Author + information
- Received October 18, 2017
- Revision received November 17, 2017
- Accepted November 23, 2017
- Published online April 16, 2018.
- Giuseppe Ciconte, MD, PhDa,
- Vincenzo Santinelli, MDa,
- Josep Brugada, MD, PhDb,
- Gabriele Vicedomini, MDa,
- Manuel Conti, MDa,
- Michelle M. Monasky, PhDa,
- Valeria Borrelli, BMSca,
- Walter Castracane, MDc,
- Tommaso Aloisio, MDc,
- Luigi Giannelli, MDa,
- Umberto Di Dedda, MDc,
- Paolo Pozzi, BEngd,
- Marco Ranucci, MDc and
- Carlo Pappone, MD, PhDa,∗ ()
- aArrhythmology Department, IRCCS Policlinico San Donato, San Donato Milanese, Milan, Italy
- bCardiovascular Institute, Hospital Clinic, University of Barcelona, Barcelona, Spain
- cDepartment of Cardiothoracic and Vascular Anesthesia and ICU, IRCCS Policlinico San Donato, San Donato Milanese, Milan, Italy
- dJohnson & Johnson, Biosense Webster, Pomezia, Rome, Italy
- ↵∗Address for correspondence:
Dr. Carlo Pappone, Department of Arrhythmology, IRCCS Policlinico San Donato, Piazza E. Malan 1, 20097 San Donato Milanese, Milan, Italy.
Objectives This study investigates the electrocardiographic-electrophysiological effects of administration of anesthetic drugs for general anesthesia (GA) in patients with BrS at high risk of sudden cardiac death (SCD).
Background The safety of anesthetic agents in Brugada syndrome (BrS) is under debate.
Methods All consecutive patients with spontaneous type 1 BrS electrocardiographic (ECG) patterns undergoing epicardial ablation of the arrhythmogenic substrate (AS) under GA were enrolled. Anesthesia was induced with single bolus of propofol and maintained with sevofluorane. ECG measurements were collected before, immediately after, and 20 min after induction of GA. Three-dimensional maps during GA and after ajmaline indicated the epicardial AS before ablation.
Results Thirty-six patients with BrS (32 male, 88.9%; mean age 38.8 ± 12.0 years) with a spontaneous type 1 ECG pattern underwent GA. Induction was performed using propofol at mean dose of 1.6 to 2.6 mg/kg (2.1 ± 0.3 mg/kg). Twenty-eight (28 of 36, 77.8%) patients showed a reversion to a nondiagnostic pattern. ST-segment elevation (0.32 ± 0.01 mV vs. 0.19 ± 0.02 mV; p < 0.001) and J-wave amplitude (0.47 ± 0.02 mV vs. 0.31 ± 0.03 mV; p < 0.001) decreased after propofol. The AS area during GA, in the absence of BrS pattern, significantly enlarged after administration of ajmaline (3.6 ± 0.5 cm2 vs. 20.3 ± 0.8 cm2). No patient developed malignant arrhythmias during GA induction and maintenance.
Conclusions This study shows that GA using single-bolus propofol and volatile anesthetics is safe in high-risk patients with BrS, and it may exert a modulating effect by reducing the manifestation of type 1 BrS pattern and AS in the form of epicardial abnormal ECGs. (Epicardial Ablation in Brugada Syndrome: An Extension Study of 200 BrS Patients; NCT03106701)
The Brugada syndrome (BrS) is an inherited disease characterized by coved-type ST-segment elevation in the right precordial leads on the electrocardiogram (ECG) and increased risk of sudden cardiac death (SCD) (1) in the absence of structural heart disease (2). The presence of a spontaneous type 1 pattern generally confers a higher risk of ventricular tachycardia/fibrillation (VT/VF), potentially leading to SCD (2,3). The electrophysiological substrate responsible for ECG abnormalities appears to be located in the epicardial surface of the right ventricular outflow tract (RVOT) (4,5). Therefore, recent clinical studies highlighted the value of epicardial radiofrequency catheter ablation (RFA) of such regions, resulting in the normalization of ECG pattern and thus preventing recurrences of life-threatening ventricular arrhythmia (VA) (4,6–8).
Since the systematic introduction of active screening in unmasking BrS using sodium-channel blockers, the diagnosis and incidence of the disease has increased considerably as the true prevalence is still unknown (9). As a result, not only cardiologists but also anesthesiologists and critical care physicians need to be aware of the potential proarrhythmic effect and interaction of drugs commonly used in clinical practice when dealing with BrS (10).
Among intravenous anesthetics, propofol is one of the most frequently administered drugs for induction and maintenance of general anesthesia (GA). However, despite the conflicting data available in the literature (11,12), it is currently indicated as a drug to be avoided in patients with BrS (10) owing to its reported arrhythmogenic effects (13–16).
The aim of the current study is to evaluate the electrocardiographic and electrophysiological effects of GA in a large population of patients with BrS at high risk of SCD, exhibiting spontaneous type 1 BrS pattern, and undergoing epicardial RFA of the arrhythmogenic substrate (AS).
All patients referred to the Arrhythmology Department of IRCCS Policlinico San Donato, scheduled for epicardial RFA for BrS, have been prospectively enrolled (NCT03106701). The data analyzed for this study were prospectively collected as part of a predefined secondary analysis during the main study. All patients with spontaneous type 1 BrS ECG patterns were considered for this analysis. Medical history, physical examination, and baseline ECGs were obtained. Underlying structural cardiac abnormalities were excluded using cardiac magnetic resonance (MR) and echocardiogram in 21 and 15 patients, respectively. Spontaneous type 1 ECG pattern was defined in presence of a coved type ST-segment elevation ≥2 mm in ≥1 lead from V1 to V3, or in the high right precordial leads (V1 and V2 up to the second, third, and fourth intercostal space [IS]) in the absence of a sodium-channel blocker agent, according to the most recent guidelines (9). Patients were considered to be symptomatic if they had presented with previous aborted cardiac arrest (CA), syncope, or documented VAs. Patients without typical BrS-related symptoms may have experienced other symptoms (i.e., weakness, dizziness, or palpitations) without ECG documentation at the time of events, but all with inducible VT/VF. All patients enrolled had implantable cardioverter-defibrillators (ICDs). The study was approved by the local ethics committee, and all patients provided written informed consent.
GA and ECG assessment
All procedures were performed under GA and were conducted in the hybrid catheterization laboratory, where external cardioverter defibrillators were attached to patients with adhesive pads prior to the procedure (8). Blood pressure was constantly monitored through a radial arterial access. Further monitoring comprised pulse oximetry and continuous carbon dioxide monitoring through side sampling from the ventilator tubes. Induction of anesthesia was performed in all cases using propofol as a single bolus over a few seconds. Fentanyl, at a dose of 0.5 to 2 μg/kg, was always combined with propofol before securing the airways with an endotracheal tube. Anesthesia was maintained with volatile anesthetics (sevoflurane, 2% to 3%) in a 50:50 oxygen-air mixture.
ECG was continuously recorded at the beginning and throughout the entire procedure with the right precordial leads positioned at the sternal margin of the second, third, and fourth IS. All ECG parameters were analyzed before, while the patient was fully awake, and immediately after administration of propofol. Further ECG measurements were collected 20 min after administration of propofol, a time when its action is considered to be expired (17). PR interval, QRS duration, and QTc interval (Bazett’s formula) were measured in milliseconds. The J-wave amplitude was measured at the J point (18), and the analysis of ST-segment elevation was performed at 40 ms from the J point in the high right precordial lead showing the greatest elevation in each patient (V1 or V2 at the second, third, or fourth IS) (18,19). The same ECG lead was used to compare all measurements before and after anesthesia. ECG intervals were digitally measured by an expert physician and verified by a second reviewer using the EP recording system calipers (Claris, Abbott, Minneapolis, Minnesota). ECG pattern changes were analyzed at 25 mm/s, and ECG intervals were measured at 200 mm/s paper speed.
Endocardial-epicardial electroanatomical mapping and potential duration map
Our standard approach has been previously described in detail (8). Briefly, after having performed endocardial (Endo) electroanatomical mapping of the right ventricle (RV), epicardial (Epi) access was obtained using fluoroscopy-guided subxyphoidal puncture, and a steerable sheath (Agilis EPI, St Jude Medical, St. Paul, Minnesota) was introduced, as previously described (20). Detailed RV Endo-Epi mapping was performed using a 3-dimensional (3D) mapping system (CARTO 3, Biosense Webster, Diamond Bar, California) with the ablation catheter (ThermoCool SF, Biosense Webster) and/or high-density mapping catheter (DecaNAV, Biosense Webster). All Epi-maps were obtained at baseline conditions and after drug challenge (ajmaline 1 mg/kg in 5 min). The provocative test was used in case of significant reduction or disappearance of the spontaneous type 1 pattern. Ajmaline was administered (1) to achieve the maximal ST-segment elevation and unmask, if necessary, the type 1 pattern and (2) to identify the real extent of the regions displaying fragmented and abnormal electrograms (EGMs). All the potential duration maps (PDMs) were performed by collecting the duration of each bipolar EGM. Bipolar EGMs were filtered from 16 Hz to 500 Hz, displayed at 200 mm/s speed, and were recorded between the distal electrode pair. Measurements were interpreted and validated online by 2 observers using CARTO3 system electronic calipers. Abnormal EGMs were identified if they met at least 1 of the following characteristics: 1) a wide duration (>110 ms) with fragmented component (>3 distinct peaks); 2) late component of low-voltage amplitude ranging from 0.05 to 1.5 mV; 3) distinct and delayed component exceeding the end of the QRS complex; or 4) discrete double activity. EGM acquisition was performed only if the multipolar catheter was stable in each epicardial position and if the EGM morphology, evaluated by the operators, was consistent and repetitive for at least 3 consecutive beats, thus avoiding artifacts. Acquisition was excluded if their technical quality was insufficient (noise due to catheter movement or poor catheter contact). Total duration of signal was measured for each potential before and after drug challenge. As a result, a color-coded map was obtained showing the regions displaying the shortest (<110 ms cut-off, red color) and the longest (>200 ms cut-off, purple color) durations.
Data are presented as mean ± SD or SEM and as absolute values and percentages, as appropriate. Significance testing was performed using univariate analysis of variance (ANOVA), and then multiple comparisons were corrected using Tukey’s approach. A p value < 0.05 was considered statistically significant. Statistical analyses were conducted using SPSS version 21 (IBM SPSS Statistics, Armonk, New York).
A total of 36 patients with BrS (32 male, 88.9%; mean age 38.8 ± 12.0 years; range 18 to 63 years) undergoing epicardial ablation and showing a spontaneous type 1 ECG pattern were enrolled in this study. All patients were European, except for one Southeast-Asian patient. Eight patients (8 of 36, 22.2%) had survived previous CAs, and 11 (11 of 36, 30.6%) had at least 1 episode of syncope with documented VA or VA inducibility at EPS. The remaining 17 patients (17 of 36, 47.2%) had VT/VF inducibility during EPS without typical Brugada-related symptoms. Baseline clinical characteristics of the study population are listed in Table 1.
GA-induced BrS pattern modifications
ECG parameters were measured at baseline, immediately after induction of anesthesia using propofol, and every 20 min thereafter. The induction dose ranged between 1.6 and 2.6 mg/kg (2.1 ± 0.3 mg/kg). No patient received propofol to maintain GA. Among 36 patients, 23 (23 of 36, 63.9%) showed the highest ST-segment elevation in V2 second IS, 10 (10 of 36, 27.8%) in V2 third IS, and 3 (3 of 36, 8%) in V1 second IS before GA.
After administration of propofol, among 36 patients exhibiting a typical type 1 pattern while awake, 28 (28 of 36, 77.8%) showed a reversion to a nondiagnostic pattern (Figures 1, 2, and 3⇓⇓⇓). Eight subjects (8 of 36, 22.2%) continued to show type 1 morphology with a reduced ST-segment elevation, whereas only 1 of them did not experience any ST-segment or J-wave change during induction and maintenance of GA. Fifteen patients (15 of 36, 41.6%) showed reduction of T-wave negativity, and 16 (16 of 36, 44.4%) shifted to a positive T-wave (Figure 3). In 2 patients (2 of 36, 5.5%), the T-wave became isoelectric, whereas in 2 others (2 of 36, 5.5%), it did not show significant changes.
No statistically significant differences could be observed regarding PR, QRS, and QTc interval duration before and during GA (Figure 4, Table 2). The ST-segment elevation significantly decreased during GA (0.32 ± 0.01 mV vs. 0.19 ± 0.02 mV; p < 0.001) (Figure 4). The latter effect was significantly more pronounced immediately after administration of propofol compared with 20 min after (0.19 ± 0.02 mV vs. 0.21 ± 0.02 mV; p < 0.001) (Figure 4). Similarly, the J-wave showed a statistically significant reduction of amplitude after administration of propofol (awake 0.47 ± 0.02 mV vs. propofol 0.31 ± 0.03 mV; p < 0.001) (Figure 4), which persisted throughout the GA period (propofol 0.31 ± 0.03 min vs. 20 min after 0.34 ± 0.03 mV; p = 0.056) (Figure 4).
In 35 patients (35 of 36, 97.2%), ajmaline challenge was performed to fully exhibit the type 1 pattern in order to identify the epicardial AS. Only 1 patient (1 of 36, 2.8%) did not receive the drug challenge, as the ECG-pattern did not change overtime during GA. Administration of ajmaline significantly increased the PR, QRS, and QTc duration of interval compared with the awake condition and during GA (Figure 4, Table 2). All patients undergoing drug challenge showed typical type 1 BrS patterns after administration of ajmaline, without differences in ST-segment elevation and J-wave amplitude, compared with the awake condition (ST-awake 0.31 ± 0.13 mV vs ST-ajmaline 0.33 ± 0.03 mV; p = 0.53; J-awake 0.46 ± 0.02 mV vs. J-ajmaline 0.48 ± 0.03 mV; p = 0.85) (Figure 4). After administration of ajmaline, the ST-segment elevation and the J-wave amplitude significantly increased compared with both parameters measured immediately after and then 20 min after infusion with propofol (ST-ajmaline 0.33 ± 0.03 min vs. propofol 0.19 ± 0.02 vs. 20 min after 0.21 ± 0.01 mV; both p < 0.0001; J-ajmaline 0.48 ± 0.03 min vs. propofol 0.31 ± 0.03 vs. 20 min after 0.34 ± 0.03; both p < 0.0001) (Figure 4). No patients developed VAs during induction and maintenance of anesthesia or during ajmaline challenge.
Arrhythmogenic electrophysiological substrate
All patients underwent electroanatomical mapping to assess the epicardial AS area. The PDM was performed before and after administration of ajmaline to compare the different distribution of the prolonged and fragmented EGMs over the RV epicardium, according to the different degrees of ST-segment elevation and presence of type 1 pattern.
Before ajmaline challenge, in the absence of typical type 1 BrS ECG pattern, the AS area exhibiting delayed and fragmented activities accounted for 3.6 ± 0.5 cm2 (Figures 5 and 6⇓⇓). The pre-ajmaline AS was identified during GA, when spontaneous type 1 pattern had disappeared or been modified by anesthetic drugs.
After administration of ajmaline, the epicardial EGMs were significantly prolonged, resulting in a significant enlargement of the AS region (20.3 ± 0.8 cm2 vs. 3.6 ± 0.5 cm2; p < 0.001) (Figures 5 and 6). After the epicardial mapping/ablation procedure, no adverse events were noticed during the recovery phase. All patients were then safely discharged from the postanesthesia care unit after 1 h of intensive monitoring.
To the best of our knowledge, this is the first study assessing the electrophysiological effect of anesthetics in patients with BrS and spontaneous type 1 pattern. The main findings of this study are the following: (1) GA can be conducted safely in high-risk patients with BrS without occurrence of VAs; (2) administration of propofol consistently reduces ST-segment elevation, converting type 1 ECG into nondiagnostic pattern; (3) ECG changes are associated with a marked reduction of the epicardial arrhythmogenic substrate.
Risk of SCD using anesthetic drugs in BrS
It is known that the Brugada type 1 ECG is a marker of SCD, and the arrhythmogenic risk increases in the presence of a spontaneous pattern, which is associated with the epicardial AS area (9). Moreover, patients with BrS are more prone to develop potentially lethal malignant arrhythmias in case of fever, conditions determining increased vagal tone, or after administration of certain medications (9).
Among anesthetic drugs, propofol has been proposed as a contributor to such arrhythmias by provoking Brugada-like pattern (21) and increasing the risk of malignant arrhythmias (12), thus questioning its safety in patients with BrS (10). Although the safety and efficacy of propofol has been demonstrated for induction and maintenance of GA (22), it is known that its intravenous administration at high doses for prolonged periods is associated with propofol infusion syndrome (PRIS) (16). Vernooy et al. (21) described the occurrence of a coved-type ST-segment elevation in the right precordial leads as a preceding marker of imminent arrhythmic SCD in 6 patients while they were receiving extremely high doses of propofol (average 6.4 mg/kg/h); these high doses are rarely used in current practice. Therefore, considering the apparent similarity in ECG pattern among those developing life-threatening arrhythmias and in patients with BrS, a common arrhythmogenic mechanism was postulated, suggesting great caution or avoidance of administration of propofol, especially for patients with BrS.
Moreover, the risk of VAs was claimed to be associated with propofol in a retrospective cohort of patients with BrS receiving this drug for acute medical events (14). However, neither clinical characteristics of these patients nor type of acute event requiring sedation were reported nor was the administered dose with the duration of infusion defined. In the case of an acute event, as described in the latter series, it may be difficult to prove a causative association between ECG abnormalities and fatal outcome of 1 single drug, especially when underlying comorbidities may exist and multiple drugs may have been administered. The role of propofol in the development of arrhythmias, as reported in other studies, is still unclear. It has been speculated that it may have an indirect effect on myocardial cells through a metabolite, and—in the presence of suitable factors (i.e., electrolytes imbalance, acidosis, fever and drug combinations)—it might contribute to both ECG abnormalities and life-threatening arrhythmias (21). In fact, by carefully analyzing the 7 patients with PRIS described by Vernooy et al. (21), 3 patients had fever, hyperkalemia was documented in the other 3 patients, and 1 patient experienced metabolic acidosis. However, as occurred in this study, propofol was administered safely to a cohort of patients with BrS at higher risk of SCD without any arrhythmic event. In addition, while on GA, patients received ajmaline, aiming at full expression of the substrate, and—also in this case—no VA occurred. These findings suggest that such anesthetic drugs may be used safely and effectively in this subset of patients.
Although several drugs may be dangerous, considering their potential action on cardiac ion channels, the basis for establishing some anesthetic agents—as is nearly forbidden in patients with BrS—seems to lack strong evidence. As reported in the literature, previous retrospective studies have shown the safety of GA in patients with BrS (11,23).
The results of our study extend the above-mentioned experiences regarding the safety of GA in BrS. In fact, this represents the first prospective study conducted in a “high-risk” BrS population undergoing epicardial AS ablation that assesses the safety of this anesthesia strategy. According to our experience, GA carried out with single-bolus administration of propofol for induction and volatile anesthetics for maintenance is a safe and effective strategy for patients with BrS. Of note, it was associated with the absence of VAs and reduction of ST-segment elevation, and such ECG changes were maintained over time until administration of ajmaline. In addition, Brugada-pattern reversion was accompanied by a reduction of the epicardial AS, which showed its full extent only after administration of the sodium channel blocker, ajmaline, aiming at type 1 ECG-pattern reappearance, as occurred in our series.
The data analyzed in the current study were prospectively collected as part of the main study, in which the findings were as follows: 1) patients with BrS have well-defined electrophysiological substrate located in the RV epicardium; 2) ajmaline test facilitates the identification of the epicardial AS, proving an objective relationship between the presence of coved-type pattern and the extent of the AS; and 3) extensive ablation of the AS normalized the ECG pattern, resulting in VT/VF noninducibility in all patients (8).
As occurred in this cohort, GA has altered the phenotype expression of the BrS, and this may be a unique phenomenon. In fact, unlike other diseases, BrS seems to be the only condition showing a close relationship between coved-type ECG and extent of AS (8). Therefore, it is reasonable that any factor, such as temperature or drugs, affecting BrS ECG pattern may also influence the epicardial substrate (24,25). We also believe that GA may not alter the arrhythmogenic substrate in non-Brugada conditions; however, future studies are needed to confirm this hypothesis.
The Brugada ECG pattern is often concealed and can be unmasked with a wide variety of drugs and conditions including febrile state, vagotonic agents and maneuvers, electrolyte imbalance, and alcohol/cocaine toxicity (9). According to the data available in the literature, it has been suggested to avoid some medications (i.e., propofol) in patients with BrS, as it may increase the risk of life-threatening VAs, which is associated with the presence of type 1 ECG pattern (9). However, as occurred in our cohort, the use of this drug for induction of GA was associated with attenuation of the ST-segment elevation, downgrading of the ECG pattern, and absence of VAs in all patients. Most importantly, GA modulated and reduced the BrS epicardial AS. Single-bolus propofol, expiring in 15 min, was followed by sevofluorane 5 to 10 minthereafter, potentially showing a sequential rather than synergistic effect. Moreover, volatile anesthetics are very practical for their rapid onset and offset in patients under mechanical ventilation, compared with long-term propofol infusion, which is discouraged for patients with BrS and might be less feasible for maintenance of GA. According to this experience, not only propofol but the anesthesia strategy described herein may be recommended safely even for patients with BrS undergoing noncardiac interventions.
A high density of the transient outward potassium current (Ito) in RVOT epicardial cells has been implicated as a principal mechanism underlying the repolarization abnormalities giving rise to the arrhythmogenic substrate in BrS. For this reason, pharmacologic inhibition of Ito is regarded to be of therapeutic value (26,27). Moreover, propofol has been shown to inhibit Ito in a concentration-dependent manner (IC50 = 33.5 ± 2.0 μM) in human myocytes (28). Administration of single-dose propofol may acutely cause a rebalancing of ion channel currents, resulting in a reduction of the ST-segment elevation. This potential mechanism may explain how GA ameliorates the BrS phenotype, as occurred in this study. Moreover, propofol induces systemic vasodilatation, which, in turn, may result in a reactive increase in catecholaminergic tone. Accordingly, one might speculate that the above-mentioned mechanisms could modulate the autonomic tone and equalize ion currents.
Considering that anesthesia-induced ECG changes were associated with lower expression of the abnormal epicardial area, it could also be postulated that GA could be of benefit in the acute management of life-threatening VAs and cardiac resuscitation maneuvers in this cohort of patients, given the potential antiarrhythmic effect.
This study bears the relative limitation of being a single-center and nonrandomized trial. Therefore, considering the low prevalence of spontaneous type 1 pattern in the general population, we believe that the size and characteristics of our study population produced a homogenous “high-risk” cohort group with an appropriate sample size. Considering that only those patients having documented or inducible VAs underwent ablation, the effect of GA and propofol in the low-risk population has not been evaluated. However, GA had been successfully conducted in a true high-risk cohort (spontaneous type 1 ECG, CA survivors, documented arrhythmias and inducibility of VAs), thus potentially overcoming this limitation.
The same ECG lead was always used to collect ECG parameter changes in each patient. It was chosen according to the lead showing the highest ST-segment elevation, which could be different according to each patient’s characteristics. However, we have demonstrated a clear and consistent ST-segment elevation and reduction of J-wave amplitude in all right precordial leads.
General anesthesia was induced with propofol and maintained with volatile anesthetics; no patient received continuous infusion of propofol. The potential arrhythmogenic effect of continuous administration of propofol in this patient population is beyond the scope of the current study and requires further evaluation.
General anesthesia carried out with a single bolus of propofol, followed by volatile anesthetics, is not only safe but may also exert a modulating effect by reducing the phenotype expression of type 1 Brugada ECG and arrhythmogenic epicardial substrate.
These findings may provide new and relevant information regarding the use of these anesthetic agents in BrS, suggesting that current recommendations to avoid administration of propofol in this cohort of patients should be reconsidered.
COMPETENCY IN MEDICAL KNOWLEDGE: General anesthesia using single-bolus propofol and volatile anesthetics resulted in attenuation of BrS type 1 ECG pattern and reduction of the epicardial arrhythmogenic substrate area without the occurrence of malignant arrhythmias.
TRANSLATIONAL OUTLOOK: The described general anesthesia approach may be safely recommended in patients with BrS, as it could prove to be beneficial in the short-term management of patients with BrS, exerting a potential antiarrhythmic effect.
All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Abbreviations and Acronyms
- anti arrhythmic drugs
- arrhythmogenic substrate
- Brugada syndrome
- general anesthesia
- implantable cardioverter-defibrillator
- intercostal space
- potential duration map
- radiofrequency ablation
- right ventricle outflow tract
- sudden cardiac death
- ventricular arrhythmia
- ventricular tachycardia/ventricular fibrillation
- Received October 18, 2017.
- Revision received November 17, 2017.
- Accepted November 23, 2017.
- 2018 American College of Cardiology Foundation
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