Stepwise ablation strategy in radiofrequency ablation improves acute and long-term outcomes of scar-related ventricular tachycardias

Abstract

Background

The optimal intervention procedures for scar-related ventricular tachycardia (VT) is still unclear.

Objective

This study aimed to compare the acute and long-term outcomes of a stepwise ablation approach targeting critical sites identified through activation mapping during VT or pace mapping followed by substrate ablation with substrate modification alone in patients with scar-related VT.

Methods

Data of 41 patients with scar-related VTs treated with stepwise ablation (Group 1, n = 29) or substrate modification alone during sinus rhythm (Group 2, n = 12) were retrospectively reviewed. The procedure acute success and long-term success during follow-up were compared.

Results

There was no statistical difference between the two groups on basic characteristics. Group 1 demonstrated shorter ablation time (P = 0.02), longer VT-free survival rates at a median follow-up of 24.0 months (P = 0.02) and a lower VT recurrence rate (hazard ratio: 0.17, 95% confidence interval: [0.03, 0.93], P = 0.04) compared to Group 2. The acute success and ratio of ablation area to scar area were comparable between the two groups (P ≥ 0.05).

Conclusion

The stepwise ablation strategy shows promise for improving acute and long-term outcomes and reducing the recurrence risk in patients with scar-related VT.

Keywords

scar ventricular tachycardia radiofrequency ablation activation mapping substrate ablation

1 Introduction

Scar-related ventricular tachycardia (VT) is a severe arrhythmia usually caused by myocardial infarction and associated with a high rate of sudden cardiac death in patients with ischemic cardiomyopathy (ICM) or non-ischemic cardiomyopathy (NICM).¹ Antiarrhythmic drugs are often moderately effective but have inevitable side effects.² Although implantable cardioverter defibrillators (ICDs) are life-saving, they do not prevent VT and ICD shocks lead to a decreased quality of life.³ Over the past 30 years, with the development of new methods and tools, radiofrequency ablation technology targeting and modifying the isolated channels of surviving myocardium within the scar to treat scar-related VTs and prevent their recurrence has become a promising therapeutic option.^4,5

Conventional ablation approaches that are widely accepted for the treatment of scar-related VTs include the ablation of critical areas based on activation, entrainment, or pace mapping, or the substrate ablation strategy, such as the elimination of local abnormal ventricular activities (LAVAs), late potential, scar dechanneling and homogenization.^6–9 Hemodynamic intolerance, lack of inducibility, and unsustainability are common during the radiofrequency ablation procedure of scar-related VTs, which preclude complete activation mapping and the identification of the critical isthmus of reentry.⁹ The substrate ablation approach overcomes these difficulties by targeting areas of low voltage and/or abnormal potential during normal sinus rhythm (NSR) for ablation. However, the complete elimination of all abnormal substrates using radiofrequency energy is difficult. The success rate ranged from 55% to 81%, which is not a satisfactory outcome.¹⁰ Despite the suboptimal long-term results of radiofrequency ablation, depending on the underlying structural heart disease, various observational studies and randomized trials have demonstrated a favorable outcome in terms of VT recurrence.^4,11,12

In recent years, physicians in many electrophysiological centers induce a VT or VTs, and perform activation mapping, entrain maneuvers, ablation of critical areas following with substrate ablation during NSR if the VTs are hemodynamically tolerated. In case the VTs are not hemodynamically tolerated, pace mapping of the VTs or premature ventricular contractions (PVCs) and substrate modification targeting LAVAs, late potentials, fractionated electrogram (EGM), were performed. Although this kind of stepwise ablation strategy has been reported,¹³ few studies compare the stepwise ablation strategy with the traditional substrate ablation strategy. During the last few years, we conducted the stepwise ablation strategy targeting ablation to critical sites identified during VT or pace mapping followed by substrate modification during NSR in scar-related VT patients and achieved a relatively high success rate. This study aimed to report our experience and compare the acute and long-term outcomes of the stepwise ablation strategy followed by substrate modification with substrate ablation alone.

2 Methods

2.1 Study population

Forty-one patients with scar-related VT underwent radiofrequency catheter ablation at the Cardiac Electrophysiology Center of the Second Hospital of Hebei Medical University between December 2018 and August 2022 were retrospectively reviewed. The indications for radiofrequency catheter ablation were recurrent VT recorded using electrocardiography (ECG) or ICD devices, and at least one antiarrhythmic drug was ineffective or patients required repeated anti-tachycardia pacing (ATP) or shock therapy with ICD or electrical cardioversion (ECD). The diagnosis of ICM was established by a previous history of infarction with Q waves, focal wall motion abnormalities with or without ventricular aneurysm formation on echocardiography, definite coronary angiography results, or previous coronary intervention. NICM was defined as the presence of scarring in areas without coronary stenosis. Patients with severe renal insufficiency, ventricular thrombosis, unstable angina, end-stage heart failure (New York Heart Association (NYHA) functional class IV, and expected survival of less than 1 year) were excluded. The baseline characteristics, the risk of periprocedural acute hemodynamic decompensation evaluated using the PAINESD score,^14–16 and the inducibility of VT in each patient were collected and compared between groups. The study protocol adhered to the tenets of the Declaration of Helsinki and was approved by the Research Ethics Committee of the second hospital of Hebei Medical University (Approval No.2023-R604). The Institutional Review Board waived consent from the patients due to retrospective nature of this study.

2.2 Intervention procedures

The patients were divided into two groups depending on the ablation strategy they received: Group 1 received the stepwise ablation strategy and Group 2 received substrate ablation alone. All patients underwent echocardiography before the procedure to evaluate cardiac function, including left ventricular ejection fraction (LVEF), and to aid in the identification of scar areas and ventricular aneurysms. Antiarrhythmic drugs were discontinued several days before the procedure, if applicable.

The procedures were performed under conscious sedation with fentanyl citrate (2 μg/kg/h). Arterial blood pressure and real-time oxygen saturation were monitored continuously. The ICD or cardiac resynchronization therapy defibrillator (CRTD) was deactivated to prevent discharge.

2.2.1 Group 1

The first step was to manage to induce VT. If VT can be induced, activation and entrainment mapping were performed to identify and ablate the critical isthmus under VT. If VT cannot be induced, pace mapping was performed to identify the most likely critical reentrant sites and ablated them. Subsequently, the arrhythmogenic substrate was modified for all patients.

The procedures for patients in group 1 were as follow:

Step 1: VT inducing, mapping and ablating of critical sites

A quadripolar catheter (Supreme Electrophysiology Catheter, St Jude Medical, St Paul, Minnesota, USA) was positioned in the right ventricular apex and a decapolar (Inquiry Steerable Diagnostic Catheter, St Jude Medical, St Paul, Minnesota) was placed in the coronary sinus. A loading dose of heparin (100 U/kg) was administered after accessing the left ventricle. The activated clotting time was maintained at > 250 s. Attempts were made at the beginning of the procedure to induce VT from the right ventricular apex by (1) giving stimulation trains consisting of single stimuli with incremental pacing, and/or (2) delivering programmed stimulation with a drive train of 500 ms for 6–8 stimuli followed by one to two extra stimuli, until the ventricular refractory period or 220 ms, to evaluate the inducibility and hemodynamic stability and to confirm the morphology of the QRS complex of the VT. Subsequently, VTs were terminated by overdriving pacing or ECD in patients with hemodynamic intolerance (after sedation with midazolam).

Voltage mapping and tagging of LAVAs during NSR were performed for each index procedure using a 3-dimensional electroanatomic mapping (3D EAM) Carto system with Pentaray or Deca (Biosense Webster, Diamond Bar, California), with a filling threshold set at 17–20 mm. Intracardiac electrical signals were filtered at 20–500 Hz for bipolar signals and at 2–250 Hz for unipolar signals. Activation mapping during the NSR was performed at the discretion of the operator. The left ventricular mapping was performed using a retrograde aortic or transseptal approach, and the right ventricular mapping was performed via the femoral vein. Epicardial access¹⁷ was performed via a subxiphoid approach using a steerable sheath (Agilis, St Jude Medical, St Paul, Minnesota) to guide the catheter into the pericardial cavity in cases where an endocardial scar was insignificant, ablation was ineffective or the EGM suggested an epicardial origin.

Bipolar voltage mapping was performed as follows: scar <1.5 mV, dense scar <0.5 mV, and border zone 0.5∼1.5 mV. LAVAs were considered to be poorly coupled in scar tissue and described as fractionated (multiple high-frequency deflections), split (double or multi-components separated by an isoelectric interval), or late potentials.¹⁸ During the mapping process, abnormal potentials were tagged with colored dots by an experienced engineer to denote the type of EGM.

Step 2: Mapping and ablating of critical isthmus of VT

Depending on the inducibility, different subsequent steps were performed after re-induction of VT. Activation mapping was performed, and isolated diastolic or continuous potentials were tagged. Entrainment mapping was performed whenever possible. An isthmus was defined as a site that demonstrated concealed fusion with (1) a post-pacing interval within 30 ms of the VT cycle length (CL), (2) a stimulus to the QRS (S-QRS) interval equal to the EGM-QRS, and/or (3) 30%< S-QRS < 70% VTCL.¹⁹ Radiofrequency energy was delivered focusing on the critical sites. We proceeded to the next step: whether the VT was terminated and uninducible or whether it could still be induced after detailed activation and entrainment mapping. If other mappable VT were observed, the previous step was repeated.

For patients with hemodynamic intolerance or non-inducible VTs, activation mapping of PVCs with the same morphology as the clinical VT and/or pace mapping was performed from the LAVAs during NSR (15 mA at 2 ms, and 500 ms step length). At least 10/12 leads exhibiting QRS morphology consistent with clinical VT were considered to have the same exit.^20,21 Exhibiting multiple morphologies, pace mapping matching with S-QRS > 30 ms, initiating VT,²² or an abrupt change from poor to well-matched QRS morphology²³ were considered surrogates for VT isthmuses and satisfactory pace mappings. The radiofrequency energy was limited and focused on common exits or sites those were satisfactory for pace mapping.

Step 3: Substrate modification

The abnormal potentials in the scar were remapped and radiofrequency energy was applied to those remained. If the LAVAs and far-field potentials appeared as fusion, we used stimulation to verify whether the potential had decremental conduction properties and separated from the far-field wave since this feature has been proven to be associated with slow conduction zones of VT reentry.²⁴

2.2.2 Group 2

All patients only underwent substrate ablation after VT inducing and substrate mapping, which is the current mature ablation strategy described elsewhere. Radiofrequency energy was applied to all abnormal potentials within the scar and the endpoints were defined as potential disappearance, separation, or loss of capture. If the potential was too close to the coronary artery or the intramural area, no excessive ablation was performed.

In both groups, the radiofrequency ablation procedures were performed with a 3.5-mm-tip open-irrigated catheter (ThermoCool NaviStar or SmartTouch, Biosense Webster, Diamond Bar, California) with a power of 35–50 W, temperature limit 45°C at a 17–20 mL flow rate. Radiofrequency energy was applied for 60 s for each application.

2.3 Post-procedure management

Antiarrhythmic drugs were administered for at least 3 months after the procedure. Postprocedural hospitalization was approximately 2–4 days with electrocardiographic monitoring. The ICD or CRTD was turned on, and the treatment threshold was set lower than the clinical VT.

2.4 Definition of acute and long-term outcomes

Acute procedural success was defined as the non-inducibility of any VT (except for non-clinical VTs with CL < 200 ms, polymorphic non-sustained VTs, and ventricular fibrillation).^25,26 Long-term success was defined as VT-free survival for at least 1 year.

2.5 Follow-up

All patients were followed up at 1, 3, and 6 months after the procedure and then every 6 months for at least 1 year. Transthoracic echocardiography, Holter monitoring, and ICD/CRTD programming were performed every 6 months. VT recurrence was defined as symptomatic VT lasting > 30 s or an episode detected by ECG or ICD/CRTD.

2.6 Statistical analysis

All statistical analyses were performed using SPSS software (version 21.0; IBM Corp., Armonk, NY, USA). Normal distribution of continuous variables was tested by Shapiro-Wilk method. Data were presented as means ± standard deviation for those with normal distribution or as median and interquartile range (IQR: 25th-75th) for those not conforming to a normal distribution. Comparisons between groups were performed using the Student's T-test for normal distribution data or the Mann–Whitney U test for non-normal distribution data. Categorical variables were shown as frequencies and percentages, and compared with Pearson's chi-square test or Fisher's exact test. Differences in VT-free survival were plotted using Kaplan–Meier curves and compared between groups using the log-rank test. Cox proportional hazards models were used to identify the predictors of VT recurrence, and hazard ratios (HR) and 95% confidence intervals (CI) were calculated. Co-localization of the different methods on the VT isthmus was examined using the kappa consistency test. All tests were two-sided, and a P-value <0.05 was considered statistically significant.

3 Results

3.1 Study population

The baseline characteristics of patients in the two groups are displayed in Table 1. A total of 41 patients completing the procedure and subsequent follow-up were reviewed, of whom 29 were in Group 1 (22 ICM and 7 NICM) and 12 were in Group 2 (7 ICM and 5 NICM). There was no statistical difference between the two groups in terms of mean age of the study population (64.79 ± 11.13 years in Group 1 and 59.33 ± 10.08 years in Group 2, respectively, P = 0.15) and sex distribution (82.8% males in Group 1 and 100.0% males in Group 2, respectively, P = 0.31). Besides, no significant differences in types of cardiomyopathies, LVEF, NYHA function class, hypertension, or the use of antiarrhythmic drugs between the two groups was observed.

Table 1.
Baseline characteristics of patients in the two groups.

Group 1 Group 2

(n = 29) (n = 12) P Value

Age, years 64.79 ± 11.13 59.33 ± 10.08 0.15

Male 24 (82.8%) 12 (100.0%) 0.31

ICM 22 (75.9%) 7 (58.3%) 0.46

NYHA III/IV 15 (51.7%) 4 (33.3%) 0.28

LVEF (%) 40.86 ± 11.26 44.58 ± 9.49 0.32

Hypertension 14 (48.3%) 4 (33.3%) 0.38

Diabetes 4 (13.8%) 1 (8.3%) 1.00

History of cardiac surgery 3 (10.3%) 2 (16.7%) 0.97

ICD/CRTD implanted 4 (13.8%) 1 (8.3%) 1.00

Previous RF 3 (10.3%) 1 (8.3%) 1.00

AADs

Amiodarone 17 (58.6%) 10 (83.3%)

Beta-blockers 16 (55.2%) 5 (41.7%)

≥2AADs 11 (37.9%) 6 (50.0%) 0.72

	Group 1	Group 2
Age, years	64.79 ± 11.13	59.33 ± 10.08	0.15
Male	24 (82.8%)	12 (100.0%)	0.31
ICM	22 (75.9%)	7 (58.3%)	0.46
NYHA III/IV	15 (51.7%)	4 (33.3%)	0.28
LVEF (%)	40.86 ± 11.26	44.58 ± 9.49	0.32
Hypertension	14 (48.3%)	4 (33.3%)	0.38
Diabetes	4 (13.8%)	1 (8.3%)	1.00
History of cardiac surgery	3 (10.3%)	2 (16.7%)	0.97
ICD/CRTD implanted	4 (13.8%)	1 (8.3%)	1.00
Previous RF	3 (10.3%)	1 (8.3%)	1.00
AADs
Amiodarone	17 (58.6%)	10 (83.3%)
Beta-blockers	16 (55.2%)	5 (41.7%)
≥2AADs	11 (37.9%)	6 (50.0%)	0.72

Variables are presented as means ± standard deviation, or frequency (percentage). AADs, antiarrhythmic drugs; CRTD, cardiac resynchronization therapy defibrillator; ICD, implantable cardioverter defibrillator; ICM, ischemic cardiomyopathy; LVEF, left ventricular ejection fraction; NYHA, New York Heart Association; RF, radiofrequency.

There were no significant differences in PAINESD scores (9.0 [6–15] vs. 7.5 [0.75–9], P = 0.059) or risk stratification of periprocedural acute hemodynamic decompensation between the two groups (P = 0.162).

3.2 Mapping and ablation

VT was induced in 22 patients (75.9%) in Group 1 and in 5 patients (41.7%) in Group 2 (P = 0.08). Two patients (6.9%) in Group 1 and four patients (33.3%) in Group 2 (P = 0.09) had access to the left ventricular chamber via the transseptal approach, and the others via the retrograde aortic route. Voltage maps during NSR were obtained from all endocardial surfaces, including five from right ventricular due to arrhythmic right ventricular cardiomyopathy or right ventricular surgical scars. Seven patients also underwent epicardial mapping, including four patients in Group 1 and three patients in Group 2 (P = 0.68). The location of the scars based on voltage mapping is given in Table 2.

Table 2.
Location of the scars based on voltage mapping.

Group 1 Group 2

LV

Septal 9 (31.0%) 2 (16.7%)

Anterior 13 (44.8%) 3 (25.0%)

Lateral 8 (27.6%) 4 (33.3%)

Post-inferior 14 (48.3%) 7 (58.3%)

RV

RVOT 2 (6.9%) 1 (8.3%)

Anterior 1 (3.4%) 1 (8.3%)

	Group 1	Group 2
LV
Septal	9 (31.0%)	2 (16.7%)
Anterior	13 (44.8%)	3 (25.0%)
Lateral	8 (27.6%)	4 (33.3%)
Post-inferior	14 (48.3%)	7 (58.3%)
RV
RVOT	2 (6.9%)	1 (8.3%)
Anterior	1 (3.4%)	1 (8.3%)

Variables are represented as frequencies and percentages.

LV: left ventricle; RV: right ventricle; RVOT: right ventricular outflow tract.

Activation mapping was performed in 22 cases of Group 1, with complete mapping in 10 cases and a limited mapping in 12 cases. PVC activation mapping and/or pace mapping were performed in seven cases.

A total of 32 types of VTs were identified in 22 patients. Thirteen types were induced in ten patients in whom the reentrant circuits could be completely mapped, and the critical sites were identified (Figure 1). Ten of the 13 VTs terminated during tachycardia. Three types of VTs were non-sustained and ablated during NSR at critical sites identified during activation mapping. No VTs were re-induced.

Figure 1.

Endo- and epicardial activation mapping and ablation of VT in a patient with ICM (color online). (A): The left panel depicts a scar on the lateral wall of the left ventricular endocardium during NSR and the right is the activation mapping during VT. The EGMs on the right correspond to the local potentials at points [a], [b], and [e], respectively. The red arrows and numbers indicate the LAT. The EGM at [e] occurred at the onset of QRS, indicating an exit of the reentry. Endocardial mapping failed to map the total cycle length, with a missing segment near the exit (the block from [b] to [e]). (B): Voltage and activation mapping on the epicardium of left ventricle during VT. [c] was activated first and conducted toward [d], the direction of which aligned with the endocardial structure's incapability to form a reentrant. Thus, the probable reentry pathway of this VT was [e]→[a]→[b]→[c]→[d]→[e]. (C): The left panel is a schematic depicting the conduction path. The thick black line on the endocardium denotes the conduction block region. The right panel shows a histogram of LAT during VT mapping on the endocardium, suggesting a cycle length deficiency. (D): The substrate mapping on the endocardium and epicardium during NSR, respectively. Ablation at the endocardium was ineffective while discharge on the epicardium terminated the VT. Solid red dots represent the ablation points. (EGM, electrogram; ICM, ischemic cardiomyopathy; LAT, local activation time; LV: Left ventricle; NSR, normal sinus rhythm; VT, ventricular tachycardia.).

Limited activation mapping for 19 types of VTs was performed in 12 patients. Six types of VTs were terminated upon discharge and two VTs were terminated mechanically at the designated critical sites. Radiofrequency energy was delivered during NSR to nine VTs because of non-sustained or hemodynamic instability. The two VTs were terminated using ECDs without further activation mapping due to hemodynamic intolerance.

Eighteen of the above VTs (in 16 patients) were terminated during tachycardia via ablation or mechanical collision. The activation maps during the NSR were analyzed in these 16 patients. Fifteen (83.3%) of the 18 VTs had diastolic potentials at the VT termination sites, whereas 15 (83.3%) VTs terminated in areas with slow or discontinuous conduction during NSR, which predicted the isthmus of the VT with an agreement test of Kappa = 0.60 (P = 0.01), suggesting moderate agreement.

Of the seven patients without induced VT, activation mapping combined with pace mapping was performed for PVCs to locate the common exit in three patients, and only pace mapping was conducted in four patients.

As shown in Figure 2, VT was not induced in the patient with noncompaction of the ventricular myocardium. A scar is observed in the epicardium of the LV lateral wall. Pace mapping was performed at abnormal potentials, giving rise to a QRS pattern similar to that of the PVC, which was then ablated and consolidated in the periphery.

Figure 2.

Epicardial pace mapping and substrate ablation of VT in a NICM patient (color online). (A): The left panel shows a short-axis section of an enhanced cardiac MRI scan, with a yellow arrow pointing to non-compaction of ventricular myocardium at the lateral wall of left ventricle, corresponding to the low-voltage area of epicardial EAM on the right. (B). The EAM map in the center displays epicardial activation mapping during NSR and exhibits a conduction abnormality area corresponding to the scar in A (right). [a] was the earliest activated point, [c] located in the slow conduction area while [d] was the latest activated point. The signal was transmitted from the septal side to the lateral wall ([b] →[d] →[e]). At [d] and [e], the signals from [a] and [b] collided, resulting in [d] being the latest activated point compared to nearby points (as indicated by red arrows in the bottom left panel), indicating that [d] was not the ablation target. Deca recorded abnormal far-field potentials originating from the scar area (yellow arrows). The varied colored arrows and boxes mirror the color-coded conduction sequence in the activation mapping and the numbers represent LAT. (C): Pace mapping was performed within the scar. The large orange dots indicated points where the morphology of the paced-QRS matches with PVCs, while the small yellow dots did not. The electrocardiography showed the pace mapping graphics, representing the two orange dots in the picture. The ablation area in the bottom plane included satisfactory pacing locations, the dominating path to the epicardium ([a]), and the slow conduction zone ([c]) during NSR. (EAM, electroanatomic mapping; ECG, electrocardiogram; LAT, local activation time; LV: Left ventricle; MRI, magnetic resonance imaging; NICM, nonischemic cardiomyopathy; NSR, normal sinus rhythm; PD, pacing dots; PVC, premature ventricular contraction.).

Nearly all abnormal potentials in the scar area were ablated during NSR in 12 patients of Group 2 (Figure 3), except for those less than 5 mm from the coronary artery and those located in the mid-myocardium. Only the substrate modification of VT was performed during NSR, and VT was induced and mapped to prove that it was related to scarring.

Figure 3.

Substrate ablation of VT in a patient with ICM (color online). The image shows the scarred areas on the posterior wall of the left ventricle. The EAMs were the activation and voltage maps during the NSR. Multiple slow or discontinued conduction areas were observed in dense scars and border zones. The pink dots represent the abnormal potentials tagged by Pentaray in the mid-to-end phase of the QRS complex and are represented as fractionated or multicomponent potentials. The red dots represent ablation points covering most scarred areas. From top to bottom, the EGM panels are CS5-6, V1-4, and Pentaray1-20. (EAM: electroanatomic mapping; EGM: electrogram; ICM: ischemic cardiomyopathy; VT: ventricular tachycardia.).

3.3 Duration and area of radiofrequency ablation

The duration of radiofrequency energy delivery was 16.00 min (13.30–22.32) in Group 1, which was significantly shorter than that in Group 2 (29.65 min [20.00–34.00] (P = 0.02). The total procedure time was comparable between the two groups (151.56 min [133.24–164.10] in Group 1 vs. 145.33 min [131.62–167.39] in Group 2, respectively, P = 0.75). The median scar area/low voltage area was 69.1 cm² (45.1–146.7) in Group 1 and 47.5 cm² (23.9–92.3) in Group 2 (P = 0.173). The ratio of ablation area to scar area (A/S) was 31.89% (17.74–58.79) and 53.28% (27.17–78.06), respectively (P = 0.05).

3.4 Acute and long-term outcomes

Acute procedural success was achieved in 100% in Group 1 and 91.7% in Group 2 (P = 0.65). The overall follow-up was 24.0 months (15.5–24.0) for Group 1 and 24.0 months (14.5–24.0) for Group 2 (P = 0.86). No patient died or was lost to follow-up. Two patients in Group 1 and four in Group 2 experienced VT recurrence. Figure 4 shows the Kaplan–Meier curves that plot the status of the patients and those at-risk during follow-up. The VT-free survival rate in Group 1 (93.1%) was significantly higher than that in Group 2 (66.7%) (P = 0.02). The univariate Cox proportional hazards model revealed that only the ablation strategy was associated with VT recurrence. The stepwise ablation strategy reduced the risk of VT recurrence (HR: 0.17, 95% CI: [0.03, 0.93], P = 0.04).

Figure 4.

Kaplan–Meier survival curve (color online). The Kaplan–Meier Curves describe the VT-free survival of patients in both groups during the entire follow-up period, and the bottom table shows the patients at risk. There was a significant difference in the VT-free survival between the two groups.

3.5 Complications

In Group 1, two patients presented with pseudoaneurysms, one of which disappeared after compression hemostasis, and the other was embolized by injecting lyophilized thrombin powder into the aneurysm. Additionally, one patient in Group 1 developed an arteriovenous fistula. In Group 2, one patient developed an arteriovenous fistula with pelvic hemorrhage, which was successfully treated with blood transfusion, anti-infection medication, and intravenous fluid therapy.

3.6 Application of antiarrhythmic drugs

Except for six patients who developed VT recurrence and were on long-term amiodarone, all patients discontinued antiarrhythmic drugs other than β-blockers within 1 year, and many patients remained on β-blockers primarily for hypertension or coronary heart disease.

4 Discussion

This study compared the acute and long outcomes of two different ablation procedures. Our results showed that the stepwise ablation strategy can improve the long-term success rate of VT-free and reduce the risk of recurrence and decrease the time of radiofrequency energy application.

Theoretically, the critical isthmus for maintaining VT episodes must satisfy a variety of conditions, such as conduction velocity and CL, and matching refractory period or specific stimuli.^27,28 Abnormal potentials and low voltage areas during NSR do not equally contribute to VT reentry. A significant proportion of abnormal myocardium may not meet all requisite conditions.²⁹ It is essential to recognize that certain abnormal potentials may be attributed to poor coupling between the local myocardium and its surrounding structures located at the blind end of conduction or bystanders rather than being directly involved in causing or maintaining VT, thus not embodying the actual arrhythmogenic substrate. The spatial distribution of slow or discontinued conduction during NSR may not correspond to the VT isthmus.³⁰ Indiscriminate ablation in substrate ablation is not conducive to producing focused and enduring lesions at sites that are critical for VT reentry. This nonspecific nature can easily result in extensive ablation and may create new blocks or deceleration zones that may induce new VTs.³¹ Activation mapping and entrainment mapping can identify the critical isthmus of VT reentry and enable stable and durable ablative lesions to critical sites. Although undifferentiated ablation lesions can also delay, separate, or eliminate LAVAs, there may only be a temporary injury or suppression of arrhythmia with the re-emergence of VT in the early post-procedure period.³² Although the ablation of the critical isthmuses is the primary target of VT, it may not always be sufficient. The VT substrate is dynamic in nature. Even if the VT is terminated during ablation, it may only intervene in one part of the functional barrier rather than the anatomical barrier, and the real isthmus can still drive reentry under certain conditions.^29,33 Besides, other areas of pathological myocardium may also function as the critical isthmus for different types of VTs that are not necessarily induced during the procedure, thereby becoming the substrate for future VT recurrence. In addition, some patients with NICM experience continuous progression of myocardial lesions, and bystander pathological myocardium may lead to new VT with aggravation of the lesions. Previous studies have demonstrated that complete substrate ablation has positive effects on long-term outcomes.^6,11,34 Therefore, it is advantageous to perform substrate ablation after the critical sites of VT have been ablated. Our study supports this perspective by demonstrating improved long-term outcomes in patients who underwent a stepwise ablation strategy.

The stepwise ablation strategy significantly reduced the ablation time. In Group 1, the first step was to manage to induce VT. Then, we identified the VT isthmus by activation mapping, entrainment mapping or pace mapping and ablated them. The abnormal EGMs were significantly reduced because ablation of critical sites was usually performed at abnormal potentials, which were often key factors inducing VT, and the mechanism of arrhythmia can be disrupted after ablating these abnormal potentials. This is because the occurrence of arrhythmia often depends on specific electrical conduction pathways. Precise targeting of critical isthmuses may destroy the central pathway, exit, or entrance to the reentry circuit. Specifically, by ablating the isthmus near the entrance of the VT reentry, an anatomical barrier was established that effectively blocked the re-entry of the VT and prevented the activity from being transmitted to a deeper depth, resulting in a reduction in the number of abnormal potentials and ablation time.^35,36 At the same time, the destroyed critical sites may serve as anchors of multiple VTs in the same case³⁰ and form different reentry circuits or conduction patterns in myocardial tissue under a certain condition, thus achieving the purpose of increasing the success rate. The A/S ratio tended to be lower in Group 1, but the difference was not statistically significant, perhaps because of the small sample size.

In clinical practice, there has been increasing interest in functional substrate mapping during NSR to identify surrogates of the critical sites of VT for targeted ablation³⁷ thereby avoiding extensive ablation. The scar dechanneling technique has been reported to reduce recurrence and mortality rates in over 50% of study patients.³⁵ The decrement-evoked potential mapping achieved a VT-free rate of 75% at 6 months post-procedure.³¹ Eliminating hidden slow conduction has been reported to achieve a long-term success rate of 75.7%,³⁸ and locating conduction deceleration zones during NSR has been shown to have a 70% success rate.³⁹ These methods are particularly applicable in cases in which VT cannot be induced or the patient is hemodynamically intolerant. Activation mapping during NSR provides the activation sequence and wavefront conduction characteristics that help identify arrhythmogenic substrates and guide targeted ablation. In our study, the diastolic potentials in the VT and slow or discontinued conduction in the NSR were at the upper limit of the moderate range for colocalization of the critical isthmus of the VT. However, the diastolic potential is only one of the predictors of the critical isthmus. In addition, the interpretation of the diagnostic medical imaging results depends a lot on the specialized knowledge of doctor, which might result in high susceptible to human error and subjectivity.^40,41 Therefore, artificial intelligence, such as artificial neural networks, is necessary to increase the standardization of interpretation of medical images and shows a relatively higher accuracy.^42,43 We anticipate that in future studies, functional substrate mapping and ablation during NSR may be incorporated into stepwise ablation strategies, leading to more accurate targeted ablation.

The primary contribution of this research is the proposition that a stepwise ablation strategy may mitigate the recurrence of VT. However, there are some limitations in this study. First, this study is a retrospective study with a limited sample size in a single-center. Only 41 patients were included and the number of patients in the two groups was unbalanced. Second, VT could not be induced before radiofrequency ablation in some patients, which may have limited our ability to evaluate the acute effects of the procedure. Third, the patients were heterogeneous, including both ICM and NICM and the proportion of epicardial ablation was also different. Unfortunately, we did not perform subgroup analysis due to the small sample size. Though there were no statistical differences in proportions of ICM and NICM patients between the two groups, conclusion should be made with cautious due to statistical power.

5 Conclusion

The stepwise radiofrequency ablation might be a promising effective strategy for scar-related VT in achieving long-term success VT-free survival than substrate ablation alone. Furthermore, it reduces the time required for radiofrequency energy application and may decrease the ratio of the ablation-damaged area to the scarred area. Further randomized controlled, multi-center studies with larger sample size are still needed to confirm the conclusion.

Footnotes

Abbreviations

Acknowledgements

We thank Professor Chenglong Miao for providing his valuable expertise on radiofrequency ablation for scar-related ventricular tachycardia in this study. We also express special appreciation to Professor Asia Li for his support throughout this process, which was like sunshine slanted in during the difficult times.

Ethical considerations

The study protocol adhered to the tenets of the Declaration of Helsinki. The retrospective study was approved by the Research Ethics Committee of the second hospital of Hebei Medical University (Approval Letter No.2023-R604). The Institutional Review Board did not require consent from the patients.

Authors’ contributions

PW, CM and BG have given substantial contributions to the conception or the design of the manuscript, PW, CM, LX, YW, RX, YZ and SL to acquisition, analysis and interpretation of the data. All authors have participated to drafting the manuscript, BG revised it critically. All authors read and approved the final version of the manuscript.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Availability of data and materials

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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	Group 1	Group 2
	(n = 29)	(n = 12)	P Value
Age, years	64.79 ± 11.13	59.33 ± 10.08	0.15
Male	24 (82.8%)	12 (100.0%)	0.31
ICM	22 (75.9%)	7 (58.3%)	0.46
NYHA III/IV	15 (51.7%)	4 (33.3%)	0.28
LVEF (%)	40.86 ± 11.26	44.58 ± 9.49	0.32
Hypertension	14 (48.3%)	4 (33.3%)	0.38
Diabetes	4 (13.8%)	1 (8.3%)	1.00
History of cardiac surgery	3 (10.3%)	2 (16.7%)	0.97
ICD/CRTD implanted	4 (13.8%)	1 (8.3%)	1.00
Previous RF	3 (10.3%)	1 (8.3%)	1.00
AADs
Amiodarone	17 (58.6%)	10 (83.3%)
Beta-blockers	16 (55.2%)	5 (41.7%)
≥2AADs	11 (37.9%)	6 (50.0%)	0.72

Stepwise ablation strategy in radiofrequency ablation improves acute and long-term outcomes of scar-related ventricular tachycardias

Abstract

Background

Objective

Methods

Results

Conclusion

Keywords

1 Introduction

2 Methods

2.1 Study population

2.2 Intervention procedures

2.2.1 Group 1

2.2.2 Group 2

2.3 Post-procedure management

2.4 Definition of acute and long-term outcomes

2.5 Follow-up

2.6 Statistical analysis

3 Results

3.1 Study population

Table 2. Location of the scars based on voltage mapping. Group 1 Group 2 LV Septal 9 (31.0%) 2 (16.7%) Anterior 13 (44.8%) 3 (25.0%) Lateral 8 (27.6%) 4 (33.3%) Post-inferior 14 (48.3%) 7 (58.3%) RV RVOT 2 (6.9%) 1 (8.3%) Anterior 1 (3.4%) 1 (8.3%)

3.4 Acute and long-term outcomes

3.6 Application of antiarrhythmic drugs

4 Discussion

5 Conclusion

Footnotes

Abbreviations

Acknowledgements

Ethical considerations

Authors’ contributions

Funding

Declaration of conflicting interests

Availability of data and materials

References

Table 2.
Location of the scars based on voltage mapping.

Group 1 Group 2

LV

Septal 9 (31.0%) 2 (16.7%)

Anterior 13 (44.8%) 3 (25.0%)

Lateral 8 (27.6%) 4 (33.3%)

Post-inferior 14 (48.3%) 7 (58.3%)

RV

RVOT 2 (6.9%) 1 (8.3%)

Anterior 1 (3.4%) 1 (8.3%)