https://orcid.org/0000-0001-6722-1826
Abstract
J-wave syndrome in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) has been linked to an increased risk of ventricular arrhythmia. We investigated the significance of J waves with respect to substrate manifestations and ablation outcomes in patients with ARVC.
Forty-five patients with ARVC undergoing endocardial/epicardial mapping/ablation were studied. Patients were classified into two groups: 13 (28.9%) and 32 (71.1%) patients with and without J waves, respectively. The baseline characteristics, electrophysiological features, ventricular substrate, and recurrent ventricular tachycardia/fibrillation (VT/VF) were compared. Among the 13 patients with J waves, only the inferior J wave was observed. More ARVC patients with J waves fulfilled the major criteria of ventricular arrhythmias (76.9% vs. 21.9%, P = 0.003). Similar endocardial and epicardial substrate characteristics were observed between the two groups. However, patients with J waves had longer epicardial total activation time than those without (224.7 ± 29.9 vs. 200.8 ± 21.9 ms, P = 0.005). Concordance of latest endo/epicardial activation sites was observed in 29 (90.6%) patients without J waves and in none among those with J waves (P < 0.001). Complete elimination of endocardial/epicardial abnormal potentials resulted in the disappearance of the J wave in 8 of 13 (61.5%) patients. The VT/VF recurrences were not different between ARVC patients with and without J waves.
The presence of J waves was associated with the discordance of endocardial/epicardial activation pattern in terms of transmural depolarization discrepancy in patients with ARVC.
The presence of J waves was associated with the endocardial/epicardial activation pattern in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC).
The J waves in the patients with ARVC could be modified by the endocardial/epicardial substrate modification.
Introduction
Arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC) is an inherited cardiomyopathy. The major pathogenesis of ARVC is caused by mutations in the desmosomal proteins, which leads to the dysfunction of cellular adhesion molecules.1 The right ventricle is predisposed to fibro-fatty infiltration between cardiomyocytes,2 which could result in delayed wavefront propagation and inhomogeneity of electrical conduction, thereby provoking ventricular tachycardia/fibrillation (VT/VF) in ARVC.3 Currently, the modified Task Force Criteria have been proposed for the clinical diagnosis of ARVC.4 In addition to the clinical manifestations in the Task Force Criteria, several electrocardiographic features (such as early repolarization, fragmented QRS, and T-wave inversion in the inferior leads) have been reported in ARVC, and these characteristics are also associated with a higher risk of future ventricular arrhythmic events or mortality.5
Early repolarization has been defined by a distinct J-wave or J-point elevation. The electrocardiography (ECG) pattern is characterized by notching or slurring of the terminal portion of the QRS and ST elevation.6 Several studies have demonstrated that J waves in the inferior leads, lateral leads, or both were associated with an increased risk of ventricular fibrillation (VF) and sudden cardiac death in patients without heart disease.7 In addition to the repolarization hypothesis owing to an electrical gradient resulting from a faster transient outward potassium current (Ito) in the epicardium than in the endocardium,8 emerging evidence has demonstrated that depolarization abnormalities from epicardial arrhythmogenic substrate can lead to the presence of J waves in patients with Brugada syndrome.9 Previous report showed that the presence of an inferior J wave in patients with ARVC may be associated with ventricular arrhythmia (VA).10 However, the substrate characteristics in ARVC patients with J waves have not been investigated. Therefore, we assessed the clinical manifestations, epicardial and endocardial substrate characteristics, and ablation outcomes in ARVC patients with and without J waves.
Methods
Study population
We enrolled patients diagnosed with ARVC based on the 2010 Revised Task Force Criteria4 and who had undergone both epicardial and endocardial substrate mapping and radiofrequency catheter ablation (RFCA) for drug-refractory VAs between 2013 and 2019. The Institutional Review Board approved this retrospective study (VGH-IRB: 2017–01-020C). All patients underwent 12-lead ECG, signal-averaged ECG (SAECG), 24-h Holter monitoring, transthoracic echocardiography and/or cardiac magnetic resonance imaging, coronary arteriography, and electrophysiological (EP) studies.
The patients were categorized into two groups according to the presence of J waves in 12-lead ECG.6 After ablation, the patients with J waves were further categorized into two groups according to the persisted J waves in 12-lead ECG or not.6 The J-wave was defined by the presence of J-point elevation ≥1 mm in ≥2 contiguous inferior and/or lateral leads of a standard 12-lead ECG.6 The J-wave agreement was reviewed by two independent and experienced electrophysiologists. Baseline characteristics, echocardiographic, EP parameters, and substrate characteristics were compared between patients with and without J wave.
Electrophysiological study, mapping, and ablation
The details of EP study, substrate mapping, and ablation strategies have been described in our previous works.11 In brief, after obtaining informed consent, we performed a standardized EP study for all patients under fasting and sedated status. All anti-arrhythmic drugs except amiodarone were discontinued for at least five half-lives prior to RFCA.11 Both endocardial and epicardial mapping was performed in all patients.11 Rapid ventricular pacing and/or programmed stimulation up to three extrastimuli were performed from the RV apex and/or RV outflow tract (RVOT) to induce VT/VF with and without intravenous isoprenaline (1–5 μg/min). The QRS morphologies and cycle lengths of spontaneous and/or induced VTs were compared with those of clinically-documented VTs. Activation mapping and/or entrainment mapping of stable VT was performed to localize VT isthmus, whereas a substrate-based ablation strategy targeting the late and fractionated electrograms within or surrounding the scar/low-voltage zone (LVZ) recorded during sinus rhythm or ventricular pacing was achieved in all patients.
Right ventricular endocardial bipolar scar and LVZ were defined as areas with a peak-to-peak bipolar voltage <0.5 and 0.5—1.5 mV, respectively, while the RV endocardial unipolar LVZ area was defined as an area with a peak-to-peak unipolar voltage <5.5 mV.12 Right ventricular epicardial bipolar scar and LVZ were defined as areas with a peak-to-peak bipolar voltage <0.5 and 0.5–1.0 mV, respectively. The voltage maps were edited manually to avoid intracavitary points. The average bipolar or unipolar median voltage was calculated. The area of scar, LVZ, and area with abnormal electrograms (defined as late or continuous fragmented potentials)13 were measured using the standard surface area measurement tool on the navigation system. When multiple areas with confluent low voltage were present, the aggregate area from the individual regions of interest was calculated. Successful ablation is defined as the absence of any spontaneous and inducible VA using the same stimulation protocol at the end of the procedure with and without isoproterenol.11 Partial success was defined as the presence of either spontaneous or inducible non-clinical VA after ablation, while failed ablation was considered for those with inducible clinical VAs.
Late potential area and definition of right ventricular regions
Late potentials were defined as local ventricular potentials occurring after the terminal portion of the surface QRS, including either continuous fragmented activity (bridging from the main component within the QRS to the latest signal recorded) or isolated potentials recorded after the offset of QRS, without a definite voltage cut-off.13 The interval from the end of the QRS complex to the end of the local abnormal electrogram and the local ventricular activity (defined by the total duration of fractionated electrograms) were measured to characterize late potentials. The area with clustering of late potentials was measured.
Based on fluoroscopy and electroanatomic mapping, the distribution of epicardial and endocardial late potentials at the free wall was categorized into seven distinct anatomical RV segments (Supplementary material online, Figure S1). These include the RVOT (from the pulmonic valve to the top of the tricuspid valve), superior tricuspid annulus (TA; 2 cm anterior to the valve, superior portion), inferior TA (2 cm anterior to the valve, inferior portion), superior free wall, inferior free wall, anterior wall, and apex.14
Transmural activation gradient
The epi-endocardial transmural activation gradient was defined as the absolute difference in activation time between the endocardium and its corresponding epicardium. The largest activation gradient of each anatomic segment was obtained. Prolonged transmural conduction was defined as an epi-endocardial activation gradient of >30 ms.15
Follow-up and recurrences of ventricular arrhythmia
Patients underwent regular follow-up at 1, 3, and 6 months after ablation in the first year and every 3–6 months thereafter. Implantable cardioverter-defibrillator interrogation, ECG, and Holter monitoring were performed every 3 or 6 months. Recurrent VAs were defined as recurrent VT/VF in patients who received appropriate implantable cardioverter-defibrillator therapies.16
Statistical analysis
Continuous variables were expressed as mean±standard deviation while categorical variables as percentages. Differences between continuous variables were assessed using Student’s t-test, whereas categorical variables were compared using the χ2 test with or without Yate’s correction or Fisher’s exact test, as indicated. A P-value of <0.05 was considered statistically significant. All statistical analyses were performed using the Statistical Package for the Social Sciences version 22.0 (IBM Corporation, Armonk, NY, USA).
Results
Baseline characteristics of patients with arrhythmogenic right ventricular cardiomyopathy
Forty-five patients [33 (73.3%) men; mean age, 46.4 ± 13.8 years] with a diagnosis of definite ARVC based on the 2010 Revised Task Force Criteria received endocardial and epicardial mapping and ablation. Among these, 32 (71.1%) patients were classified as J wave (−), while J waves in inferior leads were observed in 13 (28.9%) patients. No anterior or lateral J waves were identified in our patients. Table 1 shows the comparison of baseline characteristics between patients with and without J waves. More patients with ARVC and J waves fulfilled the major criteria of VA than those without J waves (76.9% vs. 21.9%, P = 0.003). There were no significant differences in baseline parameters, repolarization abnormalities, depolarization abnormalities, family history, gene mutation, and histopathological evidence of fibrofatty infiltration between the two groups.
Comparison of baseline characteristics between patients with ARVC with and without J waves
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Baseline characteristics | |||
| Age | 51.8 ± 12.9 | 44.2 ± 13.7 | 0.094 |
| Sex (men, %) | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Syncope | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Hypertension | 3 (30.0%) | 10 (35.7%) | 0.999 |
| Diabetes mellitus | 1 (7.7%) | 2 (6.2%) | 0.999 |
| Structural assessment | |||
| LVEF (%) | 52.9 ± 10.2 | 54.1 ± 8.4 | 0.706 |
| RVEF (%) | 34.6 ± 10.7 | 37.8 ± 11.7 | 0.404 |
| Medications | |||
| Amiodarone prior to ablation | 7 (53.8%) | 22 (68.8%) | 0.494 |
| β-Blocker | 9 (69.2%) | 21 (65.6%) | 0.999 |
| Class I AAD | 1 (7.7%) | 5 (15.6%) | 0.656 |
| Task Force Criteriaa | |||
| Structural abnormalities | |||
| Major | 8 (61.5%) | 17 (53.1%) | 0.625 |
| Minor | 5 (38.5%) | 13 (40.6%) | |
| Fibrofatty replacement | |||
| Major | 1 (7.7%) | 8 (25.0%) | 0.408 |
| Minor | 5 (38.5%) | 9 (28.1%) | |
| Depolarization abnormalities | |||
| Major | 6 (46.2%) | 5 (15.6%) | 0.085 |
| Minor | 6 (46.2%) | 25 (78.1%) | |
| Repolarization abnormalities | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.326 |
| Minor | 4 (30.8%) | 16 (50.0%) | |
| Ventricular arrhythmias | |||
| Major | 10 (76.9%) | 7 (21.9%) | 0.003 |
| Minor | 3 (23.1%) | 25 (78.1%) | |
| Clinical manifestation with VF | 7 (53.8%) | 12 (37.5%) | 0.341 |
| Family history | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.284 |
| Minor | 0 (0.0%) | 2 (6.2%) | |
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Baseline characteristics | |||
| Age | 51.8 ± 12.9 | 44.2 ± 13.7 | 0.094 |
| Sex (men, %) | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Syncope | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Hypertension | 3 (30.0%) | 10 (35.7%) | 0.999 |
| Diabetes mellitus | 1 (7.7%) | 2 (6.2%) | 0.999 |
| Structural assessment | |||
| LVEF (%) | 52.9 ± 10.2 | 54.1 ± 8.4 | 0.706 |
| RVEF (%) | 34.6 ± 10.7 | 37.8 ± 11.7 | 0.404 |
| Medications | |||
| Amiodarone prior to ablation | 7 (53.8%) | 22 (68.8%) | 0.494 |
| β-Blocker | 9 (69.2%) | 21 (65.6%) | 0.999 |
| Class I AAD | 1 (7.7%) | 5 (15.6%) | 0.656 |
| Task Force Criteriaa | |||
| Structural abnormalities | |||
| Major | 8 (61.5%) | 17 (53.1%) | 0.625 |
| Minor | 5 (38.5%) | 13 (40.6%) | |
| Fibrofatty replacement | |||
| Major | 1 (7.7%) | 8 (25.0%) | 0.408 |
| Minor | 5 (38.5%) | 9 (28.1%) | |
| Depolarization abnormalities | |||
| Major | 6 (46.2%) | 5 (15.6%) | 0.085 |
| Minor | 6 (46.2%) | 25 (78.1%) | |
| Repolarization abnormalities | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.326 |
| Minor | 4 (30.8%) | 16 (50.0%) | |
| Ventricular arrhythmias | |||
| Major | 10 (76.9%) | 7 (21.9%) | 0.003 |
| Minor | 3 (23.1%) | 25 (78.1%) | |
| Clinical manifestation with VF | 7 (53.8%) | 12 (37.5%) | 0.341 |
| Family history | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.284 |
| Minor | 0 (0.0%) | 2 (6.2%) | |
AAD, anti-arrhythmic drug; ARVC, arrhythmogenic right ventricular cardiomyopathy; ICD, implantable cardioverter-defibrillator; LVEF, left ventricular ejection fraction; RVEF, right ventricular ejection fraction; VF, ventricular fibrillation.
According to the 2010 Revised Task Force Criteria.5
Comparison of baseline characteristics between patients with ARVC with and without J waves
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Baseline characteristics | |||
| Age | 51.8 ± 12.9 | 44.2 ± 13.7 | 0.094 |
| Sex (men, %) | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Syncope | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Hypertension | 3 (30.0%) | 10 (35.7%) | 0.999 |
| Diabetes mellitus | 1 (7.7%) | 2 (6.2%) | 0.999 |
| Structural assessment | |||
| LVEF (%) | 52.9 ± 10.2 | 54.1 ± 8.4 | 0.706 |
| RVEF (%) | 34.6 ± 10.7 | 37.8 ± 11.7 | 0.404 |
| Medications | |||
| Amiodarone prior to ablation | 7 (53.8%) | 22 (68.8%) | 0.494 |
| β-Blocker | 9 (69.2%) | 21 (65.6%) | 0.999 |
| Class I AAD | 1 (7.7%) | 5 (15.6%) | 0.656 |
| Task Force Criteriaa | |||
| Structural abnormalities | |||
| Major | 8 (61.5%) | 17 (53.1%) | 0.625 |
| Minor | 5 (38.5%) | 13 (40.6%) | |
| Fibrofatty replacement | |||
| Major | 1 (7.7%) | 8 (25.0%) | 0.408 |
| Minor | 5 (38.5%) | 9 (28.1%) | |
| Depolarization abnormalities | |||
| Major | 6 (46.2%) | 5 (15.6%) | 0.085 |
| Minor | 6 (46.2%) | 25 (78.1%) | |
| Repolarization abnormalities | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.326 |
| Minor | 4 (30.8%) | 16 (50.0%) | |
| Ventricular arrhythmias | |||
| Major | 10 (76.9%) | 7 (21.9%) | 0.003 |
| Minor | 3 (23.1%) | 25 (78.1%) | |
| Clinical manifestation with VF | 7 (53.8%) | 12 (37.5%) | 0.341 |
| Family history | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.284 |
| Minor | 0 (0.0%) | 2 (6.2%) | |
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Baseline characteristics | |||
| Age | 51.8 ± 12.9 | 44.2 ± 13.7 | 0.094 |
| Sex (men, %) | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Syncope | 12 (92.3%) | 21 (65.6%) | 0.134 |
| Hypertension | 3 (30.0%) | 10 (35.7%) | 0.999 |
| Diabetes mellitus | 1 (7.7%) | 2 (6.2%) | 0.999 |
| Structural assessment | |||
| LVEF (%) | 52.9 ± 10.2 | 54.1 ± 8.4 | 0.706 |
| RVEF (%) | 34.6 ± 10.7 | 37.8 ± 11.7 | 0.404 |
| Medications | |||
| Amiodarone prior to ablation | 7 (53.8%) | 22 (68.8%) | 0.494 |
| β-Blocker | 9 (69.2%) | 21 (65.6%) | 0.999 |
| Class I AAD | 1 (7.7%) | 5 (15.6%) | 0.656 |
| Task Force Criteriaa | |||
| Structural abnormalities | |||
| Major | 8 (61.5%) | 17 (53.1%) | 0.625 |
| Minor | 5 (38.5%) | 13 (40.6%) | |
| Fibrofatty replacement | |||
| Major | 1 (7.7%) | 8 (25.0%) | 0.408 |
| Minor | 5 (38.5%) | 9 (28.1%) | |
| Depolarization abnormalities | |||
| Major | 6 (46.2%) | 5 (15.6%) | 0.085 |
| Minor | 6 (46.2%) | 25 (78.1%) | |
| Repolarization abnormalities | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.326 |
| Minor | 4 (30.8%) | 16 (50.0%) | |
| Ventricular arrhythmias | |||
| Major | 10 (76.9%) | 7 (21.9%) | 0.003 |
| Minor | 3 (23.1%) | 25 (78.1%) | |
| Clinical manifestation with VF | 7 (53.8%) | 12 (37.5%) | 0.341 |
| Family history | |||
| Major | 5 (38.5%) | 6 (18.8%) | 0.284 |
| Minor | 0 (0.0%) | 2 (6.2%) | |
AAD, anti-arrhythmic drug; ARVC, arrhythmogenic right ventricular cardiomyopathy; ICD, implantable cardioverter-defibrillator; LVEF, left ventricular ejection fraction; RVEF, right ventricular ejection fraction; VF, ventricular fibrillation.
According to the 2010 Revised Task Force Criteria.5
Endocardial and epicardial substrate characteristics
Table 2shows the comparison of substrate characteristics of RV endocardium and epicardium. There was no significant difference in bipolar voltage, unipolar voltage, area of bipolar and unipolar LVZ, and area of bipolar scar. It is notable that the total activation time of the RV epicardium in ARVC patients with J waves was significantly longer than in those without J waves (224.7 ± 29.9 vs. 200.8 ± 21.9 ms, P = 0.005) in the RV epicardium.
Comparison of RV substrate between patients with ARVC with or without J waves
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| RV endocardium | |||
| Averaged bipolar voltagea | 2.0 ± 0.8 | 1.9 ± 0.8 | 0.525 |
| Averaged unipolar voltagea | 5.1 ± 2.1 | 4.8 ± 1.2 | 0.512 |
| Total activation time (ms) | 171.5 ± 22.2 | 157.1 ± 27.8 | 0.105 |
| Bipolar low-voltage zone (cm2) | 37.4 ± 26.1 | 32.8 ± 18.6 | 0.504 |
| Bipolar low-voltage zone (%) | 15.4 ± 8.7 | 14.7 ± 7.3 | 0.800 |
| Bipolar scar (cm2) | 16.0 ± 12.9 | 18.2 ± 13.2 | 0.623 |
| Bipolar scar (%) | 6.5 ± 4.4 | 8.7 ± 5.7 | 0.214 |
| Unipolar low-voltage zone (cm2) | 84.3 ± 39.6 | 71.1 ± 31.0 | 0.239 |
| Unipolar low-voltage zone (%) | 29.6 ± 8.7 | 28.7 ± 11.9 | 0.804 |
| RV epicardium | |||
| Averaged bipolar voltage (mV)a | 1.2 ± 0.4 | 1.4 ± 0.5 | 0.280 |
| Total activation time (ms) | 224.7 ± 29.9 | 200.8 ± 21.9 | 0.005 |
| Bipolar low-voltage zone (cm2) | 140.3 ± 103.5 | 90.4 ± 45.0 | 0.116 |
| Bipolar low-voltage zone (%) | 39.3 ± 23.5 | 28.9 ± 12.9 | 0.153 |
| Bipolar scar (cm2) | 53.7 ± 30.6 | 44.2 ± 29.3 | 0.510 |
| Bipolar scar (%) | 19.6 ± 12.6 | 14.1 ± 6.3 | 0.155 |
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| RV endocardium | |||
| Averaged bipolar voltagea | 2.0 ± 0.8 | 1.9 ± 0.8 | 0.525 |
| Averaged unipolar voltagea | 5.1 ± 2.1 | 4.8 ± 1.2 | 0.512 |
| Total activation time (ms) | 171.5 ± 22.2 | 157.1 ± 27.8 | 0.105 |
| Bipolar low-voltage zone (cm2) | 37.4 ± 26.1 | 32.8 ± 18.6 | 0.504 |
| Bipolar low-voltage zone (%) | 15.4 ± 8.7 | 14.7 ± 7.3 | 0.800 |
| Bipolar scar (cm2) | 16.0 ± 12.9 | 18.2 ± 13.2 | 0.623 |
| Bipolar scar (%) | 6.5 ± 4.4 | 8.7 ± 5.7 | 0.214 |
| Unipolar low-voltage zone (cm2) | 84.3 ± 39.6 | 71.1 ± 31.0 | 0.239 |
| Unipolar low-voltage zone (%) | 29.6 ± 8.7 | 28.7 ± 11.9 | 0.804 |
| RV epicardium | |||
| Averaged bipolar voltage (mV)a | 1.2 ± 0.4 | 1.4 ± 0.5 | 0.280 |
| Total activation time (ms) | 224.7 ± 29.9 | 200.8 ± 21.9 | 0.005 |
| Bipolar low-voltage zone (cm2) | 140.3 ± 103.5 | 90.4 ± 45.0 | 0.116 |
| Bipolar low-voltage zone (%) | 39.3 ± 23.5 | 28.9 ± 12.9 | 0.153 |
| Bipolar scar (cm2) | 53.7 ± 30.6 | 44.2 ± 29.3 | 0.510 |
| Bipolar scar (%) | 19.6 ± 12.6 | 14.1 ± 6.3 | 0.155 |
ARVC, arrhythmogenic right ventricular cardiomyopathy; RV, right ventricular.
The average of bipolar or unipolar median voltage.
Comparison of RV substrate between patients with ARVC with or without J waves
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| RV endocardium | |||
| Averaged bipolar voltagea | 2.0 ± 0.8 | 1.9 ± 0.8 | 0.525 |
| Averaged unipolar voltagea | 5.1 ± 2.1 | 4.8 ± 1.2 | 0.512 |
| Total activation time (ms) | 171.5 ± 22.2 | 157.1 ± 27.8 | 0.105 |
| Bipolar low-voltage zone (cm2) | 37.4 ± 26.1 | 32.8 ± 18.6 | 0.504 |
| Bipolar low-voltage zone (%) | 15.4 ± 8.7 | 14.7 ± 7.3 | 0.800 |
| Bipolar scar (cm2) | 16.0 ± 12.9 | 18.2 ± 13.2 | 0.623 |
| Bipolar scar (%) | 6.5 ± 4.4 | 8.7 ± 5.7 | 0.214 |
| Unipolar low-voltage zone (cm2) | 84.3 ± 39.6 | 71.1 ± 31.0 | 0.239 |
| Unipolar low-voltage zone (%) | 29.6 ± 8.7 | 28.7 ± 11.9 | 0.804 |
| RV epicardium | |||
| Averaged bipolar voltage (mV)a | 1.2 ± 0.4 | 1.4 ± 0.5 | 0.280 |
| Total activation time (ms) | 224.7 ± 29.9 | 200.8 ± 21.9 | 0.005 |
| Bipolar low-voltage zone (cm2) | 140.3 ± 103.5 | 90.4 ± 45.0 | 0.116 |
| Bipolar low-voltage zone (%) | 39.3 ± 23.5 | 28.9 ± 12.9 | 0.153 |
| Bipolar scar (cm2) | 53.7 ± 30.6 | 44.2 ± 29.3 | 0.510 |
| Bipolar scar (%) | 19.6 ± 12.6 | 14.1 ± 6.3 | 0.155 |
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| RV endocardium | |||
| Averaged bipolar voltagea | 2.0 ± 0.8 | 1.9 ± 0.8 | 0.525 |
| Averaged unipolar voltagea | 5.1 ± 2.1 | 4.8 ± 1.2 | 0.512 |
| Total activation time (ms) | 171.5 ± 22.2 | 157.1 ± 27.8 | 0.105 |
| Bipolar low-voltage zone (cm2) | 37.4 ± 26.1 | 32.8 ± 18.6 | 0.504 |
| Bipolar low-voltage zone (%) | 15.4 ± 8.7 | 14.7 ± 7.3 | 0.800 |
| Bipolar scar (cm2) | 16.0 ± 12.9 | 18.2 ± 13.2 | 0.623 |
| Bipolar scar (%) | 6.5 ± 4.4 | 8.7 ± 5.7 | 0.214 |
| Unipolar low-voltage zone (cm2) | 84.3 ± 39.6 | 71.1 ± 31.0 | 0.239 |
| Unipolar low-voltage zone (%) | 29.6 ± 8.7 | 28.7 ± 11.9 | 0.804 |
| RV epicardium | |||
| Averaged bipolar voltage (mV)a | 1.2 ± 0.4 | 1.4 ± 0.5 | 0.280 |
| Total activation time (ms) | 224.7 ± 29.9 | 200.8 ± 21.9 | 0.005 |
| Bipolar low-voltage zone (cm2) | 140.3 ± 103.5 | 90.4 ± 45.0 | 0.116 |
| Bipolar low-voltage zone (%) | 39.3 ± 23.5 | 28.9 ± 12.9 | 0.153 |
| Bipolar scar (cm2) | 53.7 ± 30.6 | 44.2 ± 29.3 | 0.510 |
| Bipolar scar (%) | 19.6 ± 12.6 | 14.1 ± 6.3 | 0.155 |
ARVC, arrhythmogenic right ventricular cardiomyopathy; RV, right ventricular.
The average of bipolar or unipolar median voltage.
Table 3demonstrates the areas with late potentials in patients with ARVC. A total of 20 (1.5 ± 0.7/patient) and 42 (1.3 ± 0.6/patient) areas with late potentials within the RV endocardium were identified in patients with and without J waves, respectively (P = 0.148), while epicardial mapping demonstrated late potential areas of 25 (1.9 ± 1.4) and 44 (1.4 ± 0.9) in patients with and without J waves, respectively (P = 0.147). Of note, inferior TA was the most common endocardial segment with clustering of late potentials in ARVC patients with J waves (53.8%), while areas with late potentials were most frequently observed within endocardial RVOT in ARVC patients without J waves (84.4%). On the other hand, inferior RV free wall and RVOT were the most common epicardial areas with late potentials in patients with ARVC. Both endocardial and epicardial latest activation time in ARVC patients with J waves was significantly longer than that in patients without J waves (endocardium: 55.3 ± 38.4 vs. 24.2 ± 28.1 ms, P = 0.004; epicardium: 109.3 ± 67.2 vs. 50.3 ± 45.5 ms, P = 0.001). Moreover, in contrast to the endocardium, a heterogeneous distribution of the latest epicardial activation site was observed between patients with or without J waves (P = 0.002; Table 3). Figure 1 demonstrates the latest activation sites of the endocardium and epicardium. Furthermore, 29 of 32 (90.6%) ARVC patients without J waves had endocardial and epicardial latest activation sites located at the same RV segment (concordant distribution), while discordance of the latest activation areas between the endocardium and endocardium was observed in all ARVC patients with J waves (P < 0.001, Table 1). Figure 2 shows the examples of discordance and concordance of the latest endocardial and epicardial activation areas in ARVC patients with and without J waves, respectively. The heterogeneous activation pattern in patients with or without J waves is summarized in Figure 3. The largest transmural activation gradient between the endocardium and epicardium was higher in ARVC patients with J waves than in those without (110.9 ± 63.9 vs. 32.1 ± 38.1 ms, P < 0.001, Table 3). Furthermore, patients with J waves had more areas with the largest transmural gradient >30 ms than those without (92.3% vs. 34.4%, P < 0.001). A non-uniform distribution of areas with the largest transmural gradient >30 ms was observed between the two groups.
The corresponding latest activation sites between RV endocardium and epicardium. RV, right ventricular; RVOT, right ventricular outflow tract; TA, tricuspid annulus.
ARVC patients with and without a J wave. Left panel: there was no J wave on the 12-lead ECG (A1). The epicardial and endocardial activation maps (B1 and C1) demonstrated concordant latest activation sites in the RVOT area and the local electrogram of the latest activation site from epicardium (*) and endocardium (#). The bipolar voltage map demonstrated scar predominately in the RV epicardium (D1). Right panel: J wave could be observed in the inferior leads of 12-lead ECG (A2). The activation maps demonstrated discordance of latest activation sites between the epicardium (B2) and endocardium (C2). (epicardium: upper free wall; endocardium: RVOT). Local electrogram of the latest activation site from epicardium (*) and endocardium (#) was demonstrated in (B2) and (C2), respectively. The bipolar voltage map demonstrated scar predominately in the RV epicardium (D2). ARVC, arrhythmogenic right ventricular cardiomyopathy; ECG, electrocardiography; RVOT, right ventricular outflow tract.
The diverse activation pattern in ARVC patients with and without J wave. Upper panel: in patients without a J wave, the latest endocardial and epicardial activation areas were concordant, which resulted in a smaller transmural activation gradient. Lower panel: in patients with J waves, the latest epicardial activation area is frequently different from the latest endocardial activation area, which leads to greater transmural activation gradient.
Comparison of endocardial/epicardial distribution of late potentials and latest activation site between patients with and without J waves
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Distribution of late potentials | |||
| RV endocardium | |||
| Areas with late potentials | 1.5 ± 0.7 | 1.3 ± 0.7 | 0.321 |
| Superior TA | 3 (23.1%) | 5 (15.6%) | 0.672 |
| Inferior TA | 7 (53.8%) | 9 (28.1%) | 0.169 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.289 |
| Inferior free wall | 3 (23.1%) | 1 (3.1%) | 0.066 |
| RVOT | 5 (38.5%) | 27 (84.4%) | 0.004 |
| RV epicardium | |||
| Areas with late potentials | 1.8 ± 1.2 | 1.4 ± 0.8 | 0.214 |
| Superior TA | 5 (38.5%) | 6 (18.8%) | 0.251 |
| Inferior TA | 5 (38.5%) | 10 (31.2%) | 0.732 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.079 |
| Inferior free wall | 7 (53.8%) | 2 (6.2%) | 0.001 |
| RVOT | 5 (38.5%) | 26 (81.2%) | 0.011 |
| Latest activation time | |||
| RV endocardium (ms) | 55.3 ± 38.6 | 24.2 ± 28.1 | 0.004 |
| RV epicardium (ms) | 109.3 ± 67.2 | 50.3 ± 45.5 | 0.001 |
| Location of latest activation sites | |||
| RV endocardium | 0.204 | ||
| Superior TA | 1 (7.7%) | 1 (3.1%) | |
| Inferior TA | 5 (38.5%) | 7 (21.9%) | |
| Superior free wall | 1 (7.7%) | 0 (0.0%) | |
| Inferior free wall | 1 (7.7%) | 1 (3.1%) | |
| RVOT | 5 (38.5%) | 23 (71.9) | |
| RV epicardium | |||
| Superior TA | 3 (23.1%) | 2 (6.2%) | 0.002 |
| Inferior TA | 2 (15.4%) | 6 (18.8%) | |
| Superior free wall | 0 (0.0%) | 0 (0.0%) | |
| Inferior free wall | 5 (38.5%) | 1 (3.1%) | |
| RVOT | 3 (23.1%) | 23 (71.9) | |
| Largest activation gradient | 110.9 ± 63.9 | 32.1 ± 38.1 | <0.001 |
| Area with largest gradient >30 ms | |||
| No identifiable area | 1 (7.7%) | 21 (65.6%) | |
| Superior TA area | 3 (23.1%) | 1 (3.1%) | <0.001 |
| Inferior TA area | 3 (23.1%) | 3 (9.4%) | |
| Inferior free wall area | 4 (30.8%) | 0 (0.0%) | |
| RVOT area | 2 (15.4%) | 7 (21.9%) | |
| Concordance of endo/epi latest activation sites | 0 (0%) | 29 (90.6%) | <0.001 |
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Distribution of late potentials | |||
| RV endocardium | |||
| Areas with late potentials | 1.5 ± 0.7 | 1.3 ± 0.7 | 0.321 |
| Superior TA | 3 (23.1%) | 5 (15.6%) | 0.672 |
| Inferior TA | 7 (53.8%) | 9 (28.1%) | 0.169 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.289 |
| Inferior free wall | 3 (23.1%) | 1 (3.1%) | 0.066 |
| RVOT | 5 (38.5%) | 27 (84.4%) | 0.004 |
| RV epicardium | |||
| Areas with late potentials | 1.8 ± 1.2 | 1.4 ± 0.8 | 0.214 |
| Superior TA | 5 (38.5%) | 6 (18.8%) | 0.251 |
| Inferior TA | 5 (38.5%) | 10 (31.2%) | 0.732 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.079 |
| Inferior free wall | 7 (53.8%) | 2 (6.2%) | 0.001 |
| RVOT | 5 (38.5%) | 26 (81.2%) | 0.011 |
| Latest activation time | |||
| RV endocardium (ms) | 55.3 ± 38.6 | 24.2 ± 28.1 | 0.004 |
| RV epicardium (ms) | 109.3 ± 67.2 | 50.3 ± 45.5 | 0.001 |
| Location of latest activation sites | |||
| RV endocardium | 0.204 | ||
| Superior TA | 1 (7.7%) | 1 (3.1%) | |
| Inferior TA | 5 (38.5%) | 7 (21.9%) | |
| Superior free wall | 1 (7.7%) | 0 (0.0%) | |
| Inferior free wall | 1 (7.7%) | 1 (3.1%) | |
| RVOT | 5 (38.5%) | 23 (71.9) | |
| RV epicardium | |||
| Superior TA | 3 (23.1%) | 2 (6.2%) | 0.002 |
| Inferior TA | 2 (15.4%) | 6 (18.8%) | |
| Superior free wall | 0 (0.0%) | 0 (0.0%) | |
| Inferior free wall | 5 (38.5%) | 1 (3.1%) | |
| RVOT | 3 (23.1%) | 23 (71.9) | |
| Largest activation gradient | 110.9 ± 63.9 | 32.1 ± 38.1 | <0.001 |
| Area with largest gradient >30 ms | |||
| No identifiable area | 1 (7.7%) | 21 (65.6%) | |
| Superior TA area | 3 (23.1%) | 1 (3.1%) | <0.001 |
| Inferior TA area | 3 (23.1%) | 3 (9.4%) | |
| Inferior free wall area | 4 (30.8%) | 0 (0.0%) | |
| RVOT area | 2 (15.4%) | 7 (21.9%) | |
| Concordance of endo/epi latest activation sites | 0 (0%) | 29 (90.6%) | <0.001 |
RV, right ventricular; RVOT, right ventricular outflow tract; TA, tricuspid annulus.
Comparison of endocardial/epicardial distribution of late potentials and latest activation site between patients with and without J waves
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Distribution of late potentials | |||
| RV endocardium | |||
| Areas with late potentials | 1.5 ± 0.7 | 1.3 ± 0.7 | 0.321 |
| Superior TA | 3 (23.1%) | 5 (15.6%) | 0.672 |
| Inferior TA | 7 (53.8%) | 9 (28.1%) | 0.169 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.289 |
| Inferior free wall | 3 (23.1%) | 1 (3.1%) | 0.066 |
| RVOT | 5 (38.5%) | 27 (84.4%) | 0.004 |
| RV epicardium | |||
| Areas with late potentials | 1.8 ± 1.2 | 1.4 ± 0.8 | 0.214 |
| Superior TA | 5 (38.5%) | 6 (18.8%) | 0.251 |
| Inferior TA | 5 (38.5%) | 10 (31.2%) | 0.732 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.079 |
| Inferior free wall | 7 (53.8%) | 2 (6.2%) | 0.001 |
| RVOT | 5 (38.5%) | 26 (81.2%) | 0.011 |
| Latest activation time | |||
| RV endocardium (ms) | 55.3 ± 38.6 | 24.2 ± 28.1 | 0.004 |
| RV epicardium (ms) | 109.3 ± 67.2 | 50.3 ± 45.5 | 0.001 |
| Location of latest activation sites | |||
| RV endocardium | 0.204 | ||
| Superior TA | 1 (7.7%) | 1 (3.1%) | |
| Inferior TA | 5 (38.5%) | 7 (21.9%) | |
| Superior free wall | 1 (7.7%) | 0 (0.0%) | |
| Inferior free wall | 1 (7.7%) | 1 (3.1%) | |
| RVOT | 5 (38.5%) | 23 (71.9) | |
| RV epicardium | |||
| Superior TA | 3 (23.1%) | 2 (6.2%) | 0.002 |
| Inferior TA | 2 (15.4%) | 6 (18.8%) | |
| Superior free wall | 0 (0.0%) | 0 (0.0%) | |
| Inferior free wall | 5 (38.5%) | 1 (3.1%) | |
| RVOT | 3 (23.1%) | 23 (71.9) | |
| Largest activation gradient | 110.9 ± 63.9 | 32.1 ± 38.1 | <0.001 |
| Area with largest gradient >30 ms | |||
| No identifiable area | 1 (7.7%) | 21 (65.6%) | |
| Superior TA area | 3 (23.1%) | 1 (3.1%) | <0.001 |
| Inferior TA area | 3 (23.1%) | 3 (9.4%) | |
| Inferior free wall area | 4 (30.8%) | 0 (0.0%) | |
| RVOT area | 2 (15.4%) | 7 (21.9%) | |
| Concordance of endo/epi latest activation sites | 0 (0%) | 29 (90.6%) | <0.001 |
| J wave (+) (N = 13) | J wave (−) (N = 32) | P-value | |
|---|---|---|---|
| Distribution of late potentials | |||
| RV endocardium | |||
| Areas with late potentials | 1.5 ± 0.7 | 1.3 ± 0.7 | 0.321 |
| Superior TA | 3 (23.1%) | 5 (15.6%) | 0.672 |
| Inferior TA | 7 (53.8%) | 9 (28.1%) | 0.169 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.289 |
| Inferior free wall | 3 (23.1%) | 1 (3.1%) | 0.066 |
| RVOT | 5 (38.5%) | 27 (84.4%) | 0.004 |
| RV epicardium | |||
| Areas with late potentials | 1.8 ± 1.2 | 1.4 ± 0.8 | 0.214 |
| Superior TA | 5 (38.5%) | 6 (18.8%) | 0.251 |
| Inferior TA | 5 (38.5%) | 10 (31.2%) | 0.732 |
| Superior free wall | 2 (15.4%) | 0 (0.0%) | 0.079 |
| Inferior free wall | 7 (53.8%) | 2 (6.2%) | 0.001 |
| RVOT | 5 (38.5%) | 26 (81.2%) | 0.011 |
| Latest activation time | |||
| RV endocardium (ms) | 55.3 ± 38.6 | 24.2 ± 28.1 | 0.004 |
| RV epicardium (ms) | 109.3 ± 67.2 | 50.3 ± 45.5 | 0.001 |
| Location of latest activation sites | |||
| RV endocardium | 0.204 | ||
| Superior TA | 1 (7.7%) | 1 (3.1%) | |
| Inferior TA | 5 (38.5%) | 7 (21.9%) | |
| Superior free wall | 1 (7.7%) | 0 (0.0%) | |
| Inferior free wall | 1 (7.7%) | 1 (3.1%) | |
| RVOT | 5 (38.5%) | 23 (71.9) | |
| RV epicardium | |||
| Superior TA | 3 (23.1%) | 2 (6.2%) | 0.002 |
| Inferior TA | 2 (15.4%) | 6 (18.8%) | |
| Superior free wall | 0 (0.0%) | 0 (0.0%) | |
| Inferior free wall | 5 (38.5%) | 1 (3.1%) | |
| RVOT | 3 (23.1%) | 23 (71.9) | |
| Largest activation gradient | 110.9 ± 63.9 | 32.1 ± 38.1 | <0.001 |
| Area with largest gradient >30 ms | |||
| No identifiable area | 1 (7.7%) | 21 (65.6%) | |
| Superior TA area | 3 (23.1%) | 1 (3.1%) | <0.001 |
| Inferior TA area | 3 (23.1%) | 3 (9.4%) | |
| Inferior free wall area | 4 (30.8%) | 0 (0.0%) | |
| RVOT area | 2 (15.4%) | 7 (21.9%) | |
| Concordance of endo/epi latest activation sites | 0 (0%) | 29 (90.6%) | <0.001 |
RV, right ventricular; RVOT, right ventricular outflow tract; TA, tricuspid annulus.
Ventricular tachycardia mapping and ablation
Sixty-seven (1.5 ± 0.7) VTs could be induced in the EP laboratory. The mean cycle length of inducible VT was 339.0 ± 65.2 ms. VT mapping, either via entrainment or activation map, could be achieved in 41 patients, including 29 [96.6% (29/32)] and 12 [92.3% (12/13)] ARVC patients with and without J waves, respectively. All patients underwent isthmus ablation, if mappable, and complete endocardial/epicardial substrate modification. After catheter ablation, successful ablation was achieved in all patients. Notably, a disappearance of the J wave in at least one lead was observed in 8 of 13 (61.5%) patients. Figure 4 shows an example of the disappearance of the J wave after complete endocardial and epicardial substrate modification. There were no procedural-related complications in any of the patients.
An example of elimination of the J wave after ablation. The upper panel (A) showed the J wave in the inferior leads (II and aVF) before ablation. After endocardial and epicardial substrate modification, the J wave disappeared (B).
Follow-up
After a mean follow-up period of 33.9 ± 23.0 months, two (4.4%) patients died of non-cardiovascular diseases (pneumonia: 2), and seven (15.6%) patients had recurrences of sustained VT or VF. The incidence of VT/VF recurrence was similar between patients with and without J waves (log-rank P value = 0.735, Figure 5A). Among ARVC patients with J waves before ablation, the incidence of VT/VF recurrence was not statistically different between those with and without disappearance of J waves after ablation (log-rank P = 0.487, Figure 5B).
Comparison of VT/VF recurrences during longitudinal follow-up between patients with and without J wave. The Kaplan–Meier curve demonstrated no differences in VT/VF recurrences between patients with and without J waves (A) and patients with and without J-wave disappearance (B) during follow-up. VT, ventricular tachycardia; VF, ventricular fibrillation
Discussion
Main findings
There were several important findings of the present study. First, the majority of the J wave observed in patients with ARVC involved the inferior leads rather than the lateral leads. Secondly, the presence of J waves in the inferior leads in patients with ARVC was associated with non-uniform distribution of areas with late potentials between the endocardium and epicardium of the right ventricle. Furthermore, more ARVC patients with J waves had discordant endo-epicardial activation patterns, which lead to a larger transmural activation gradient, highlighting the mechanistic insight of depolarization in the presence of J waves. The above finding was also indirectly evidenced by the fact that disappearance of J waves could be observed after complete endocardial and epicardial substrate modification in certain ARVC patients. Finally, despite the presence of J waves in patients with ARVC, the long-term outcomes of endocardial and epicardial substrate modification were similar.
J waves in patients with arrhythmogenic right ventricular cardiomyopathy
J waves during hypothermia, which were known as ‘Osborn waves’, are caused by transmural differences in the early phases of the action potential and exert the potential proarrhythmic effects with an increased incidence of spontaneous VF in the experimental study.17 Yan and Antzelevitch8 demonstrated that prominent Ito-mediated notch of the action potential in the ventricular epicardium resulted in the abnormal repolarization manifested as a J wave on ECG. In addition to hypothermia, the J wave can be observed in other life-threatening cardiac arrhythmia syndromes, such as Brugada syndrome and early repolarization syndromes.18
The J wave has been previously reported in ARVC, which was also associated with a higher incidence of clinical VF and aborted sudden cardiac death.10 In our present study, the long-term outcome became similar between the patients with or without J wave after eliminating all the mappable VT circuit and targeting all the abnormal electrograms within the LVZ by epicardial–endocardial approach.
Whether ARVC and J wave syndrome have a common pathogenetic denominator remains unclear. In contrast to the J wave observed during hypothermia or J-wave syndrome in structurally normal hearts, ARVC is one of the non-ischaemic cardiomyopathies, which is caused by the dysfunction of cell adhesion and fibrofatty tissue infiltration.1 Recent experimental studies have renewed interest in identifying the mechanisms responsible for the overlapping phenotype by demonstrating a subcellular interrelationship due to the crosstalk between desmosomes and sodium channel proteins.19,20 This was also supported by the phenotypic overlap between ARVC and Brugada syndrome in a clinical study.21 Despite the link between the J waves and Brugada syndrome, future investigations are warranted to clarify the cellular mechanism of J waves in ARVC.
Correlation between substrates and J waves in arrhythmogenic right ventricular cardiomyopathy
Previously, the J wave was considered as a repolarization discrepancy between the epicardium and endocardium. Notwithstanding, mapping of the epicardial substrate in Brugada syndrome proved a mixture of repolarization and/or depolarization abnormalities in the development of J waves. To the best of our knowledge, this is the first study to illustrate the correlation between epi/endocardial depolarization in ARVC patients with J waves. First, the J wave in patients with ARVC was predominantly involved in the inferior leads, which was compatible with the observed scar or slow conduction within the RV basal inferior wall. Furthermore, our results demonstrated a higher proportion of discordant endocardial/epicardium latest activation pattern in ARVC patients with J waves. This was not observed in those without J waves, reemphasizing the potential role of depolarization discrepancy between the endocardium and epicardium in the presence of J waves. The aforementioned findings were also evidenced by the fact that disappearance of the J wave could be observed in 61.5% of patients after substrate modification. However, no significant changes in J waves were observed in the remaining patients, which could be explained by the concomitant repolarization abnormalities or the existence of intramural substrates that were not identifiable. However, the exact mechanism of the J wave in these patients remains to be clarified.
Clinical implications
Despite the similar ablation outcome in ARVC patients with and without J waves, the presence of J waves might indicate the discordance of endocardial and epicardial late potentials, which might lead to ventricular arrhythmogenesis and contribute to the failed ablation through the endocardial approach alone. Therefore, based on present results, epicardial mapping would be warranted for ARVC patients with J waves on surface ECG, especially for those with failed endocardial approaches or recurrences.
Limitations
There were some limitations to the present study. First, the study population was relatively small, particularly for the J-wave group. However, the present findings provide a novel mechanistic insight into the transmural electrical discontinuity in the development of J waves in ARVC. Secondly, this was a retrospective study, and only patients with ARVC undergoing both endocardial and epicardial mapping were selected. Whether selective bias could confound the current results remains unknown and future investigations are warranted to validate the generalizability of the present findings in a large-scale cohort. Thirdly, the presence of epicardial fat could interfere with the recognition of the latest activation site or the presence of late potentials within the epicardium. Furthermore, the activation pattern or diseased substrate within the intramural area was not clear, despite high-density mapping being performed to minimize the aforementioned concerns.
Conclusion
The majority of J waves in patients with ARVC involved the inferior leads. The presence of J waves in ARVC patients was associated with the discordance of endocardial and epicardial activation pattern, and disappearance of the J wave could be observed in 61.5% of patients after substrate modification. Despite the presence of J waves, similar VT/VF recurrences were observed after complete endocardial and epicardial substrate modification.
Supplementary material
Supplementary material is available at Europace online.
Funding
This work was supported by the Ministry of Science and Technology (MOST 109-2314-B-075-075-MY3, MOST 109-2314-B-010-058-MY2, MOST 109-2314-B-075-074-MY3, MOST 109-2314-B-075 -076 -MY3, grant nos. 107-2314-B-010-061-MY2, MOST 106-2314-B-075-006-MY3, MOST 106-2314-B-010-046-MY3, and MOST 106-2314-B-075-073-MY3), Research Foundation of Cardiovascular Medicine, Szu-Yuan Research Foundation of Internal Medicine, and Taipei Veterans General Hospital (grant nos. V106C-158, V106C-104, V107C-060, V107C-054, V108C-107, V109C-113, and V110C-116).
Conflict of interest: none declared.
Data availability
The authors were not allowed to provide the details of the research data.
