showed that in patients with heart failure who received ICD for primary prevention, the occurrence of appropriate ICD shock was associated with a markedly increased risk of death.¹³ It may be that the negative inotropic consequences of the shock itself could increase the risk of death, especially when the patient receives multiple shocks as a result of oversensing or incessant supraventricular tachycardia.¹⁴ Another study showed that a local injury current on near-field bipolar right ventricular electrogram (EGM) after induced ventricular fibrillation (VF) rescue ICD shock is associated with increased risk of congestive heart failure (CHF) progression, future hospitalizations due to CHF exacerbation, and subsequent heart failure death.¹⁵ These results showed that ICD shock was associated with a markedly increased risk of death. Using anti-tachycardia pacing (ATP) as the first therapy for fast ventricular rhythms has been shown to minimize ICD shock and their potentially detrimental effects. ICD shock was significantly associated with subsequent reduction in both physical functioning and mental wellbeing.¹⁶ ATP therapy during capacitor charging is one method to deliver ATP therapy first without delay of shock delivery when ATP fails.

Editorial p 2619

Previous studies found ATP terminates fast ventricular tachycardia (FVT) with favorable success rates (50–72%).^17–20 The etiology of VT in those studies, however, was predominantly coronary artery disease (CAD). Patient etiology differs by geography and could affect ATP efficacy rate. The primary objective of this study was to examine how often first ATP terminates FVT in Japanese ICD patients with regional etiologies.

Methods

Study Design

Survey on AnTItachycardia pacing Strategy for the termination of FAst ventricular tachycardia in Japanese implantable Cardioverter defibrillator populaTION (SATISFACTION) trial was a prospective, multicenter study in patients with ICD or CRT-D with the function of ATP during capacitor charging. This study was conducted at 41 Japanese centers. Patients with ICD or CRT-D were enrolled from January 2009 to May 2011. We enrolled 760 patients and the analysis was conducted on 715 patients. Forty-five patients were excluded due to programming non-compliance or no follow-up after enrollment. All patients were seen at least every 6 months and at least twice during the follow-up period. Patients were eligible if they had received an ICD or CRT-D equipped with ATP during capacitor charging function (ATP During Charging; Medtronic, Minneapolis, MN, USA) or the equivalent function to prevent any delay of ICD shock therapy in the case of ATP failure. Patients under the age of 20 years were excluded. Stored ICD data were transferred to a central database for analysis. The definition of VT (cycle length [CL] >320 ms), FVT (240 ms≤CL≤320 ms), very FVT (vFVT; 200 ms≤CL<240 ms) and VF (CL <200 ms) first depended on the CL of the tachycardia detected by the ICD. The tachyarrhythmias were then classified by the waveform on the EGM.

The primary endpoint was the success rate of initial ATP for FVT. The secondary endpoints were the success rate of initial ATP according to underlying etiology, the success rate of initial ATP for vFVT, and hazard ratios for occurrence of VT and VF events according to patient characteristics. Syncopal events and acceleration rate due to ATP were also identified.

This study was approved by the institutional review board/medical ethics committee of each participating center, and all patients provided signed informed consent.

Device Description and Programming

All patients had ICD or CRT-D with ATP During Charging (Virtuoso VR, Virtuoso DR, Secura VR, Secura DR, and Concerto C154DWK and C174AWK; Medtronic). Tachyarrhythmia detection and therapy settings are described in Table 1. Briefly, ATP programming for FVT was set to 8-pulse burst pacing at 88% of the FVT CL in ATP During Charging or FVT via VF zone for a CL of 240–320 ms (250–188 beats/min). ATP programming for vFVT was set to 8-pulse burst pacing at 88% of the vFVT CL only in ATP During Charging. The number of intervals to detect for VF was set to 18/24. If the first ATP was successful, investigators were allowed to modify FVT programming to perform ATP before ATP during charging. A slow VT zone was not a requisite for study participation. Supraventricular tachyarrhythmia (SVT) discrimination was programmed “on” in the VT zone of all dual-chamber ICD. Therapy programming for VT zone, SVT discrimination for single-chamber ICD and other programming was left to the discretion of the investigator.

Table 1. Device Programming

Parameter	Programmed setting
Required programming
Detection
VF DI	320 ms
VF NID	18/24
VF redetect NID	12/16
FVT detection	OFF
PR-Logic	ON (dual chamber only)
SVT-limit	320 ms (dual chamber only)
Therapy
ATP during charging	ON
Deliver ATP last 8 R-R≥	200 ms
Amplitude	8 V
Pulse width	1.5 ms
Therapy type	Burst
Initial no. pulses	8
R-S1 interval=(%RR)	88%
Minimum ATP Interval	170 ms
Optional programming
Detection
FVT detection	ON-via VF
FVT DI	240 ms
Therapy
Therapy type	Burst
Amplitude	8 V
Pulse width	1.5 ms
Initial no. pulses	8
R-S1 interval=(%RR)	88%

ATP, anti-tachycardia pacing; DI, detection interval; FVT, fast ventricular tachyarrhythmia; NID, no. intervals to detect; SVT, supraventricular tachyarrhythmia; VF, ventricular fibrillation.

Sample Size

Sample size calculation was based on confidence interval (CI). Assuming a 70% success rate of first ATP for FVT in this study (given that this in the PainFREE trial was 77%¹⁷), the range of the 95% CI of the expected success rate in 78 patients with at least 1 FVT episode was at least 20%. Additionally, assuming that 15% of all patients would experience episodes detected as FVT during the follow-up period, it was necessary to register and follow more than 520 patients in total.

Statistical Analysis

Continuous data are expressed as mean±SD, whereas categorical data are expressed as count and percentile. Device EGM episodes adjudicated as true VT (appropriate) by investigators were analyzed for the primary and secondary endpoint. Risk of ventricular tachyarrhythmia was evaluated univariately and multivariately using the hazard ratio, which was the ratio of episode per person-year for the various predictive factors, using Poisson regression models with forward variable selection. The episode rates were calculated using Poisson regression adjusting for overdispersion. To evaluate the effects of background factor on ATP efficacy, the odds ratios adjusted for within-patient correlation were estimated on univariate and multivariate logistic regression. The success rate for ATP was calculated with 95% CI, considering repeated episodes for each patient, using the generalized estimating equation (GEE) for binomial distribution. GEE is a widely used method to estimate marginal regression parameters for correlated responses. ATP success was defined as confirmation of 2 consecutive heartbeats with a rate equal to or below the tachycardia detection rate. Episode acceleration after ATP was defined as ≥10% CL reduction in mono-VT or a change from mono to poly-VT or VF. All tests were done at the 5% type I error level. Statistical analysis was carried out with SAS (version 8.2).

Results

Baseline Characteristics

Table 2 lists the patient demographics. Of 715 patients who underwent implantation, 77% were male, with a mean age of 65.3±12.6 years, 40% with biventricular pacing and the others with ICD (51% with dual-, 49% with single-chamber), and mean ejection fraction (EF) of 42.9±17.2%. CAD was present in 41% of patients. In the non-CAD group, 50.4% had dilated cardiomyopathy, 21.4% hypertrophic cardiomyopathy, 8.9% sarcoidosis, 3.9% arrhythmogenic right ventricular cardiomyopathy and 16.6% others. A total of 43% were classified in New York Heart Association (NYHA) class I, 36% in class II, 19% in class III, and 3% in class IV. Indications for ICD implantation were primary prevention in 42%. Most patients were on β-blockers (73%) and angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blocker (ARB; 65%). A total of 157 (22%) out of all 715 patients had a history of paroxysmal or persistent atrial fibrillation (AF).

Table 2. Subject Characteristics vs. Presence of Ischemia

Characteristic	Total (n=715)	Ischemic (n=293)	Non-ischemic (n=337)	P-value†
Age (years)	65.3±12.6	68.4±10.8	64.3±12.3	<0.01
Male	550 (76.9)	257 (87.7)	229 (68.0)	0<0.01
Underlying heart disease
Ischemic	293 (41.0)	293 (100)	0 (0)	–
Non-ischemic	337 (47.1)	0 (0)	337 (100)
DCM	170 (50.4)
HCM	72 (21.4)
Sarcoidosis	30 (8.9)
ARVC	13 (3.9)
Others	56 (16.6)
Idiopathic	85 (11.9)
NYHA class		0.73
I	305 (42.7)	106 (36.2)	131 (38.9)
II	254 (35.5)	119 (40.6)	125 (37.1)
III	135 (18.9)	58 (19.8)	71 (21.1)
IV	21 (2.9)	10 (3.4)	10 (3.0)
QRS interval (ms)	124.6±33.7	123.7±31.8	129.8±33.2	0.02
LVEF (%)	42.9±17.2	39.8±14.7	41.6±17.8	0.18
Hypertension	341 (47.7)	193 (65.9)	122 (36.2)	<0.01
Syncope	342 (47.8)	161 (54.9)	123 (36.5)	<0.01
Primary prevention	301 (42.1)	106 (36.2)	163 (48.4)	<0.01
Atrial tachyarrhythmia
AT/AFl	57 (8.0)	24 (8.2)	31 (9.2)	0.67
AF	157 (22.0)	59 (20.1)	76 (22.6)	0.50
Ventricular tachyarrhythmia
Non-sustained VT	184 (25.7)	74 (25.3)	106 (31.5)	0.09
Sustained VT	231 (32.3)	100 (34.1)	114 (33.8)	1.00
VF	185 (25.9)	88 (30.0)	61 (18.1)	<0.01
Bi-ventricular pacing	229 (32.0)	86 (29.4)	136 (40.4)	<0.01
Baseline medications
ACEI	175 (24.5)	88 (30.0)	78 (23.1)	0.06
ARB	286 (40.0)	131 (44.7)	141 (41.8)	0.47
β-blocker	522 (73.0)	220 (75.1)	267 (79.2)	0.22
AAD (Amiodarone)	285 (39.9)	131 (44.7)	141 (41.8)	0.47
AAD (Class I)	135 (18.9)	44 (15.0)	77 (22.8)	0.01

Data given as mean±SD or n (%). ^†Fisher exact test or Student t-test between ischemic and non-ischemic groups.AAD, anti-arrhythmic drug; ACEI, angiotensin-converting enzyme inhibitor; AF, atrial fibrillation; AFl, atrial flutter; ARB, angiotensin receptor blocker; ARVC, arrhythmogenic right ventricular cardiomyopathy; AT, atrial tachycardia; DCM, dilated cardiomyopathy; HCM, hypertrophic cardiomyopathy; LVEF, left ventricular ejection fraction; NYHA, New York Heart Association; VT, ventricular tachycardia. Other abbreviation as in Table 1.

Appropriate and Inappropriate Device Therapy

During a mean follow-up of 11.3±5.4 months, a total of 1,039 treated episodes were observed in 163 patients (23%); 888 episodes (85%) were true VT/VF consisting of 575 (55%) detected as VT in 70 patients, 276 (27%) as FVT in 42 patients, 20 (2%) as vFVT in 7 patients, and 17 (2%) as VF in 10 patients. Four of 276 FVT and 14 of 20 vFVT episodes were not treated by ATP due to the last 8 ventricular intervals prior to detection being less than the ATP delivery threshold or due to a restriction feature of ATP During Charging. The other 151 episodes (15%) in 34 patients were detected inappropriately; 88% of those in the VT zone (Figure 1). Figure 2 shows the CL of VT according to detection zone.

Figure 1.

Study flow of the SATISFACTION study and final successful intervention. ATP, anti-tachycardia pacing; FVT, fast ventricular tachycardia; VF, ventricular fibrillation; vFVT, very fast ventricular tachycardia; VT, ventricular tachycardia.

Figure 2.

No. episodes of ventricular tachycardia (VT), fast ventricular tachycardia (FVT), very fast ventricular tachycardia (vFVT) and ventricular fibrillation (VF) vs. median cycle length.

On multivariate Cox regression analysis for the risk of true VT/VF, male sex, non-CAD, secondary prevention, no history of AF and absence of amiodarone were identified as independent predictors for the occurrence of VT/VF episodes (Table 3).

Table 3. Risk of Ventricular Tachyarrhythmia

Variable	Univariate		Multivariate
	HR (95% CI)	P-value	HR (95% CI)	P-value
Age (<65 years)	1.45 (1.01–2.10)	0.05
Gender (male)	2.32 (1.30–4.11)	<0.01	4.07 (2.30–7.21)	<0.01
Etiology (ischemic)	0.30 (0.19–0.48)	<0.01	0.19 (0.13–0.30)	<0.01
NYHA (0/I)
II	0.65 (0.43–1.00)	0.05
III	0.61 (0.35–1.05)	0.07
IV	0.52 (0.12–2.21)	0.38
LVEF (<40%)	0.86 (0.59–1.26)	0.45
Primary prevention	0.22 (0.13–0.37)	<0.01	0.16 (0.09–0.27)	<0.01
AAD (Amiodarone)	0.58 (0.38–0.87)	<0.01	0.34 (0.23–0.50)	<0.01
AAD (Class I)	2.38 (1.62–3.48)	<0.01	1.43 (0.98–2.09)	0.06
Permanent AF	0.81 (0.41–1.61)	0.54
Paroxysmal/Persistent AF	0.37 (0.20–0.69)	<0.01	0.35 (0.19–0.63)	<0.01
CRT	0.77 (0.52–1.14)	0.20
RV pacing	0.55 (0.19–1.66)	0.29

CI, confidence interval; CRT, cardiac resynchronization therapy; HR, hazard ratio; RV, right ventricular. Other abbreviations as in Table 2.

A total of 34 patients (5%) experienced at least 1 inappropriate device response. The causes of inappropriate response (ATP or shock) were AF or atrial tachycardia in 88% and sinus tachycardia in 8%.

Endpoints

The first ATP terminated 169 of 272 FVT episodes (62.1% unadjusted, 61.7% adjusted; 95% CI: 54.0–68.9; CL, 289.8±17.7 ms) in this subject group with mixed etiology (41% CAD, 59% non-CAD including 23% of idiopathic etiology). The success rate for patients with non-CAD (CL, 291.2±16.0 ms) or CAD etiology (CL, 281.3±22.2 ms) was not significantly different (61.4% adjusted and 57.5% adjusted, respectively, P=0.78; Table 4).

Table 4. ATP Success Rate vs. Presence of Ischemia

	n	ATP success rate for FVT (adjusted, %) (95% CI)	P-value†
Total	715	61.7 (54.0–68.9)	–
Non-ischemic	337	61.4 (54.1–68.3)	0.78
Ischemic	293	57.5 (31.2–80.2)

^†Calculated between non-ischemic and ischemic. Abbreviations as in Tables 1,2.

Univariate and multivariable analysis was done on baseline clinical variables in order to determine their potential correlation with ATP success in the overall group. The independent significant predictors of ATP efficacy for FVT were: female sex, CAD, primary prevention, narrow QRS, FVT CL, ACEI/ARB and absence of β-blocker (Table 5).

Table 5. Predictors of Efficacy of First ATP for FVT^†

Variables	Univariate analysis			Multivariate analysis
	OR	95% CI	P-value	OR	95% CI	P-value
Age <65 years	0.99	0.51–1.93	0.98
Gender male	0.32	0.09–1.17	0.09	0.08	0.02–0.43	<0.01
Ischemic Cardiomyopathy	0.85	0.27–2.65	0.78	9.71	2.32–40.62	<0.01
NYHA class (Ref=0,1)　4	0.09	0.07–0.11	<0.01
NYHA class (Ref=0,1)　3	0.66	0.19–2.24	0.51
NYHA class (Ref=0,1)　2	0.71	0.35–1.43	0.33
Primary prevention	1.17	0.41–3.35	0.77	6.38	1.46–27.90	0.01
LVEF <40%	0.63	0.29–1.37	0.24
QRS <120 ms	3.04	1.24–7.47	0.02	8.28	2.36–29.05	<0.01
AF	0.52	0.12–2.32	0.39	5.00	0.80–31.36	0.09
CRT	0.48	0.20–1.13	0.09
Episode cycle length　(/10)	0.01	0.00–10.64	0.19	1.53	1.26–1.86	<0.01
ACEI/ARB	1.32	0.59–2.97	0.50	3.35	1.62–6.94	<0.01
β-blocker	0.59	0.31–1.13	0.11	0.27	0.11–0.64	<0.01
Amiodarone	0.48	0.19–1.20	0.12
AAD (Class I)	0.70	0.24–2.03	0.52

^†GEE logistic model. OR, odds ratio. Other abbreviations as in Tables 1–3.

Figure 3 shows ATP efficacy for VT according to detected CL. The ATP success rates for VT, FVT, vFVT and VF were significantly different in VT vs. FVT, and in VT vs. vFVT (VT vs. FVT, P<0.0001; VT vs. vFVT, P=0.033; FVT vs. vFVT, P=0.31).

Figure 3.

Anti-tachycardia pacing (ATP) success rate vs. median cycle length. FVT, fast ventricular tachycardia; vFVT, very fast ventricular tachycardia; VT, ventricular tachycardia.

Eight FVT episodes (2.9%) in 5 patients accelerated after the first ATP attempt and 3 of those were subsequently terminated by ATP and 5 were terminated by shock in 3 patients. The acceleration rate for patients with non-CAD (1.2%) or CAD etiology (0.3%) was not significantly different (P=0.23).

Two of 6 vFVT treated by ATP (CL, 220±8.9 ms) were terminated successfully by the first ATP (33.3% unadjusted, 50.0% adjusted; 95% CI: 12.4–87.7).

During follow up, 5 patients experienced 1 syncopal event each. In 4 patients, the events were associated with VF (CL, 193.3±18.5 ms). In 1 patient, the syncopal event was associated with FVT that was not successfully terminated with ATP. The syncopal rate for patients with non-CAD (0.9%) or CAD etiology (0.7%) was not significantly different (P=0.57).

Discussion

Large randomized trials have noted a beneficial effect of ICD therapy, initially in survivors of life-threatening arrhythmias, but also more recently in the primary prevention of sudden arrhythmic death in selected ischemic and non-ischemic patients at high risk.^4–6

The 5 main findings of the present study are that (1) the first ATP for terminating FVT in the present subject group with mixed etiology was effective; (2) the efficacy of the first ATP for FVT in the present subject group was similar to that previously identified in patients mostly with CAD; (3) the efficacy of the first ATP for FVT was similar between CAD and non-CAD patients; (4) the first ATP for terminating vFVT (CL, 200–240 ms) was lower (50%); and (5) male, non-CAD, secondary prevention, no history of AF and absence of amiodarone were independent predictors for the occurrence of VT/VF episodes.

The first-ATP success rate for FVT was 62%, which is similar to those determined in the PainFREE Rx II trial¹⁸ and ADVANCE-D trial¹⁹ (72% and 64%, respectively). The ADVANCE-D trial additionally found that there was no significant difference in the first-ATP efficacy between CAD and non-CAD. In the present study, equivalently, no statistical difference was observed between the etiologies. This could explain the similar success rate of the first ATP for the whole group in the present study, as compared with previous studies. Syncope occurred in only 0.3% of FVT episodes (1 patient). The MADIT-RIT trial found that high-rate therapy and delayed ICD therapy were associated with reduction in all-cause mortality.²¹ The MADIT-RIT trial additionally showed that syncope caused by slow VT (<200 beats/min) is a rare event. The large reduction in number of shocks may reduce morbidity and mortality caused by shock as previously reported.¹³

Considering the structural difference in the underlying diseases of tachycardia (ie, CAD, cardiomyopathy or idiopathic VF), the efficacy of ATP for FVT could be different due to the varying electrophysiological mechanism of ventricular tachyarrhythmia. A total of 40% of the present patients had CAD. The majority of subjects enrolled in the PainFREE Rx II trial¹⁸ and ADVANCE-D trial¹⁹ were patients with CAD (83% and 75%, respectively). In the present study, the success rate for patients with non-CAD or CAD etiology was not significantly different. The present study data show that in patients with non-ischemic cardiomyopathy, ATP was effective for FVT.

Of 6 vFVT episodes, 33.3% (50.0% adjusted) reverted with first ATP, which otherwise would fall within the VF zone and be treated exclusively with defibrillation. ATP is efficacious and safe in patients with vFVT with no syncope event. Sivagangabalan et al reported ATP and low-energy shock (LES) efficacy for vFVT (CL, 200–250 ms).²² According to that study, the first-ATP success rate for vFVT was 35.8%. Compared with shock therapy, ATP improved quality of life,¹⁸ and produced no increase in mortality or heart failure.⁹ A single ATP burst terminated approximately one-third of VFVT episodes and, when successful, resulted in an extremely short episode duration and almost complete avoidance of syncope. Otherwise, a second ATP burst for vFVT had poor success rate with regard to episode prolongation and syncope. In the present study, ATP success rate for vFVT was similar to previous study. ATP during capacitor charging function prevents delay of ICD shock therapy in the case of ATP failure. Limitation of ATP to a single burst in vFVT is recommended to terminate VT and minimize syncope.

On multivariate Cox regression analysis, male sex, non-CAD, secondary prevention, no history of AF and absence of amiodarone remained significantly associated with VT/VF episodes. In terms of the incidence rate of VT/VF, CAD patients had fewer VT/VF episodes than non-CAD patients (Table 3).

This study also showed that female sex, CAD, primary prevention, narrow QRS, FVT CL, ACEI/ARB and absence of β-blocker were independent predictors of first-ATP efficacy for FVT. It has also been noted that increased left ventricular size and muscle mass, myocardial fibrosis, and the involvement of the conduction system in ischemic areas prolong the duration of the basal QRS complex.²³ In a previous study, duration of basal QRS >100 ms was associated with lower ATP effectiveness applied to the right ventricle apex independently of left ventricle size, suggesting that longer conduction time was the mechanism responsible.²⁴ Gender differences in left ventricular size or hormonal differences have been suggested to influence ATP effectiveness, but the relationship has not been clearly established.²⁵ The PainFREE Rx I study found that patients with NSVT in their arrhythmia history had higher ATP efficacy than patients without a history of NSVT.¹⁷ The PainFREE Rx II study found that left ventricular EF was a marginally significant predictor of first-ATP efficacy for FVT.¹⁸ The ADVANCE-D study found that primary prevention and VT CL were the significant predictors of first-ATP efficacy for FVT.¹⁹ Faster VT has a shorter excitation gap, increasing the difficulty of the paced stimulus to interact with the circuit at the critical time for terminating the arrhythmia. It was previously reported that both appropriate and inappropriate shocks are significant predictors of death. In the present study ATP was highly effective and safe in treating FVT in the general population. With regard to predictors of ATP success, in particular ACEI, the efficacy of ATP treatment greatly depended on the patient functional status. These results may have been a coincidental observation and will require further confirmation by means of a specific study. Owing to the high efficacy of ATP and the consequent reduction in shocks, it is suggested that ATP should always be programmed as a first-option electrical therapy for FVT.

There are several reports regarding the incidence rate in each etiology, but the results were still controversial due to the varying study design and sample size.^26–28 The present study consisted of 293 CAD and 422 non-CAD patients with a mean follow-up of 11.3 months. The difference in VT/VF incidence rate could be due to patient characteristics. In the CAD group there were more primary prevention patients, and more with biventricular pacing. According to previous reports, reverse remodeling by CRT was associated with a significant reduction in the risk of subsequent ventricular arrhythmia.^29–31 This could be a factor in the different VT/VF incidence rate.

Study Limitation

The primary endpoint was established with a smaller sample size than was first calculated. The lower number of patients with FVT might be due to lower NYHA class and better LVEF in the present patients than in previous studies.

Conclusions

The efficacy of first ATP for FVT in the present study was similar to that in previous studies in patients with different etiologies. ATP success was similar between patients with and without CAD etiology. We believe that ATP for FVT is favorable even in patients with varying etiology.

Acknowledgments

This study was sponsored by Association for Establishment of Evidence in Interventions (Tokyo, Japan). This study was supported by Medtronic Japan (Tokyo, Japan).

Appendix

We are grateful to all the participants who took part in each of the cohort studies.

SATISFACTION Study Group: Chair: Tetsuya Watanabe (Kansai Rosai Hospital); Executive Committee: Tetsuya Watanabe (Kansai Rosai Hospital), Koichi Inoue (Sakurabashi Watanabe Hospital), Kazunori Kashiwase (Osaka Police Hospital), Takanao Mine (Hyogo College of Medicine), Keiji Hirooka (Osaka National Hospital), Ryu Shutta (Osaka Rosai Hospital), Yuji Okuyama, Hiroya Mizuno, Shinsuke Nanto (Osaka University Graduate School of Medicine); Participating Facility: Shinya Shimoshige (Sapporo Medical University School of Medicine), Sou Takenaka (Yokohama General Hospital), Takenori Sumiyoshi (Miyagi Cardiovascular and Respiratory Center), Yuzuru Yambe (IMS Katsushika Heart Center), Kinya Shirota (Matsue Red Cross Hospital), Junichi Nitta (Saitama Red Cross Hospital), Makoto Ito (Shiga University of Medical Science), Takehiko Keida (Edogawa Hospital), Shoichi Tange (Maebashi Red Cross Hospital), Tadakatsu Yamada (Ehime Prefectural Central Hospital), Yutaka Furukawa (Kobe City Medical Center General Hospital), Yoshihisa Abe (Akita Medical Center), Takashi Komatsu (Iwate Medical University), Kenichiro Otomo (Ome Municipal General Hospital), Keijiro Saku (Fukuoka University Hospital), Toshihiro Honda (Saiseikai Kumamoto Hospital), Fumiharu Miura (Onomichi General Hospital), Eitaro Fujii (Mie University Hospital), Sonoda Masahiro, Nakashima Hitoshi (Kagoshima Medical Center), Kazuo Usuda (Toyama Prefecture Central Hospital), Akira Yamashina (Tokyo Medical University Hospital), Masayuki Inagaki (Funabashi Municipal Medical Center), Ryousuke Takeuchi (Shizuoka Hospital), Satoru Miyanaga (Saitama Cardiovascular and Respiratory Center), Hiromi Obata (Obihiro National Hospital), Toshiaki Oka (Seirei Hamamatsu General Hospital), Akiko Chishaki (Kyushu University Hospital), Yasuhiro Ishii (Ogikubo Hospital), Minoru Murata (Mito Saiseikai General Hospital), Takahisa Noma (Kagawa University School of Medicine), Akihiko Yotsukura (Hokko Memorial Hospital), Takahiro Muroya (National Hospital Organization Ureshino Medical Center), Masato Watarai (Anjo Kosei Hospital).

References

• 1.    Moss  AJ,  Hall  WJ,  Cannom  DS,  Daubert  JP,  Higgins  SL,  Klein  H, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia: Multicenter automatic defibrillator implantation trial investigators. N Engl J Med 1996; 335: 1933–1940.
• 2.   The Antiarrhythmics Versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias: The Antiarrhythmics Versus Implantable Defibrillators (AVID) Investigators. N Engl J Med 1997; 337: 1576–1583.
• 3.    Buxton  AE,  Lee  KL,  Fisher  JD,  Josephson  ME,  Prystowsky  EN,  Hafley  G. A randomized study of the prevention of sudden death in patients with coronary artery disease: Multicenter unsustained tachycardia trial investigators. N Engl J Med 1999; 341: 1882–1890.
• 4.    Connolly  SJ,  Gent  M,  Roberts  RS,  Dorian  P,  Roy  D,  Sheldon  RS, et al. Canadian Implantable Defibrillator Study (CIDS): A randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation 2000; 101: 1297–1302.
• 5.    Kuck  KH,  Cappato  R,  Siebels  J,  Ruppel  R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: The Cardiac Arrest Study Hamburg (CASH). Circulation 2000; 102: 748–754.
• 6.    Moss  AJ,  Zareba  W,  Hall  WJ,  Klein  H,  Wilber  DJ,  Cannom  DS, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002; 346: 877–883.
• 7.    Bristow  MR,  Saxon  LA,  Boehmer  J,  Krueger  S,  Kass  DA,  De Marco  T, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 2004; 350: 2140–2150.
• 8.    Kadish  A,  Dyer  A,  Daubert  JP,  Quigg  R,  Estes  NA,  Anderson  KP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med 2004; 350: 2151–2158.
• 9.    Bardy  GH,  Lee  KL,  Mark  DB,  Poole  JE,  Packer  DL,  Boineau  R, et al; Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005; 352: 225–237.
• 10.   JCS Joint Working Group. Guidelines for non-pharmacotherapy of cardiac arrhythmias (JCS 2011): Digest version. Circ J 2013; 77: 249–274.
• 11.    Murakoshi  N,  Aonuma  K. Epidemiology of arrhythmias and sudden cardiac death in Asia. Circ J 2013; 77: 2419–2431.
• 12.    Daubert  JP,  Zareba  W,  Cannom  DS,  McNitt  S,  Rosero  SZ,  Wang  P, et al. Inappropriate implantable cardioverter-defibrillator shocks in MADIT II: Frequency, mechanisms, predictors, and survival impact. J Am Coll Cardiol 2008; 51: 1357–1365.
• 13.    Poole  JE,  Johnson  GW,  Hellkamp  AS,  Anderson  J,  Callans  DJ,  Raitt  MH, et al. Prognostic importance of defibrillator shocks in patients with heart failure. N Engl J Med 2008; 359: 1009–1017.
• 14.    Tokano  T,  Bach  D,  Chang  J,  Davis  J,  Souza  JJ,  Zivin  A, et al. Effect of ventricular shock strength on cardiac hemodynamics. J Cardiovasc Electrophysiol 1998; 9: 791–797.
• 15.    Tereshchenko  LG,  Faddis  MN,  Fetics  BJ,  Zelik  KE,  Efimov  IR,  Berger  RD. Transient local injury current in right ventricular electrogram after implantable cardioverter-defibrillator shock predicts heart failure progression. J Am Coll Cardiol 2009; 54: 822–828.
• 16.    Daniel  BM,  Kevin  JA,  Jie  LS,  Nancy  EC,  Anastasios  AT,  Linda  DR, et al. Quality of life with defibrillator therapy or amiodarone in heart failure. N Engl J Med 2008; 359: 999–1008.
• 17.    Wathen  MS,  Sweeney  MO,  DeGroot  PJ,  Stark  AJ,  Koehler  JL,  Chisner  MB, et al. Shock reduction using antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with coronary artery disease. Circulation 2001; 104: 796–801.
• 18.    Wathen  MS,  DeGroot  PJ,  Sweeney  MO,  Stark  AJ,  Otterness  MF,  Adkisson  WO, et al. Prospective randomized multicenter trial of empirical antitachycardia pacing versus shocks for spontaneous rapid ventricular tachycardia in patients with implantable cardioverter-defibrillators: Pacing Fast Ventricular Tachycardia Reduces Shock Therapies (PainFREE Rx II) trial results. Circulation 2004; 110: 2591–2596.
• 19.    Santini  M,  Lunati  M,  Defaye  P,  Mermi  J,  Proclemer  A,  del Castillo-Arroys  S, et al. Prospective multicenter randomized trial of fast ventricular tachycardia termination by prolonged versus conventional anti-tachyarrhythmia burst pacing in implantable cardioverter-defibrillator patients-Atp DeliVery for pAiNless ICD thErapy (ADVANCE-D) Trial results. J Interv Card Electrophysiol 2010; 27: 127–135.
• 20.    Gasparini  M,  Anselme  F,  Clementy  J,  Santini  M,  Martínez-Ferrer  J,  De Santo  T, et al. BIVentricular versus right ventricular antitachycardia pacing to terminate ventricular tachyarrhythmias in patients receiving cardiac resynchronization therapy: The ADVANCE CRT-D Trial. Am Heart J 2010; 159: 1116–1123.
• 21.    Moss  AJ,  Schuger  C,  Beck  CA,  Brown  MW,  Cannom  DS,  Daubert  JP, et al. Reduction in inappropriate therapy and mortality through ICD programming. N Engl J Med 2012; 367: 2275–2283.
• 22.    Sivagangabalan  G,  Chik  W,  Zaman  S,  Stafford  W,  Hayes  J,  Denman  R, et al. Antitachycardia pacing for very fast ventricular tachycardia and low-energy shock for ventricular arrhythmias in patients with implantable defibrillators. Am J Cardiol 2013; 112: 1153–1157.
• 23.    Mazzoleni  A,  Curtin  ME,  Wolff  R,  Reiner  L,  Somes  G. On the relationship between heart weights, fibrosis, and QRS duration. J Electrocardiol 1975; 8: 233–236.
• 24.    Jiménez-Candil  J,  Ruiz  M,  Herrero  J,  León  V,  Martín  A,  Moriñigo  J, et al. Relationship between the duration of the basal QRS complex and electrical therapies for ventricular tachycardias among ICD patients. Pacing Clin Electrophysiol 2010; 33: 596–604.
• 25.    Haigney  MC,  Zareba  W,  Nasir  JM,  McNitt  S,  McAdams  D,  Gentlesk  PJ, et al. Gender differences and risk of ventricular tachycardia or ventricular fibrillation. Heart Rhythm 2009; 6: 180–186.
• 26.    Boriani  G,  Gasparini  M,  Lunati  M,  Santini  M,  Landolina  M,  Vincenti  A, et al. Characteristics of ventricular tachyarrhythmias occurring in ischemic versus nonischemic patients implanted with a biventricular cardioverter-defibrillator for primary or secondary prevention of sudden death. Am Heart J 2006; 152: 527.e1–e11, doi:10.1016/j.ahj.2006.03.003.
• 27.    Koa-Wing  M,  Wright  I,  Peters  NS,  Davies  DW,  Francis  DP,  Kanagaratnam  P. Experience of ICD management at a UK center: Cardiovascularly stable VT presentation predicts higher risk for appropriate ICD therapy. Pacing Clin Electrophysiol 2007; 30: 1369–1375.
• 28.    Streitner  F,  Kuschyk  J,  Dietrich  C,  Mahl  E,  Streitner  I,  Doesch  C, et al. Comparison of ventricular tachyarrhythmia characteristics in patients with idiopathic dilated or ischemic cardiomyopathy and defibrillators implanted for primary prevention. Clin Cardiol 2011; 34: 604–609.
• 29.    Ouellet  G,  Huang  DT,  Moss  AJ,  Hall  WJ,  Barsheshet  A,  McNitt  S, et al. Effect of cardiac resynchronization therapy on the risk of first and recurrent ventricular tachyarrhythmic events in MADIT-CRT. J Am Coll Cardiol 2012; 60: 1809–1816.
• 30.    Shahrzad  S,  Soleiman  NK,  Taban  S,  Alizadeh  A,  Aslani  A,  Tavoosi  A, et al. The effect of left ventricular (LV) remodeling on ventricular arrhythmia in cardiac resynchronization therapy (CRT-D) patients (antiarrhythmic effect of CRT). Pacing Clin Electrophysiol 2012; 35: 592–597.
• 31.    Barsheshet  A,  Wang  PJ,  Moss  AJ,  Solomon  SD,  Al-Ahmad  A,  McNitt  S, et al. Reverse remodeling and the risk of ventricular tachyarrhythmias in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy). J Am Coll Cardiol 2011; 57: 2416–2423.