CASE SUMMARY:A 73-year-old man with severe aortic stenosis and preexisting right bundle branch block (RBBB) underwent transcatheter aortic valve replacement. Postprocedural day 4 mobile cardiac outpatient telemetry revealed intermittent atrioventricular block. A 12-lead electrocardiogram obtained in the emergency department revealed PR interval alternans with RBBB, with longer PR following longer preceding RP intervals, and shorter PR following shorter RP intervals. He suddenly experienced cardiac arrest due to proximal atrioventricular block, requiring cardiopulmonary resuscitation. TAKE-HOME MESSAGES:Inverse decremental conduction, known as Yan conduction, demonstrates an inverse relationship between conduction time and frequency of upstream stimulation. Inverse decremental conduction within the left bundle branch in the setting of RBBB may manifest as PR alternans, heralding proximal atrioventricular block.

ABSTRACT Pheochromocytoma typically presents with sustained or paroxysmal hypertension, but initial manifestation as acute non‐ST‐segment elevation myocardial infarction (NSTEMI) is rare. Peri‐procedural hemodynamic fluctuations are often dramatic, making diagnosis and management challenging. We report a 51‐year‐old male admitted with chest tightness for 17 days. Elevated troponin and coronary angiography showing multivessel disease with total occlusion of the mid‐left anterior descending artery (LAD) led to a preliminary diagnosis of NSTEMI. During percutaneous coronary intervention, blood pressure surged to 240/130 mmHg; intravenous nitroprusside caused an instantaneous drop to 95/55 mmHg, with rapid rebound to >200 mmHg upon withdrawal, showing no clear temporal relationship with drug administration. Postoperatively, large rapid blood pressure oscillations persisted, associated with postural changes but without patient discomfort. Workup revealed markedly elevated plasma catecholamines: dopamine 77.58 pg/mL (normal 0–20), normetanephrine 1881.63 pg/mL (0–145), and norepinephrine 5,724.04 pg/mL (217–1,109). CT and PET‐CT identified a left retroperitoneal mass (59×34×44 mm, SUVmax 14.6), suggestive of pheochromocytoma. Surgical resection was performed, and histopathology with immunohistochemistry confirmed the diagnosis. Postoperatively, the patient required no antihypertensive medications and blood pressure remained stable. This case illustrates a rare pheochromocytoma presentation as secondary hypertension manifesting as acute myocardial infarction, characterized by extreme peri‐procedural hemodynamic instability during PCI and an “all‐or‐none” response to conventional antihypertensive therapy, ultimately cured by surgical resection.

CASE SUMMARY:An 83-year-old man with a history of atrial fibrillation on amiodarone therapy was admitted for direct-current cardioversion because of recurrent atrial fibrillation with a ventricular rate of approximately 105 beats per minute. Cardioversion successfully restored sinus rhythm. Postcardioversion 12-lead electrocardiography revealed an unexpectedly short QTc of 344 ms despite chronic treatment with a QT-prolonging agent. This finding was attributed to QT hysteresis, reflecting delayed adaptation of ventricular repolarization to the abrupt reduction in heart rate after rhythm conversion. TAKE-HOME MESSAGE:QT hysteresis can result in transient QTc shortening and has important implications for interpretation of QT intervals during antiarrhythmic therapy.

BACKGROUND:Cardiac syncope can be life-threatening, but there is no clinical tool for initial screening. The study explored and developed optimal artificial intelligence methods for automatic diagnosis of cardiac syncope based on combinations of electrocardiogram parameters and clinical characteristics. METHODS:The patients presenting with syncope and hospitalized between June 21, 2018 and August 23, 2022 at the Second Hospital of Tianjin Medical University. The patients enrolled were divided into development cohort who were then randomly split into a training set and an internal validation set (4: 1) and temporal validation cohort. Fifteen features of syncope patients were ranked and valuable features were selected. Six supervised machine learning models were developed to explore a potential prediction model for cardiac syncope. The area under the curve (AUC) was the primary metric used to evaluate classification performance. RESULTS:A total of 380 patients (340 in the development cohort and 40 in the temporal validation cohort) were included in the final analysis. The random forest showed the best performance using the top twelve features ranked by importance, demonstrating an AUC of 0.85 (sensitivity: 0.72, specificity: 0.85, F1 score: 0.74) in the development cohort, and an AUC of 0.75 (sensitivity: 0.70, specificity: 0.65, F1 score: 0.68) in the validation cohort. The novel approach for automatic diagnosis of cardiac syncope has been proposed as web service for further application. CONCLUSIONS:Artificial intelligence methods may assist in syncope classification, and which have the potential to serve as a cost-effective and efficient screening tool for cardiac syncope.

This review explores the ionic and cellular mechanisms that underlie antiarrhythmic drug therapy, focusing on how modulation of ionic currents influences cardiac action potentials and refractory periods. Reentrant arrhythmias, the most common type of tachyarrhythmias, are managed by strategies that prolong the effective refractory period. The review also discusses the proarrhythmic risks associated with use-dependence and reverse use-dependence of ion channel blockers. Special attention is given to J-wave syndromes, where Ito blockade plays a pivotal role in preventing phase 2 reentry and polymorphic ventricular tachycardia. Mechanistic understanding is essential for enhancing drug safety and therapeutic efficacy in clinical practice.

Inflammation plays a crucial role in the pathogenesis of ST-segment elevation myocardial infarction (STEMI). However, the precise immunological mechanisms remain incompletely understood. Single-cell RNA sequencing (scRNA-seq) provides a powerful approach to dissect immune cell heterogeneity and dynamic changes at single-cell resolution. Peripheral blood mononuclear cells (PBMCs) were collected from 7 STEMI patients (within 6h after primary percutaneous coronary intervention) and 3 healthy controls. Single-cell suspensions were prepared and subjected to scRNA-seq using the 10x Genomics Chromium platform and Illumina NovaSeq 6000. Data were processed using Cell Ranger and analyzed with Seurat for quality control, clustering, and annotation. Differentially expressed genes (DEGs) were identified and analyzed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), gene set variation analysis (GSVA), and gene set enrichment analysis (GSEA). Cell-cell communication was inferred using CellChat. And protein–protein interaction (PPI) network analysis was performed via STRING and Cytoscape. Key genes were validated using quantitative real-time PCR (qRT-PCR). A total of 71,288 PBMCs were analyzed. Significant differences in immune cell composition were observed between groups, especially in monocytes and T cells. Monocytes were divided into 10 subclusters; subclusters 0, 1, and 6 showed marked expansion and were functionally associated with inflammation, antigen presentation, and cytokine regulation. PPI network analysis identified JUN as a key hub gene, which was confirmed by qRT-PCR. T cells were divided into 7 subtypes, and GSEA revealed enrichment of IL-2/STAT5 and TNF-α/NF-κB signaling in STEMI. CD69 and ICOS were significantly upregulated in T cells. CellChat analysis revealed enhanced intercellular communication in STEMI, with the CXCL signaling pathway (notably PF4–CXCR3 interaction) being highly upregulated. This study reveals key inflammatory and immune characteristics of PBMCs in STEMI patients. JUN and the CXCL signaling axis represent potential targets for immunomodulatory therapy in acute myocardial infarction.

One marker of arterial stiffness (AS) is the brachial-ankle pulse wave velocity (baPWV). We aim to investigate the predictive value of baPWV with regard to new-onset atrial fibrillation (AF). All participants without AF from 2010 to 2020 in the Kailuan cohort were included. The primary endpoint was new-onset AF. Participants were categorized into three study groups based on baPWV, with a normal baPWV group as a reference. The predictive value of baPWV was analyzed as a continuous variable. Multivariable Cox proportional hazard regression models were used to investigate the association. A total of 49,872 subjects (mean age: 47.57 years old, 74.2% male) were included with a mean follow-up of 6.17 (3.95–8.46) years. The risk of AF increased as the baseline baPWV increased, whereby the adjusted hazard ratio (aHR) of the borderline AS group and the elevated AS group were 1.82 (95% confidence interval [CI]: 1.18–2.80) and 2.08 (95% CI: 1.31–3.30), respectively. When considered as a continuous variable, each 361 cm/s increase in baseline baPWV, increased the risk of AF by 21.7% (aHR: 1.22; 95% CI: 1.08–1.37). In the subgroup analysis of non-hypertensive patients, the risks of AF were significantly higher in the borderline AS group (aHR: 3.16, 95% CI: 1.74–5.74) and elevated AS group (aHR: 2.26, 95% CI: 1.02–5.05). For patients with elevated BMI, the risk of AF in the elevated AS group was significantly higher (aHR: 1.69, 95% CI: 1.00–2.83). Baseline baPWV was associated with new-onset AF after adjustments. (Trial registration site and registration number are, respectively, http://www.chictr.org.cn/index.aspx and ChiCTR-TNRC-11001489).

Background: It is known that the Class Ic antiarrhythmic drugs exhibit strong use-dependent blockade of fast sodium current (I Na ) due to their slow dissociation kinetics from the sodium channel. Clinically, Class Ic I Na blockers are linked to increased mortality in patients with coronary artery disease or ventricular systolic dysfunction. However, the mechanisms by which Class Ic I Na blockers influence ventricular conduction and mechanical function, thereby contributing to increased mortality, have not been well studied. We hypothesized that Class Ic I Na blockers may transition conduction of normal ventricular myocytes from an "all-or-none" pattern to Wenckebach or decremental conduction, features typically associated with slow response action potentials (APs). This change could markedly alter ventricular electrophysiology and mechanical function. Methods: APs, with ECG and contractility, were recorded concurrently from ventricular epicardium (Epi) and endocardium (Endo) in the isolated arterially perfused rabbit ventricular wedge in control and in presence of flecainide, a class Ic I Na blocker, at 10 microM. The preparations were paced from Endo at basic cycle lengths (BCL) ranging from 300 to 1000 ms. Results: Pacing from a BCL of 1000 ms down to BCLs of 300 to 600 ms resulted in decremental conduction between the ventricular Endo and Epi during pacing rate acceleration or Wenckebach conduction at a constant rapid pacing rate in the presence of flecainide. This unique conduction (Figure 1) was observed in 8 of 8 preparations under flecainide perfusion versus 0 of 8 in the control perfusion (p<0.01). Decremental and Wenckebach conduction was always associated with reduced and dyssynchronous contraction. Additionally, flecainide blunted or even reversed physiologically positive staircase response of contractility (Figure 2). Notably, 2 to 1 conduction and paroxysmal conduction block between the Endo and Epi occurred in 4 of 8 (Figure 3). On the other hand, conduction delay between the ventricular Endo and Epi also promoted echo beats and non-sustained ventricular tachycardia via a reentrant mechanism. Conclusions: Flecainide due to its strong use-dependent blockage of I Na has a capability to transition ventricular fast response APs to slow response APs, leading to Wenckebach or decremental conduction. This conduction not only reduces ventricular contraction but also induces dyssynchrony. Intraventricular conduction block also promotes reentrant arrhythmias.

Background: New onset left bundle branch block (LBBB) is the most common complication following transcatheter aortic valve replacement (TAVR), occurring in up to 35% of cases. Previous case studies have shown that in some patients with new onset LBBB, the QRS duration is positively correlated with the preceding RR interval. This unique phenomenon, known as inverse decremental conduction (IDC) or Yan conduction, prompted us to investigate its clinical features and implications. Methods: We reviewed 12-lead ECGs and available in-patient telemetry for patients with new onset LBBB within 14 days following any types of cardiac surgery from 2018 to 2023 at two medical centers. Patients with ≥3 different degrees of LBBB in response to different preceding RR on 12-lead ECGs or on telemetry were included in the analysis. Results: A total of 22 patients (19 males) with a mean age of 75±8 years were identified to exhibit varying degrees of LBBB, with QRS duration that was positively correlated to the preceding RR interval within a certain range of heart rates. Among these patients, 17 had undergone TAVR, while the remaining 5 underwent surgical aortic valve replacement (AVR) and/or mitral valve replacement. 13 of the 22 patients were in sinus rhythm with premature atrial beats or sinus arrhythmias, while the remaining 9 patients were in atrial fibrillation. Figure 1 shows the typical manifestations of IDC in the left bundle on ECG in a patient post TAVR, with a positive correlation between QRS duration and the preceding RR (r = 0.87, p < 0.01). IDC in the left bundle in patients with new-onset LBBB occurred within three days following cardiac surgeries in 20 of the 22 patients, while the remaining 2 patients exhibited IDC in the left bundle > 7 days after the surgeries. IDC in the left bundle is a temporary phenomenon, commonly lasting <24 hours in most cases, and evolving into either a normal QRS or permanent LBBB. Interestingly, alternating LBBB occurred in 5 patients with IDC in the left bundle as shown in Figure 2 . Conclusion and Comment: 1) there is a positive correlation between the preceding RR interval and QRS duration, indicating IDC in left bundle, in the patients with new onset of LBBB following cardiac surgeries particularly AVR; 2) this unique phenomenon is often short-lived; 3) theoretically, IDC in left bundle can translate into PR interval changes consistent with IDC in patients with preexisting right bundle branch block, leading to paroxysmal AV block.

Objective:This study aimed to explore the impact of a combination of hyperuricemia (HUA) and excessive high-sensitivity C-reactive protein (hs-CRP) levels on the likelihood of developing cardiac conduction block (CCB). Additionally, it sought to assess whether the influence of uric acid (UA) on CCB is mediated by hs-CRP. Methods:A prospective study was executed utilizing data from the Kailuan cohort, including 81,896 individuals initially free from CCB. The participants were categorized into four groups depending on the existence of HUA and low-grade inflammation (hs-CRP>3 mg/L). Cox regression analysis was employed to ascertain hazard ratios (HRs) and 95% confidence intervals (CIs) for the risk of incident CCB. A mediation analysis was performed to determine if hs-CRP functioned as a mediator in the connection between UA levels and the incidence of CCB. Results:During a median observation period of 11.8 years, we identified 3160 cases of newly occurring CCB. Compared with the low UA/low CRP group, the combination of HUA and low-grade inflammation elevated the CCB risks (HR:1.56, 95% CI:1.22-1.99), atrioventricular block (AVB) (HR:1.88, 95% CI:1.27-2.77), and right bundle branch block (HR:1.47, 95% CI:1.02-2.12), respectively. Mediation analysis revealed that in the HUA group, compared with the non-HUA group, the risk of CCB elevated by 14.0%, with 10.3% of the increase mediated through hs-CRP. Conclusion:HUA combined with elevated hs-CRP increased the risk of CCB, especially AVB. The connection between UA and the CCB risk was partly mediated by hs-CRP.

Background: We previously observed a positive correlation between QRS duration and the preceding RP interval in sinus rhythm in certain patients experiencing new onset left bundle branch block (LBBB) after transcatheter aortic valve replacement (TAVR). This unique phenomenon, termed inverse decremental conduction ( IDC ) or Yan conduction, prompted us to investigate whether IDC in the left bundle could manifest as AV conduction in an IDC pattern in patients with preexisting right bundle branch block (RBBB) and its association with atrioventricular block (AVB). Methods: 12 lead ECGs, available in-patient telemetry and mobile cardiac outpatient telemetry were reviewed in patients with sinus rhythm and preexisting RBBB who developed paroxysmal AVB requiring temporary or permanent pacemaker within 7 days following any types of cardiac surgery from 2014 to 2023 in Lankenau Medical Center. Results: A total of 9 patients (5 males) with a mean age of 71±15 years were identified to exhibit PR interval changes consistent with IDC prior to paroxysmal AVB. Among these patients, 6 had undergone TAVR, while the remaining 3 had undergone surgical aortic valve replacement, mitral valve repair, and ventricular septal defect repair, respectively. Specifically, PR interval alternation in the setting of RBBB occurred during sinus rhythm in a pattern that the longer RP interval is followed by a longer PR interval (Figure 1). This pattern exhibits the following features: 1) 8 of 9 patients had RBBB plus left anterior fascicular block (LAFB); 2) PR alternation occurred at sinus rates from 68 to 91 bpm within 5 days following surgical procedures; 3) proximal AVB occurred within 1 to 12 hours after PR interval alternation began. A positive correlation was established between PR and preceding RP interval in 2 of 9 patients whose telemetry data were available for analysis ( Figure 2A ). In a patient with RBBB who developed paroxysmal AVB without IDC changes in the PR interval post TAVR, intracardiac recording showed a decrease in AH interval but an increase in HV interval with slowing heart rates ( Figure 2B ), indicating that decremental conduction in AV node can mask IDC in Purkinje system. Conclusion: 1) PR alternation with longer PR following longer preceding RP interval in presence of RBBB, likely due to IDC in left bundle, heralds paroxysmal AVB; 2) PR interval changes resulting from IDC in left bundle in the setting of RBBB may be masked by decremental conduction in AV node.

During drug discovery, small molecules are typically assayed in vitro for secondary pharmacology effects, which include ion channels relevant to cardiac electrophysiology. Compound A was an irreversible inhibitor of myeloperoxidase investigated for the treatment of peripheral artery disease. Oral doses in dogs at ≥5 mg/kg resulted in cardiac arrhythmias in a dose-dependent manner (at Cmax, free ≥1.53 μM) that progressed in severity with time. Nevertheless, a panel of 13 different cardiac ion channel (K, Na, and Ca) assays, including hERG, failed to identify pharmacologic risks of the molecule. Compound A and a related Compound B were evaluated for electrophysiological effects in the isolated rabbit ventricular wedge assay. Compounds A and B prolonged QT and Tp-e intervals at ≥1 and ≥.3 μM, respectively, and both prolonged QRS at ≥5 μM. Compound A produced early after depolarizations and premature ventricular complexes at ≥5 μM. These data indicate both compounds may be modulating hERG (I kr ) and Nav1.5 ion channels. In human IPSC cardiomyocytes, Compounds A and B prolonged field potential duration at ≥3 μM and induced cellular dysrhythmia at ≥10 and ≥3 μM, respectively. In a rat toxicology study, heart tissue: plasma concentration ratios for Compound A were ≥19X at 24 hours post-dose, indicating significant tissue distribution. In conclusion, in vitro ion channel assays may not always identify cardiovascular electrophysiological risks observed in vivo, which can be affected by tissue drug distribution. Risk for arrhythmia may increase with a “trappable” ion channel inhibitor, particularly if cardiac tissue drug levels achieve a critical threshold for pharmacologic effects.

Journal Article Accepted manuscript Association between cumulative uric acid exposure and the risk of incident cardiac conduction block Get access Na Li, MD, Na Li, MD Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, ChinaDepartment of Rheumatology and Immunology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Liufu Cui, MD, Liufu Cui, MD Department of Rheumatology and Immunology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Panagiotis Korantzopoulos, MD, PhD, Panagiotis Korantzopoulos, MD, PhD First Department of Cardiology, University of Ioannina Medical School, Ioannina, Greece Search for other works by this author on: Oxford Academic PubMed Google Scholar Nan Zhang, BS, Nan Zhang, BS Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Rong Shu, MD, Rong Shu, MD Department of Rheumatology and Immunology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Haicheng Song, MD, Haicheng Song, MD Department of Rheumatology and Immunology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Jierui Wang, MD, Jierui Wang, MD Department of Rheumatology and Immunology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Shuohua Chen, MD, Shuohua Chen, MD Department of Cardiology, Kailuan General Hospital, Tangshan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Gregory Y H Lip, MD, FESC, Gregory Y H Lip, MD, FESC Liverpool Centre for Cardiovascular Sciences at University of Liverpool, Liverpool John Moores University and Liverpool Heart & Chest Hospital, Liverpool, United KingdomDanish Center for Clinical Health Services Research, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark Search for other works by this author on: Oxford Academic PubMed Google Scholar Gary Tse, MD, PhD, Gary Tse, MD, PhD Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, ChinaSchool of Nursing and Health Studies, Hong Kong Metropolitan University, Hong Kong, China Search for other works by this author on: Oxford Academic PubMed Google Scholar ... Show more Konstantinos P Letsas, MD, PhD, Konstantinos P Letsas, MD, PhD Arrhythmia Unit, Laboratory of Cardiac Pacing and Electrophysiology, Onassis Cardiac Surgery Center, Athens, Greece Search for other works by this author on: Oxford Academic PubMed Google Scholar George Bazoukis, MD, PhD, George Bazoukis, MD, PhD Department of Cardiology, Larnaca General Hospital, Larnaca, CyprusEuropean University Cyprus, Medical School, Nicosia, Cyprus https://orcid.org/0000-0003-1009-9772 Search for other works by this author on: Oxford Academic PubMed Google Scholar Gan-Xin Yan, MD, PhD, Gan-Xin Yan, MD, PhD Lankenau Medical Center and Lankenau Institute for Medical Research, Wynnewood, Pennsylvania, USAFuwai Huazhong Hospital, Zhengzhou, Henan, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Xuemei Yang, BS, Xuemei Yang, BS School of Clinical Medicine, North China University of Science and Technology, Tangshan, Hebei, China Search for other works by this author on: Oxford Academic PubMed Google Scholar Shouling Wu, MD, Shouling Wu, MD Department of Cardiology, Kailuan General Hospital, Tangshan, China Corresponding authors: Prof. Tong Liu, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, No. 23, Pingjiang Road, Hexi District, Tianjin 300211, People's Republic of China. E-mail: liutong@tmu.edu.cn or liutongdoc@126.com; Prof. Shouling Wu, Department of Cardiology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China. E-mail: drwusl@163.com Search for other works by this author on: Oxford Academic PubMed Google Scholar Tong Liu, MD, PhD, FESC Tong Liu, MD, PhD, FESC Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin 300211, China Corresponding authors: Prof. Tong Liu, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, No. 23, Pingjiang Road, Hexi District, Tianjin 300211, People's Republic of China. E-mail: liutong@tmu.edu.cn or liutongdoc@126.com; Prof. Shouling Wu, Department of Cardiology, Kailuan General Hospital, North China University of Science and Technology, Tangshan, China. E-mail: drwusl@163.com https://orcid.org/0000-0003-0482-0738 Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, cvae115, https://doi.org/10.1093/cvr/cvae115 Published: 04 June 2024 Article history Received: 22 November 2023 Revision received: 25 December 2023 Accepted: 05 January 2024 Published: 04 June 2024

Mexiletine, a class Ib antiarrhythmic drug, exhibits its major antiarrhythmic effect via inhibition of the fast and late Na + currents in myocardial tissues that are dependent on the opening of Na + channels for their excitation. Through a comprehensive examination of mexiletine's therapeutic benefits and potential risks, we aim to provide valuable insights that reinforce its role as a vital therapeutic option for patients with ventricular arrhythmias, long QT syndrome, and other heart rhythm disorders. This review will highlight the current understandings of the antiarrhythmic effects and rationales for recent off‐label use and address the mortality and proarrhythmic effects of mexiletine utilizing published basic and clinical studies over the past five decades.

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 16, No. 1Characteristics of Patients with Spontaneous Versus Drug-Induced Brugada Electrocardiogram: Sub-Analysis From the SABRUS Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBCharacteristics of Patients with Spontaneous Versus Drug-Induced Brugada Electrocardiogram: Sub-Analysis From the SABRUS Anat Milman, Avi Sabbag, Giulio Conte, Pieter G. Postema, Antoine Andorin, Jean-Baptiste Gourraud, Frederic Sacher, Philippe Mabo, Sung-Hwan Kim, Shingo Maeda, Yoshihide Takahashi, Tsukasa Kamakura, Takeshi Aiba, Jimmy JM Juang, Yoav Michowitz, Eran Leshem, Yuka Mizusawa, Elena Arbelo, Zhengrong Huang, Isabelle Denjoy, Carla Giustetto, Yanushi D. Wijeyeratne, Andrea Mazzanti, Ramon Brugada, Ruben Casado-Arroyo, Jean Champagne, Leonardo Calo, Georgia Sarquella-Brugada, Jacob Tfelt-Hansen, Silvia G. Priori, Masahiko Takagi, Christian Veltmann, Pietro Delise, Domenico Corrado, Elijah R. Behr, Fiorenzo Gaita, Gan-Xin Yan, Josep Brugada, Antoine Leenhardt, Arthur A.M. Wilde, Pedro Brugada, Kengo F. Kusano, Kenzo Hirao, Gi-Byoung Nam, Vincent Probst and Bernard Belhassen Anat MilmanAnat Milman Correspondence to: Anat Milman, MD PhD, Davidai Arrhythmia Center, Leviev Heart Center Sheba Medical Center, Tel Hashomer 5265601, Israel. Email E-mail Address: [email protected] https://orcid.org/0000-0002-8551-4101 Leviev Heart Institute, The Chaim Sheba Medical Centre, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel (A.M., A.S., E.L.). Search for more papers by this author , Avi SabbagAvi Sabbag https://orcid.org/0000-0003-4295-6679 Leviev Heart Institute, The Chaim Sheba Medical Centre, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel (A.M., A.S., E.L.). Search for more papers by this author , Giulio ConteGiulio Conte https://orcid.org/0000-0003-2248-3456 Heart Rhythm Management Centre, UZ-VUB, Brussels, Belgium (G.C., P.B.). Search for more papers by this author , Pieter G. PostemaPieter G. Postema https://orcid.org/0000-0003-2863-9159 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Amsterdam UMC, University of Amsterdam, Heart Centre and Department of Clinical and Experimental Cardiology, Amsterdam, the Netherlands (P.G.P., Y.M., A.A.M.W.). Search for more papers by this author , Antoine AndorinAntoine Andorin https://orcid.org/0000-0001-6848-5452 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Service de Cardiologie, CHU de Nantes (A.A., J.B.G., V.P.). Search for more papers by this author , Jean-Baptiste GourraudJean-Baptiste Gourraud https://orcid.org/0000-0002-6961-2131 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Service de Cardiologie, CHU de Nantes (A.A., J.B.G., V.P.). Search for more papers by this author , Frederic SacherFrederic Sacher https://orcid.org/0000-0001-8348-9320 Hôpital Cardiologique du Haut-Lévêque and University Bordeaux, LIRYC Instituteitute (F.S.). Search for more papers by this author , Philippe MaboPhilippe Mabo Cardiology and Vascular Disease Division, Rennes University Health Centre, Rennes, France (P.M.). Search for more papers by this author , Sung-Hwan KimSung-Hwan Kim https://orcid.org/0000-0001-6805-0416 Division of Cardiology, College of Medicine, The Catholic University of Korea, Seoul, Korea (S.-H.K.). Search for more papers by this author , Shingo MaedaShingo Maeda https://orcid.org/0000-0001-6964-0653 Heart Rhythm Centre, Tokyo Medical and Dental University, Tokyo (S.M., Y.T., K.H.). Search for more papers by this author , Yoshihide TakahashiYoshihide Takahashi https://orcid.org/0000-0003-0335-996X Heart Rhythm Centre, Tokyo Medical and Dental University, Tokyo (S.M., Y.T., K.H.). Search for more papers by this author , Tsukasa KamakuraTsukasa Kamakura https://orcid.org/0000-0003-2964-2544 Division of Arrhythmia & EleCentreophysiology, National Cerebral & Cardiovascular Centre, Osaka, Japan (T.K., T.A.). Search for more papers by this author , Takeshi AibaTakeshi Aiba https://orcid.org/0000-0003-1779-7282 Division of Arrhythmia & EleCentreophysiology, National Cerebral & Cardiovascular Centre, Osaka, Japan (T.K., T.A.). Search for more papers by this author , Jimmy JM JuangJimmy JM Juang https://orcid.org/0000-0003-4767-7636 Cardiovascular Centre and Division of Cardiology, National Taiwan University Hospital and University College of Medicine, Taipei, Taiwan (J.J.M.J.). Search for more papers by this author , Yoav MichowitzYoav Michowitz https://orcid.org/0000-0002-5665-3735 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Cardiology Department, Shaare Zedek Hospital, Affiliated to the Faculty of Medicine, Hebrew University, Jerusalem, Israel (Y.M.). Search for more papers by this author , Eran LeshemEran Leshem https://orcid.org/0000-0002-8896-460X Leviev Heart Institute, The Chaim Sheba Medical Centre, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel (A.M., A.S., E.L.). Search for more papers by this author , Yuka MizusawaYuka Mizusawa https://orcid.org/0000-0003-1858-0923 Amsterdam UMC, University of Amsterdam, Heart Centre and Department of Clinical and Experimental Cardiology, Amsterdam, the Netherlands (P.G.P., Y.M., A.A.M.W.). Search for more papers by this author , Elena ArbeloElena Arbelo https://orcid.org/0000-0003-0424-6393 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Arrhythmia Section, Cardiology Department, Hospital Clínic, Universityersitat de Barcelona and bIDIBAPS, Instituteitut d’Investigació August Pi i Sunyer (IDIBAPS), Barcelona (E.A.). Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain (E.A.). Search for more papers by this author , Zhengrong HuangZhengrong Huang https://orcid.org/0000-0003-0007-9321 Department of Cardiology, the First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China (Z.H.). Search for more papers by this author , Isabelle DenjoyIsabelle Denjoy https://orcid.org/0000-0002-1786-9461 Service de Cardiologie et CNMR Maladies Cardiaques Héréditaires Rares, Hôpital Bichat, Paris and Université Paris Diderot, Sorbonne, France (I.D.). Search for more papers by this author , Carla GiustettoCarla Giustetto https://orcid.org/0000-0002-5102-3398 Division of Cardiology, Department of Medical Sciences, Città della Salute e della Scienza Hospital, University of Torino, Italy (C.G., F.G.). Search for more papers by this author , Yanushi D. WijeyeratneYanushi D. Wijeyeratne https://orcid.org/0000-0003-0656-5769 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Cardiovascular Sciences, St. George’s University of London and Cardiology Clinical Academic Group St. George’s University Hospitals NHS Foundation Trust, London, UK (Y.D.W., E.R.B.). Search for more papers by this author , Andrea MazzantiAndrea Mazzanti https://orcid.org/0000-0002-0208-2172 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Molecular Cardiology, Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy (A.M.). Search for more papers by this author , Ramon BrugadaRamon Brugada https://orcid.org/0000-0001-6607-3032 Cardiovascular Genetics Center, University of Girona-IDIBGI and Medical Science Department, School of Medicine, University of Girona, Spain (R.B.). Search for more papers by this author , Ruben Casado-ArroyoRuben Casado-Arroyo Department of Cardiology, Erasme University Hospital, Universityersité Libre de Bruxelles, Belgium (R.C.-A.). Search for more papers by this author , Jean ChampagneJean Champagne https://orcid.org/0000-0001-9861-9351 Quebec Heart & Lung Institute, Quebec City, Canada (J.C.). Search for more papers by this author , Leonardo CaloLeonardo Calo https://orcid.org/0000-0002-6062-5286 Division of Cardiology, Policlinico Casilino, Roma, Italy (L.C.). Search for more papers by this author , Georgia Sarquella-BrugadaGeorgia Sarquella-Brugada https://orcid.org/0000-0002-6857-8904 Pediatric Arrhythmias, EleCentreophysiology and Sudden Death Unit Cardiology, Department Hospital Sant Joan de Déu, Barcelona - Universityersitat de Barcelona, Spain (G.S.-B.). Search for more papers by this author , Jacob Tfelt-HansenJacob Tfelt-Hansen European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). The Heart Centre, Copenhagen University Hospital and Department of Forensic Medicine, Faculty of Medical Sciences, University of Copenhagen, Denmark (J.T.-H.). Search for more papers by this author , Silvia G. PrioriSilvia G. Priori https://orcid.org/0000-0001-6877-0288 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Search for more papers by this author , Masahiko TakagiMasahiko Takagi https://orcid.org/0000-0001-7712-8529 Division of Cardiac Arrhythmia, Kansai Medical University Medical Centre, Moriguchi, Japan (M.T.). Search for more papers by this author , Christian VeltmannChristian Veltmann https://orcid.org/0000-0001-7587-1124 Hannover Heart Rhythm Centre, Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany (C.V.). Search for more papers by this author , Pietro DelisePietro Delise https://orcid.org/0000-0001-7190-4830 Division of Cardiology, Hospital of Peschiera del Garda, Veneto (P.D.). Search for more papers by this author , Domenico CorradoDomenico Corrado https://orcid.org/0000-0003-1487-0392 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Department of Cardiac, Thoracic & Vascular Sciences University of Padova, Italy (D.C.). Search for more papers by this author , Elijah R. BehrElijah R. Behr https://orcid.org/0000-0002-8731-2853 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Cardiovascular Sciences, St. George’s University of London and Cardiology Clinical Academic Group St. George’s University Hospitals NHS Foundation Trust, London, UK (Y.D.W., E.R.B.). Search for more papers by this author , Fiorenzo GaitaFiorenzo Gaita European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Division of Cardiology, Department of Medical Sciences, Città della Salute e della Scienza Hospital, University of Torino, Italy (C.G., F.G.). Search for more papers by this author , Gan-Xin YanGan-Xin Yan https://orcid.org/0000-0002-3118-5680 Lankenau Medical Centre, Wynnewood, PA (G.X.Y.). Search for more papers by this author , Josep BrugadaJosep Brugada https://orcid.org/0000-0002-5662-8302 Search for more papers by this author , Antoine LeenhardtAntoine Leenhardt https://orcid.org/0000-0001-7368-4528 Search for more papers by this author , Arthur A.M. WildeArthur A.M. Wilde https://orcid.org/0000-0002-0528-0852 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Amsterdam UMC, University of Amsterdam, Heart Centre and Department of Clinical and Experimental Cardiology, Amsterdam, the Netherlands (P.G.P., Y.M., A.A.M.W.). Search for more papers by this author , Pedro BrugadaPedro Brugada https://orcid.org/0000-0003-3172-6106 Heart Rhythm Management Centre, UZ-VUB, Brussels, Belgium (G.C., P.B.). Search for more papers by this author , Kengo F. KusanoKengo F. Kusano Search for more papers by this author , Kenzo HiraoKenzo Hirao Heart Rhythm Centre, Tokyo Medical and Dental University, Tokyo (S.M., Y.T., K.H.). Search for more papers by this author , Gi-Byoung NamGi-Byoung Nam https://orcid.org/0000-0003-4391-5406 Division of Cardiology, Asan Medical Centre, University of Ulsan College of Medicine, Seoul, Korea (Gi-Byoung Nam). Search for more papers by this author , Vincent ProbstVincent Probst https://orcid.org/0000-0002-5492-8619 European Reference Network for Rare & Low Prevalence Complex Diseases of the Heart (P.G.P., A.A., J.B.G., Y.M., E.A., Y.D.W., A.M., J.T.-H., S.G.P., D.C., E.R.B., F.G., A.A.M.W., V.P.). Service de Cardiologie, CHU de Nantes (A.A., J.B.G., V.P.). Search for more papers by this author and Bernard BelhassenBernard Belhassen https://orcid.org/0000-0002-7468-2054 Heart Institute, Hadassah University Hospital, Jerusalem, Israel (B.B.) Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel (B.B.). Search for more papers by this author Originally published3 Jan 2023https://doi.org/10.1161/CIRCEP.122.011360Circulation: Arrhythmia and Electrophysiology. 2023;16Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 3, 2023: Ahead of Print Patients with Brugada syndrome (BrS) may display either a spontaneous (S) or a drug-induced (DI) ECG pattern. The latter group is considered at a lower risk of arrhythmic events (AE) and sudden cardiac death (SCD). The only study that compared these 2 groups in BrS associated with AEs comprised a small cohort of 44 patients.1The SABRUS study (Survey on Arrhythmic events in Brugada Syndrome) gathers the largest cohort of patients with BrS and AEs published to date.2 The data that support the findings of this study are available from the corresponding author upon reasonable request. Patients were divided into 2 groups according to their AE presentation: group A presented with aborted cardiac arrest before diagnosis of BrS and group B were Brugada patients implanted prophylactically with an ICD, which proved to be justified during follow-up. The present study compares DI-BrS and S-BrS patients from SABRUS. The study was approved by the Institutional Committee on Human Research at the Tel Aviv Sourasky Medical Center. Continuous variables are presented as mean±SD or median (interquartile range) and compared using the student t test or Mann-Whitney U test as appropriate. Categorical variables are presented by absolute numbers and proportions and compared using the χ2 test or Fisher exact test. All tests were 2-tailed, and a P<0.05 was considered statistically significant.Of the 678 SABRUS patients, 451 (66.5%) had S-BrS ECG and 227 (33.5%) had DI-BrS ECG (Table 1). Females predominated in the DI-ECG group (15.4% versus 5.3% in the S-ECG group, P<0.001), with less Asians than Whites (33.9% versus 42.8% in the S-ECG group, P=0.036). Higher inducibility rates of ventricular fibrillation (VF) at electrophysiologic study (EPS) were found in the S-ECG group (67.3% versus 55%.7 in the DI-ECG groups, respectively, P=0.022), with a similar rate of EPS performed in both groups (61.7% in the DI-ECG group versus 57.6% in the S-ECG group, P=0.315). There were no differences between DI-BrS ECG and S-BrS ECG patients regarding age at AE, proband status, history of syncope, AE presentation, family history of sudden cardiac death, fever-related events, and genetic analysis.Table 1. Patient Characteristics According to Brugada ECG TypeDrug-Induced BrECGSpontaneous BrECGPn=227 (33.5%)n=451 (66.5%)Age at AE, y (mean±SD)42±1442±150.969 Age at AE ≤169 (4)23 (5.1)0.532 Age at AE >16218 (96)428 (94.9)Gender Men192 (84.6)427 (94.7)<0.001 Women35 (15.4)24 (5.3)Ethnicity White130 (57.3)234 (51.9)0.036 Asian77 (33.9)193 (42.8) Other/unknown20 (8.8)24 (5.3)Arrhythmic event documentation Group A150 (66.1)276 (61.2)0.214 Group B77 (33.9)175 (38.8)Proband status181 (85.4)361 (86.4)0.736History of syncope82 (36.1)183 (40.6)0.262Fever during AE11 (5.9)24 (6)0.961Family history of SCD Yes46 (20.3)99 (22)0.851 No158 (69.6)310 (68.7) Unknown23 (10.1)42 (9.3)EPS performed140 (61.7)260 (57.6)0.315VF inducibility during EPS78 (55.7)175 (67.3)0.022Genetic analysis performed158 (69.6)327 (72.5)0.429SCN5A mutation present41 (25.9)102 (31.2)0.235AE indicates arrhythmic event; BrECG, Brugada electrocardiogram; EPS, electrophysiologic study; SCD, sudden cardiac death; and VF, ventricular fibrillation.To the best of our knowledge, this is the first study comparing BrS patients with S-ECG and DI-ECG in a large population cohort with AEs. Although a previous article by Tadros et al3 showed that 8% of patients tested by drug provocation for BrS could have false positive results, we assume, based on our findings of the SABRUS cohort,4 that all our patients with DI-ECG have proven BrS, and that the results of our study should be taken in this context only.Syncope combined with a spontaneous type 1 Brugada ECG has been shown to be useful for identifying Brugada patients at risk for AE. However, this is not relevant when a DI-ECG is encountered. In addition, the use of programmed ventricular stimulation has shown conflicting results. In a large series of patients with DI-BrS ECG, Sieira et al5 showed that VF inducibility rate was significantly lower than in patients with S-BrS ECG (13.2% versus 42.4%, respectively, P<0.01); however their cohort comprised a minority of patients with AEs. In our cohort comprising only patients with AEs, the lower inducibility rate is confirmed (55.7% versus 67.3%, respectively, P=0.022). These findings suggest that EPS is less useful for the management of BrS patients with DI-ECG, and do not inform necessarily on risk stratification strategies. These findings could actually represent a difference in the mechanism of arrhythmia generation of the 2 subgroups of Brugada patients, and future studies should test whether this could explain the lower arrhythmic risk of DI-ECG patients.Females predominated in our DI-ECG group. This is in line with the study by Nagayama et al1 in a smaller cohort.For the first time, SABRUS showed that Asians with AEs displayed significantly less DI-ECG compared with whites. This may suggest that a genetic predisposition of Asians plays a role in the occurrence of the S-BrS ECG type.No difference in the presence of SCN5A gene mutation was found between the DI-ECG and S-ECG groups. These findings agree with those reported by Nagayama et al1 in a similar, although significantly smaller patient cohort.In conclusion, DI-BrS patients represented a third of BrS cohort with AEs. They differed from S-BrS patients in gender, ethnicity, and VF inducibility rates. The most important observation is that this group of patients is less studied, and identifying high-risk DI-BrS patients is not an easy task. We encourage seeking new risk markers in this group in future studies.Article InformationSources of FundingNone.Nonstandard Abbreviations and AcronymsAEarrhythmic eventsBrSBrugada syndromeDIdrug-inducedICDimplantable cardiac defibrillatorSspontaneousSABRUSSurvey on Arrhythmic events in Brugada SyndromeVFventricular fibrillationDisclosures None.FootnotesFor Sources of Funding and Disclosures, see page 64.Correspondence to: Anat Milman, MD PhD, Davidai Arrhythmia Center, Leviev Heart Center Sheba Medical Center, Tel Hashomer 5265601, Israel. Email anatmilman@gmail.comReferences1. Nagayama T, Nagase S, Kamakura T, Wada M, Ishibashi K, Inoue YY, Miyamoto K, Noda T, Aiba T, Takaki HT, et al. Clinical and electrocardiographic differences in Brugada syndrome with spontaneous or drug-induced type 1 electrocardiogram.Circ J. 2019; 83:532–539. doi: 10.1253/circj.cj-18-0643CrossrefMedlineGoogle Scholar2. Milman A, Gourraud JB, Andorin A, Postema PG, Sacher F, Mabo P, Conte G, Giustetto C, Sarquella-Brugada G, Hochstadt A, et al. Gender differences in patients with Brugada syndrome and arrhythmic events: data from a survey on arrhythmic events in 678 patients.Heart Rhythm. 2018; 15:1457–1465. doi: 10.1016/j.hrthm.2018.06.019CrossrefMedlineGoogle Scholar3. Tadros R, Nannenberg EA, Lieve KV, Škorić-Milosavljević D, Lahrouchi N, Lekanne Deprez RH, Vendrik J, Reckman YJ, Postema PG, Amin AS, et al. Yield and pitfalls of ajmaline testing in the evaluation of unexplained cardiac arrest and sudden unexplained death.J Am Coll Cardiol EP. 2017; 3:1400–1408. doi: 10.1016/j.jacep.2017.04.005CrossrefGoogle Scholar4. Milman A, Andorin A, Gourraud JB, Sacher F, Mabo P, Kim SH, Maeda S, Takahashi Y, Kamakura T, Aiba T, et al. Age of first arrhythmic event in Brugada syndrome: data from the SABRUS (Survey on Arrhythmic Events in Brugada Syndrome) in 678 patients.Circ Arrhythm Electrophysiol. 2017; 10:e005222. doi: 10.1161/CIRCEP.117.005222LinkGoogle Scholar5. Sieira J, Ciconte G, Conte G, de Asmundis C, Chierchia GB, Baltogiannis G, Di Giovanni G, Saitoh Y, Casado-Arroyo R, Juliá J, et al. Long-term prognosis of drug-induced Brugada syndrome.Heart Rhythm. 2017; 14:1427–1433. doi: 10.1016/j.hrthm.2017.04.044CrossrefMedlineGoogle Scholar eLetters(0) eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. 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