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Frederic Sacher - One of the best experts on this subject based on the ideXlab platform.
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The Spectrum of Idiopathic Ventricular Fibrillation and J-Wave Syndromes: Novel Mapping Insights
2019Co-Authors: Michel Haissaguerre, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Me Le Ze Hocini, Wee Nademanee, Clémentine André, Thomas Lavergne, Masa Takigawa, Thomas PambrunAbstract:KEY POINTS Idiopathic ventricular fibrillation (IVF) is defined as unexplained sudden cardiac death due to ven-tricular fibrillation (VF) without any identifiable structural or electrical cause after extensive investigations (no phenotype). Recent data show that the use of high-density electrophysiologic mapping may ultimately offer sub-clinical diagnoses of cardiac disease in about 90% of individuals with IVF. Two maJor conditions underlie the occurrence of VF: the presence of either depolarization abnormalities due to micro-structural myocardial alteration or PurkinJe abnormalities manifesting as triggering ectopy or reentry in the peripheral network. J-Wave syndromes are defined as a distinct electrocardiographic phenotype (slurring/notch) affecting the Junction between the QRS complex and the ST segment in inferolateral leads. Recent data provide evidence for heterogeneous substrates, related to either delayed depolarization due to microstructural alterations or early repolarization abnormalities. IVF and J-Wave syndromes are the result of a wide spectrum of pathophysiologic processes. The individual phenotypic characterization is essential given its implications in therapy, genetic testing, and risk stratification.
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depolarization versus repolarization abnormality underlying inferolateral J Wave syndromes new concepts in sudden cardiac death with apparently normal hearts
Heart Rhythm, 2019Co-Authors: Michel Haissaguerre, Koonlawee Nademanee, Ghassen Cheniti, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Arnaud Denis, Me Le Ze Hocini, Antonio Frontera, Thomas PambrunAbstract:Early repolarization indicates a distinct electrocardiographic phenotype affecting the Junction between the QRS complex and the ST segment in inferolateral leads (inferolateral J-Wave syndromes). It has been considered a benign electrocardiographic variant for decades, but recent clinical studies have demonstrated its arrhythmogenicity in a small subset, supported by experimental studies showing transmural dispersion of repolarization. Here we review the current knowledge and the issues of risk stratification that limit clinical management. In addition, we report on new mapping data of patients refractory to pharmacologic treatment using high-density electrogram mapping at the time of inscription of J Wave. These data demonstrate that distinct substrates, delayed depolarization, and abnormal early repolarization underlie inferolateral J-Wave syndromes, with significant implications. Finally, based on these data, we propose a new simplified mechanistic classification of sudden cardiac deaths without apparent structural heart disease.
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Depolarization versus repolarization abnormality underlying inferolateral J Wave syndromes – new concepts in sudden cardiac death with apparently normal hearts
Heart Rhythm, 2019Co-Authors: Michel Haissaguerre, Koonlawee Nademanee, Ghassen Cheniti, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Arnaud Denis, Me Le Ze Hocini, Antonio Frontera, Thomas PambrunAbstract:Early repolarization indicates a distinct electrocardiographic phenotype affecting the Junction between the QRS complex and the ST segment in inferolateral leads (inferolateral J-Wave Syndromes). It has been considered a benign electrocardiographic variant for decades, but recent clinical studies have demonstrated its arrhythmogenicity in a small subset, supported by experimental studies showing transmural dispersion of repolarization. Here, we review the current knowledge and the issues of risk stratification which limit clinical management. In addition we report on new mapping data of patients refractory to pharmacological treatment using high-density electrogram mapping at the time of inscription of J-Wave. These data demonstrate that distinct substrates, delayed depolarization and abnormal early repolarization, underlie inferolateral J-Wave syndromes, with significant implications. Finally, based on these data, we propose a new simplified mechanistic classification of sudden cardiac deaths without apparent structural heart disease.
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J Wave syndromes expert consensus conference report emerging concepts and gaps in knowledge
Heart Rhythm, 2016Co-Authors: Charles Antzelevitch, Hiroshi Morita, Ihor Gussak, Can Hasdemir, Minoru Horie, Michael John Ackerman, Martin Borggrefe, Domenico Corrado, Heikki Huikuri, Frederic SacherAbstract:J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge Charles Antzelevitch, PhD, FHRS, Gan-Xin Yan, MD, PhD, Michael J. Ackerman, MD, PhD, Martin Borggrefe, MD, Domenico Corrado, MD, PhD, Jihong Guo, MD, Ihor Gussak, MD, PhD, Can Hasdemir, MD, Minoru Horie, MD, Heikki Huikuri, MD, Changsheng Ma, MD, Hiroshi Morita, MD, PhD, Gi-Byoung Nam, MD, PhD, Frederic Sacher, MD, PhD, Wataru Shimizu, MD, PhD, Sami Viskin, MD, Arthur A.M. Wilde, MD, PhD, FHRS
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J Wave syndromes expert consensus conference report emerging concepts and gaps in knowledge
Europace, 2016Co-Authors: Charles Antzelevitch, Hiroshi Morita, Ihor Gussak, Can Hasdemir, Minoru Horie, Michael John Ackerman, Martin Borggrefe, Domenico Corrado, Heikki Huikuri, Frederic SacherAbstract:The J-Wave syndromes (JWSs), consisting of the Brugada syndrome (BrS) and early repolarization syndrome (ERS), have captured the interest of the cardiology community over the past 2 decades following the identification of BrS as a new clinical entity by Pedro and Josep Brugada in 1992.[1][1] The
Charles Antzelevitch - One of the best experts on this subject based on the ideXlab platform.
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J Wave syndromes as a cause of malignant cardiac arrhythmias.
Pacing and clinical electrophysiology : PACE, 2018Co-Authors: José M. Di Diego, Charles AntzelevitchAbstract:The J Wave syndromes, including the Brugada (BrS) and early repolarization (ERS) syndromes, are characterized by the manifestation of prominent J Waves in the electrocardiogram appearing as an ST segment elevation and the development of life-threatening cardiac arrhythmias. BrS and ERS differ with respect to the magnitude and lead location of abnormal J Waves and are thought to represent a continuous spectrum of phenotypic expression termed J Wave syndromes. Despite over 25 years of intensive research, risk stratification and the approach to therapy of these two inherited cardiac arrhythmia syndromes are still rapidly evolving. Our obJective in this review is to provide an integrated synopsis of the clinical characteristics, risk stratifiers, as well as the molecular, ionic, cellular, and genetic mechanisms underlying these two syndromes that have captured the interest and attention of the cardiology community over the past two decades.
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J Wave syndromes expert consensus conference report emerging concepts and gaps in knowledge
Heart Rhythm, 2016Co-Authors: Charles Antzelevitch, Hiroshi Morita, Ihor Gussak, Can Hasdemir, Minoru Horie, Michael John Ackerman, Martin Borggrefe, Domenico Corrado, Heikki Huikuri, Frederic SacherAbstract:J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge Charles Antzelevitch, PhD, FHRS, Gan-Xin Yan, MD, PhD, Michael J. Ackerman, MD, PhD, Martin Borggrefe, MD, Domenico Corrado, MD, PhD, Jihong Guo, MD, Ihor Gussak, MD, PhD, Can Hasdemir, MD, Minoru Horie, MD, Heikki Huikuri, MD, Changsheng Ma, MD, Hiroshi Morita, MD, PhD, Gi-Byoung Nam, MD, PhD, Frederic Sacher, MD, PhD, Wataru Shimizu, MD, PhD, Sami Viskin, MD, Arthur A.M. Wilde, MD, PhD, FHRS
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J Wave syndromes expert consensus conference report emerging concepts and gaps in knowledge
Europace, 2016Co-Authors: Charles Antzelevitch, Hiroshi Morita, Ihor Gussak, Can Hasdemir, Minoru Horie, Michael John Ackerman, Martin Borggrefe, Domenico Corrado, Heikki Huikuri, Frederic SacherAbstract:The J-Wave syndromes (JWSs), consisting of the Brugada syndrome (BrS) and early repolarization syndrome (ERS), have captured the interest of the cardiology community over the past 2 decades following the identification of BrS as a new clinical entity by Pedro and Josep Brugada in 1992.[1][1] The
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Ionic and Cellular Mechanisms Underlying J Wave Syndromes
J Wave Syndromes, 2016Co-Authors: Charles Antzelevitch, Bence PatocskaiAbstract:Prominent J Waves are encountered in a number of life-threatening cardiac arrhythmia syndromes, including the Brugada (BrS) and early repolarization (ERS) syndromes. BrS and ERS differ with respect to the magnitude and lead location of abnormal J Waves and are thought to represent a continuous spectrum of phenotypic expression termed J Wave syndromes. Both are associated with the development of polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death (SCD) in young adults. J Wave syndromes are characterized by J-onset and ST-elevation in distinct ECG-leads. The region most affected by BrS is the anterior right ventricular outflow tract, accounting for why J-onset and ST-segment elevation are limited to the right precordial leads. The region most affected in ERS is the inferior wall of the left ventricle, accounting for why the appearance of J Waves or early repolarization in the inferior ECG leads is associated with the highest risk for development of arrhythmias and SCD. Risk stratification and the approach to therapy of the J Wave syndromes continue to be mired in controversy. Our obJective in this chapter is to provide an integrated review of the clinical characteristics, risk stratifiers, as well as the molecular, ionic, cellular and genetic mechanisms underlying the J Wave syndromes.
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J Wave Syndromes: Brugada and Early Repolarization Syndromes
Heart rhythm, 2015Co-Authors: Charles Antzelevitch, Gan-xin YanAbstract:A prominent J Wave is encountered in a number of life-threatening cardiac arrhythmia syndromes, including the Brugada syndrome and early repolarization syndromes. Brugada syndrome and early repolarization syndromes differ with respect to the magnitude and lead location of abnormal J Waves and are thought to represent a continuous spectrum of phenotypic expression termed J-Wave syndromes. Despite two decades of intensive research, risk stratification and the approach to therapy of these 2 inherited cardiac arrhythmia syndromes are still undergoing rapid evolution. Our obJective in this review is to provide an integrated synopsis of the clinical characteristics, risk stratifiers, and molecular, ionic, cellular, and genetic mechanisms underlying these 2 fascinating syndromes that have captured the interest and attention of the cardiology community in recent years.
Michel Haissaguerre - One of the best experts on this subject based on the ideXlab platform.
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The Spectrum of Idiopathic Ventricular Fibrillation and J-Wave Syndromes: Novel Mapping Insights
2019Co-Authors: Michel Haissaguerre, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Me Le Ze Hocini, Wee Nademanee, Clémentine André, Thomas Lavergne, Masa Takigawa, Thomas PambrunAbstract:KEY POINTS Idiopathic ventricular fibrillation (IVF) is defined as unexplained sudden cardiac death due to ven-tricular fibrillation (VF) without any identifiable structural or electrical cause after extensive investigations (no phenotype). Recent data show that the use of high-density electrophysiologic mapping may ultimately offer sub-clinical diagnoses of cardiac disease in about 90% of individuals with IVF. Two maJor conditions underlie the occurrence of VF: the presence of either depolarization abnormalities due to micro-structural myocardial alteration or PurkinJe abnormalities manifesting as triggering ectopy or reentry in the peripheral network. J-Wave syndromes are defined as a distinct electrocardiographic phenotype (slurring/notch) affecting the Junction between the QRS complex and the ST segment in inferolateral leads. Recent data provide evidence for heterogeneous substrates, related to either delayed depolarization due to microstructural alterations or early repolarization abnormalities. IVF and J-Wave syndromes are the result of a wide spectrum of pathophysiologic processes. The individual phenotypic characterization is essential given its implications in therapy, genetic testing, and risk stratification.
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depolarization versus repolarization abnormality underlying inferolateral J Wave syndromes new concepts in sudden cardiac death with apparently normal hearts
Heart Rhythm, 2019Co-Authors: Michel Haissaguerre, Koonlawee Nademanee, Ghassen Cheniti, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Arnaud Denis, Me Le Ze Hocini, Antonio Frontera, Thomas PambrunAbstract:Early repolarization indicates a distinct electrocardiographic phenotype affecting the Junction between the QRS complex and the ST segment in inferolateral leads (inferolateral J-Wave syndromes). It has been considered a benign electrocardiographic variant for decades, but recent clinical studies have demonstrated its arrhythmogenicity in a small subset, supported by experimental studies showing transmural dispersion of repolarization. Here we review the current knowledge and the issues of risk stratification that limit clinical management. In addition, we report on new mapping data of patients refractory to pharmacologic treatment using high-density electrogram mapping at the time of inscription of J Wave. These data demonstrate that distinct substrates, delayed depolarization, and abnormal early repolarization underlie inferolateral J-Wave syndromes, with significant implications. Finally, based on these data, we propose a new simplified mechanistic classification of sudden cardiac deaths without apparent structural heart disease.
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Depolarization versus repolarization abnormality underlying inferolateral J Wave syndromes – new concepts in sudden cardiac death with apparently normal hearts
Heart Rhythm, 2019Co-Authors: Michel Haissaguerre, Koonlawee Nademanee, Ghassen Cheniti, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Arnaud Denis, Me Le Ze Hocini, Antonio Frontera, Thomas PambrunAbstract:Early repolarization indicates a distinct electrocardiographic phenotype affecting the Junction between the QRS complex and the ST segment in inferolateral leads (inferolateral J-Wave Syndromes). It has been considered a benign electrocardiographic variant for decades, but recent clinical studies have demonstrated its arrhythmogenicity in a small subset, supported by experimental studies showing transmural dispersion of repolarization. Here, we review the current knowledge and the issues of risk stratification which limit clinical management. In addition we report on new mapping data of patients refractory to pharmacological treatment using high-density electrogram mapping at the time of inscription of J-Wave. These data demonstrate that distinct substrates, delayed depolarization and abnormal early repolarization, underlie inferolateral J-Wave syndromes, with significant implications. Finally, based on these data, we propose a new simplified mechanistic classification of sudden cardiac deaths without apparent structural heart disease.
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management of an asymptomatic patient with dynamically changing J Wave from inferior early repolarization to brugada pattern
Heart Rhythm, 2016Co-Authors: Nicolas Derval, Frederic Sacher, Arnaud Denis, Michel HaissaguerreAbstract:Case report A 33-year-old man was referred to our institution for investigation of type 1 Brugada syndrome (BS) fortuitously discovered on a routine electrocardiogram (ECG) recorded at an occupational medicine clinic. The patient had no family history of structural heart disease or sudden death and no personal medical history. He was completely asymptomatic at the time of the initial examination. The 12-lead ECG at admission (Figure 1) reveals a normal sinus rhythm with a significant ST-segment elevation of more than 2 mm in leads V1 and V2 diagnostic of a type 1 BS. We also noted the presence of a significant slurred J Wave in the inferior leads diagnostic of early repolarization (ER) pattern. At baseline, the maximal amplitude of the J Wave was 5 mm (0.5 mV) in lead V1 and 4 mm (0.4 mV) in lead III. As we performed routine Valsava maneuvers, we observed significant change in the J Wave in amplitude and distribution (Figure 2). Immediately after the end of maneuvers the J Wave became maximal in the inferior leads and extended all the way to the T Wave (amplitude of 5 mm in lead III) while J Wave decreased in the anterior leads (disappeared in lead V1 and maximal amplitude of 4 mm in lead V2). Rapidly after the end of the Valsalva maneuver, a gradual transition of the ECG back to its initial form was subsequently observed. The same phenomenon was obtained reproducibly with Valsalva maneuvers. Multiple ECG recordings and continuous heart rhythm telemetry also demonstrated extreme fluctuation of the J Wave in amplitude and distribution from predominant Brugada pattern to predominant ER pattern to normal ECG (Figure 3). During hospitalization, the patient underwent an extensive cardiac
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J Wave elevation to monitor quinidine efficacy in early repolarization syndrome
Journal of Electrocardiology, 2014Co-Authors: Frederic Sacher, Nicolas Derval, Marc Horlitz, Michel HaissaguerreAbstract:We present the case of a 14-year-old female with early repolarization syndrome who presented with recurrent ventricular fibrillation and ICD shocks which were refractory to multiple drugs and catheter ablation. Treatment with quinidine, an Ito blocker, resulted in a normalization of J Waves and suppression of VF. Interestingly, J Wave amplitude correlated with the ventricular arrhythmia susceptibility and quinidine levels. The case highlights the importance of quinidine for management of ventricular arrhythmias in the context of early repolarisation and suggests that J Wave amplitude may be an important indicator of therapeutic drug levels and arrhythmia susceptibility.
Gan-xin Yan - One of the best experts on this subject based on the ideXlab platform.
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J Wave Syndromes: History and Current Controversies.
Korean circulation journal, 2016Co-Authors: Tong Liu, Jifeng Zheng, Gan-xin YanAbstract:The concept of J Wave syndromes was first proposed in 2004 by Yan et al for a spectrum of electrocardiographic (ECG) manifestations of prominent J Waves that are associated with a potential to predispose affected individuals to ventricular fibrillation (VF). Although the concept of J Wave syndromes is widely used and accepted, there has been tremendous debate over the definition of J Wave, its ionic and cellular basis and arrhythmogenic mechanism. In this review article, we attempted to discuss the history from which the concept of J Wave syndromes (JWS) is evolved and current controversies in JWS.
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J Wave Syndromes: From Bench to Bedside
J Wave Syndromes, 2016Co-Authors: Gan-xin Yan, Jian-zeng Dong, Changcong CuiAbstract:J Wave syndromes represent a spectrum of electrocardiographic manifestations of ventricular repolarization abnormalities characterized by prominent J Waves and the potential to predispose affected individuals to polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF). J Wave syndromes include two maJor forms: early repolarization syndrome and Brugada syndrome. These syndromes share a common ionic and cellular mechanism with prominent Ito-mediated action potential (AP) spike and dome in ventricular epicardium and are linked by J Wave on the ECG. When Ito is large, an increase in net repolarization current by either a decrease in an inward current (INa or ICa) or an increase in an outward potassium current (Ito per se or IK-ATP) predisposes loss of epicardial AP dome. Loss of epicardial AP dome is often heterogeneous, resulting in two important changes at cellular levels that facilitates the development of polymorphic VT/VF: (1) the epicardial AP dome in some sites may propagate to sites where the cells has completely lost their dome, leading to phase 2 reentry that manifests short-coupled extrasystoles on the ECG; (2) an increase in transmural dispersion of repolarization that can serve as reentry substrate and manifest as downslope ST segment elevation. This chapter attempts to translate the abnormalities at cellular level associated with J Wave syndromes to their clinical ECG manifestations.
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J Wave Syndromes: Brugada and Early Repolarization Syndromes
Heart rhythm, 2015Co-Authors: Charles Antzelevitch, Gan-xin YanAbstract:A prominent J Wave is encountered in a number of life-threatening cardiac arrhythmia syndromes, including the Brugada syndrome and early repolarization syndromes. Brugada syndrome and early repolarization syndromes differ with respect to the magnitude and lead location of abnormal J Waves and are thought to represent a continuous spectrum of phenotypic expression termed J-Wave syndromes. Despite two decades of intensive research, risk stratification and the approach to therapy of these 2 inherited cardiac arrhythmia syndromes are still undergoing rapid evolution. Our obJective in this review is to provide an integrated synopsis of the clinical characteristics, risk stratifiers, and molecular, ionic, cellular, and genetic mechanisms underlying these 2 fascinating syndromes that have captured the interest and attention of the cardiology community in recent years.
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J Wave Syndromes: A Decade of Progress
Chinese medical journal, 2015Co-Authors: Lin Yang, Changcong Cui, Chaofeng Sun, Gan-xin YanAbstract:ObJective: The obJective was to provide a brief history of J Wave syndromes and to summarize our current understanding of their molecular, ionic, cellular mechanisms, and clinical features. We will also discuss the existing debates and further direction in basic and clinical research for J Wave syndromes. Data Sources: The publications on key words of J Wave syndromes, early repolarization syndrome (ERS), Brugada syndrome (BrS) and ST-segment elevation myocardial infarction (STEMI) were comprehensively reviewed through search of the PubMed literatures without restriction on the publication date. Study Selection: Original articles, reviews and other literatures concerning J Wave syndromes, ERS, BrS and STEMI were selected. Results: J Wave syndromes were firstly defined by Yan et al . in a Chinese Journal a decade ago, which represent a spectrum of variable phenotypes characterized by appearance of prominent electrocardiographic J Wave including ERS, BrS and ventricular fibrillation (VF) associated with hypothermia and acute STEMI. J Wave syndromes can be inherited or acquired and are mechanistically linked to amplification of the transient outward current (I to )-mediated J Waves that can lead to phase 2 reentry capable of initiating VF. Conclusions: J Wave syndromes are a group of newly highlighted clinical entities that share similar molecular, ionic and cellular mechanism and marked by amplified J Wave on the electrocardiogram and a risk of VF. The clinical challenge ahead is to identify the patients with J Wave syndromes who are at risk for sudden cardiac death and determine the alternative therapeutic strategies to reduce mortality.
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Cellular and ionic basis of J-Wave syndromes.
Trends in cardiovascular medicine, 2014Co-Authors: Marwan Badri, Aashay Patel, Gan-xin YanAbstract:J-Wave syndromes are disorders of ventricular repolarization characterized by prominent J Waves on the ECG and have the potential to predispose affected individuals to lethal ventricular arrhythmias. These disorders share a common cellular mechanism with prominent Ito in ventricular epicardium. This current causes transmural dispersion of repolarization and the generation of phase 2 reentry, leading to short-coupled extrasystoles and VF. Several autonomic, chemical, and hormonal factors modulate Ito and are therefore vital in attenuating or increasing the arrhythmic potential of these syndromes. Future research should focus on evaluating the arrhythmogenic potential of patients with pathogenic genotypes and/or J Waves and no history of VF.
Thomas Pambrun - One of the best experts on this subject based on the ideXlab platform.
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The Spectrum of Idiopathic Ventricular Fibrillation and J-Wave Syndromes: Novel Mapping Insights
2019Co-Authors: Michel Haissaguerre, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Me Le Ze Hocini, Wee Nademanee, Clémentine André, Thomas Lavergne, Masa Takigawa, Thomas PambrunAbstract:KEY POINTS Idiopathic ventricular fibrillation (IVF) is defined as unexplained sudden cardiac death due to ven-tricular fibrillation (VF) without any identifiable structural or electrical cause after extensive investigations (no phenotype). Recent data show that the use of high-density electrophysiologic mapping may ultimately offer sub-clinical diagnoses of cardiac disease in about 90% of individuals with IVF. Two maJor conditions underlie the occurrence of VF: the presence of either depolarization abnormalities due to micro-structural myocardial alteration or PurkinJe abnormalities manifesting as triggering ectopy or reentry in the peripheral network. J-Wave syndromes are defined as a distinct electrocardiographic phenotype (slurring/notch) affecting the Junction between the QRS complex and the ST segment in inferolateral leads. Recent data provide evidence for heterogeneous substrates, related to either delayed depolarization due to microstructural alterations or early repolarization abnormalities. IVF and J-Wave syndromes are the result of a wide spectrum of pathophysiologic processes. The individual phenotypic characterization is essential given its implications in therapy, genetic testing, and risk stratification.
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depolarization versus repolarization abnormality underlying inferolateral J Wave syndromes new concepts in sudden cardiac death with apparently normal hearts
Heart Rhythm, 2019Co-Authors: Michel Haissaguerre, Koonlawee Nademanee, Ghassen Cheniti, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Arnaud Denis, Me Le Ze Hocini, Antonio Frontera, Thomas PambrunAbstract:Early repolarization indicates a distinct electrocardiographic phenotype affecting the Junction between the QRS complex and the ST segment in inferolateral leads (inferolateral J-Wave syndromes). It has been considered a benign electrocardiographic variant for decades, but recent clinical studies have demonstrated its arrhythmogenicity in a small subset, supported by experimental studies showing transmural dispersion of repolarization. Here we review the current knowledge and the issues of risk stratification that limit clinical management. In addition, we report on new mapping data of patients refractory to pharmacologic treatment using high-density electrogram mapping at the time of inscription of J Wave. These data demonstrate that distinct substrates, delayed depolarization, and abnormal early repolarization underlie inferolateral J-Wave syndromes, with significant implications. Finally, based on these data, we propose a new simplified mechanistic classification of sudden cardiac deaths without apparent structural heart disease.
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Depolarization versus repolarization abnormality underlying inferolateral J Wave syndromes – new concepts in sudden cardiac death with apparently normal hearts
Heart Rhythm, 2019Co-Authors: Michel Haissaguerre, Koonlawee Nademanee, Ghassen Cheniti, Josselin Duchateau, Frederic Sacher, Nicolas Derval, Arnaud Denis, Me Le Ze Hocini, Antonio Frontera, Thomas PambrunAbstract:Early repolarization indicates a distinct electrocardiographic phenotype affecting the Junction between the QRS complex and the ST segment in inferolateral leads (inferolateral J-Wave Syndromes). It has been considered a benign electrocardiographic variant for decades, but recent clinical studies have demonstrated its arrhythmogenicity in a small subset, supported by experimental studies showing transmural dispersion of repolarization. Here, we review the current knowledge and the issues of risk stratification which limit clinical management. In addition we report on new mapping data of patients refractory to pharmacological treatment using high-density electrogram mapping at the time of inscription of J-Wave. These data demonstrate that distinct substrates, delayed depolarization and abnormal early repolarization, underlie inferolateral J-Wave syndromes, with significant implications. Finally, based on these data, we propose a new simplified mechanistic classification of sudden cardiac deaths without apparent structural heart disease.