Vincent Probst
University of Nantes
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The New England Journal of Medicine | 2008
Michel Haïssaguerre; Nicolas Derval; Frederic Sacher; Laurence Jesel; Isabel Deisenhofer; Luc De Roy; Jean-Luc Pasquié; Akihiko Nogami; Dominique Babuty; Sinikka Yli-Mayry; Christian de Chillou; Patrice Scanu; Philippe Mabo; Seiichiro Matsuo; Vincent Probst; Solena Le Scouarnec; Pascal Defaye; Juerg Schlaepfer; Thomas Rostock; Dominique Lacroix; Dominique Lamaison; Thomas Lavergne; Yoshifusa Aizawa; Anders Englund; Frederic Anselme; Mark O'Neill; Mélèze Hocini; Kang-Teng Lim; Sébastien Knecht; George D. Veenhuyzen
BACKGROUND Early repolarization is a common electrocardiographic finding that is generally considered to be benign. Its potential to cause cardiac arrhythmias has been hypothesized from experimental studies, but it is not known whether there is a clinical association with sudden cardiac arrest. METHODS We reviewed data from 206 case subjects at 22 centers who were resuscitated after cardiac arrest due to idiopathic ventricular fibrillation and assessed the prevalence of electrocardiographic early repolarization. The latter was defined as an elevation of the QRS-ST junction of at least 0.1 mV from baseline in the inferior or lateral lead, manifested as QRS slurring or notching. The control group comprised 412 subjects without heart disease who were matched for age, sex, race, and level of physical activity. Follow-up data that included the results of monitoring with an implantable defibrillator were obtained for all case subjects. RESULTS Early repolarization was more frequent in case subjects with idiopathic ventricular fibrillation than in control subjects (31% vs. 5%, P<0.001). Among case subjects, those with early repolarization were more likely to be male and to have a history of syncope or sudden cardiac arrest during sleep than those without early repolarization. In eight subjects, the origin of ectopy that initiated ventricular arrhythmias was mapped to sites concordant with the localization of repolarization abnormalities. During a mean (+/-SD) follow-up of 61+/-50 months, defibrillator monitoring showed a higher incidence of recurrent ventricular fibrillation in case subjects with a repolarization abnormality than in those without such an abnormality (hazard ratio, 2.1; 95% confidence interval, 1.2 to 3.5; P=0.008). CONCLUSIONS Among patients with a history of idiopathic ventricular fibrillation, there is an increased prevalence of early repolarization.
Circulation | 2010
Vincent Probst; Christian Veltmann; Lars Eckardt; Paola G. Meregalli; Fiorenzo Gaita; Hanno L. Tan; Dominique Babuty; Frederic Sacher; Carla Giustetto; Eric Schulze-Bahr; Martin Borggrefe; M. Haissaguerre; Philippe Mabo; H. Le Marec; Christian Wolpert; A. A. M. Wilde
Background— Brugada syndrome is characterized by ST-segment elevation in the right precordial leads and an increased risk of sudden cardiac death (SCD). Fundamental questions remain on the best strategy for assessing the real disease-associated arrhythmic risk, especially in asymptomatic patients. The aim of the present study was to evaluate the prognosis and risk factors of SCD in Brugada syndrome patients in the FINGER (France, Italy, Netherlands, Germany) Brugada syndrome registry. Methods and Results— Patients were recruited in 11 tertiary centers in 4 European countries. Inclusion criteria consisted of a type 1 ECG present either at baseline or after drug challenge, after exclusion of diseases that mimic Brugada syndrome. The registry included 1029 consecutive individuals (745 men; 72%) with a median age of 45 (35 to 55) years. Diagnosis was based on (1) aborted SCD (6%); (2) syncope, otherwise unexplained (30%); and (3) asymptomatic patients (64%). During a median follow-up of 31.9 (14 to 54.4) months, 51 cardiac events (5%) occurred (44 patients experienced appropriate implantable cardioverter-defibrillator shocks, and 7 died suddenly). The cardiac event rate per year was 7.7% in patients with aborted SCD, 1.9% in patients with syncope, and 0.5% in asymptomatic patients. Symptoms and spontaneous type 1 ECG were predictors of arrhythmic events, whereas gender, familial history of SCD, inducibility of ventricular tachyarrhythmias during electrophysiological study, and the presence of an SCN5A mutation were not predictive of arrhythmic events. Conclusions— In the largest series of Brugada syndrome patients thus far, event rates in asymptomatic patients were low. Inducibility of ventricular tachyarrhythmia and family history of SCD were not predictors of cardiac events.
Journal of Clinical Investigation | 2008
Hiroshi Watanabe; Tamara T. Koopmann; Solena Le Scouarnec; Tao Yang; Christiana R. Ingram; Jean-Jacques Schott; Sophie Demolombe; Vincent Probst; Frédeéric Anselme; Denis Escande; Ans C.P. Wiesfeld; Arne Pfeufer; Stefan Kääb; H.-Erich Wichmann; Can Hasdemir; Yoshifusa Aizawa; Arthur A.M. Wilde; Dan M. Roden; Connie R. Bezzina
Brugada syndrome is a genetic disease associated with sudden cardiac death that is characterized by ventricular fibrillation and right precordial ST segment elevation on ECG. Loss-of-function mutations in SCN5A, which encodes the predominant cardiac sodium channel alpha subunit NaV1.5, can cause Brugada syndrome and cardiac conduction disease. However, SCN5A mutations are not detected in the majority of patients with these syndromes, suggesting that other genes can cause or modify presentation of these disorders. Here, we investigated SCN1B, which encodes the function-modifying sodium channel beta1 subunit, in 282 probands with Brugada syndrome and in 44 patients with conduction disease, none of whom had SCN5A mutations. We identified 3 mutations segregating with arrhythmia in 3 kindreds. Two of these mutations were located in a newly described alternately processed transcript, beta1B. Both the canonical and alternately processed transcripts were expressed in the human heart and were expressed to a greater degree in Purkinje fibers than in heart muscle, consistent with the clinical presentation of conduction disease. Sodium current was lower when NaV1.5 was coexpressed with mutant beta1 or beta1B subunits than when it was coexpressed with WT subunits. These findings implicate SCN1B as a disease gene for human arrhythmia susceptibility.
Circulation | 2006
Frédéric Sacher; Vincent Probst; Philippe Maury; Dominique Babuty; Jacques Mansourati; Yuki Komatsu; Christelle Marquié; Antonio Rosa; Abou Diallo; Romain Cassagneau; Claire Loizeau; Raphael Martins; Michael E. Field; Nicolas Derval; Shinsuke Miyazaki; Arnaud Denis; Akihiko Nogami; Philippe Ritter; Jean-Baptiste Gourraud; Sylvain Ploux; Anne Rollin; Adlane Zemmoura; Dominique Lamaison; Pierre Bordachar; Bertrand Pierre; P. Jais; Jean-Luc Pasquié; M. Hocini; Pascal Defaye; Serge Boveda
Background— Implantable cardioverter-defibrillator indications in Brugada syndrome remain controversial, especially in asymptomatic patients. Previous outcome data are limited by relatively small numbers of patients or short follow-up durations. We report the outcome of patients with Brugada syndrome implanted with an implantable cardioverter-defibrillator in a large multicenter registry. Methods and Results— A total of 378 patients (310 male; age, 46±13 years) with a type 1 Brugada ECG pattern implanted with an implantable cardioverter-defibrillator (31 for aborted sudden cardiac arrest, 181 for syncope, and 166 asymptomatic) were included. Fifteen patients (4%) were lost to follow-up. During a mean follow-up of 77±42 months, 7 patients (2%) died (1 as a result of an inappropriate shock), and 46 patients (12%) had appropriate device therapy (5±5 shocks per patient). Appropriate device therapy rates at 10 years were 48% for patients whose implantable cardioverter-defibrillator indication was aborted sudden cardiac arrest, 19% for those whose indication was syncope, and 12% for the patients who were asymptomatic at implantation. At 10 years, rates of inappropriate shock and lead failure were 37% and 29%, respectively. Inappropriate shock occurred in 91 patients (24%; 4±4 shocks per patient) because of lead failure (n=38), supraventricular tachycardia (n=20), T-wave oversensing (n=14), or sinus tachycardia (n=12). Importantly, introduction of remote monitoring, programming a high single ventricular fibrillation zone (>210–220 bpm), and a long detection time were associated with a reduced risk of inappropriate shock. Conclusions— Appropriate therapies are more prevalent in symptomatic Brugada syndrome patients but are not insignificant in asymptomatic patients (1%/y). Optimal implantable cardioverter-defibrillator programming and follow-up dramatically reduce inappropriate shock. However, lead failure remains a major problem in this population.
Circulation | 2005
Lars Eckardt; Vincent Probst; Jeroen P. P. Smits; Eric Schulze Bahr; Christian Wolpert; Rainer Schimpf; Thomas Wichter; Pierre Boisseau; Achim Heinecke; Günter Breithardt; Martin Borggrefe; Herve LeMarec; Dirk Böcker; Arthur A.M. Wilde
Background—Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increased risk of sudden cardiac death as a result of ventricular fibrillation. Controversy exists with regard to risk stratification and therapeutic management, particularly in asymptomatic individuals. Methods and Results—A total of 212 individuals (mean age, 45±6 years) with a type 1 Brugada ECG pattern were studied. Of these, 123 (58%) were asymptomatic, 65 (31%) had ≥1 syncope of unknown origin, and 24 (11%) had to be resuscitated because of ventricular fibrillation. In 125 individuals (59%), a spontaneous type 1 ECG was recorded. In the remaining, drug challenge with a class I antiarrhythmic agent unmasked a Brugada ECG. The mean ST elevation was 2.3±1.2 mm in symptomatic patients and 1.9±1.5 mm in asymptomatic individuals (P=0.04). During a mean follow-up of 40±50 months, 4 of the 24 patients (17%) with aborted sudden cardiac death and 4 of 65 (6%) with a prior syncope had a recurrent arrhythmic event, whereas only 1 of 123 asymptomatic individuals (0.8%) had a first arrhythmic event. Four of 9 patients with arrhythmic events during follow-up were not inducible during programmed electrical stimulation. A previous history of aborted sudden death or syncope and the presence of a spontaneous type 1 ECG were predictors of adverse outcome. Conclusions—The present study reports data on a large population of individuals with a type 1 Brugada ECG pattern with the longest follow-up reported so far. A very low incidence of severe arrhythmic events, particularly in asymptomatic individuals, was found during follow-up. In the presence of very few arrhythmic events on follow-up, programmed electrical stimulation showed very little accuracy in predicting outcome.
Heart Rhythm | 2009
Pieter G. Postema; Christian Wolpert; Ahmad S. Amin; Vincent Probst; Martin Borggrefe; Dan M. Roden; Silvia G. Priori; Hanno L. Tan; Masayasu Hiraoka; Josep Brugada; Arthur A.M. Wilde
BACKGROUND Worldwide, the Brugada syndrome has been recognized as an important cause of sudden cardiac death in individuals at a relatively young age. Importantly, many drugs have been reported to induce the characteristic Brugada syndrome-linked ECG abnormalities and/or (fatal) ventricular tachyarrhythmias. OBJECTIVE The purpose of this study was to review the literature on the use of drugs in Brugada syndrome patients, to make recommendations based on the literature and on expert opinion regarding drug safety, and to ensure worldwide online and up-to-date availability of this information to all physicians who treat Brugada syndrome patients. METHODS We performed an extensive review of the literature, formed an international expert panel to produce a consensus recommendation to each drug, and initiated a website (www.brugadadrugs.org). RESULTS The literature search yielded 506 reports for consideration. Drugs were categorized into one of four categories: (1) drugs to be avoided (n = 18); (2) drugs preferably avoided (n = 23); (3) antiarrhythmic drugs (n = 4); and (4) diagnostic drugs (n = 4). Level of evidence for most associations was C (only consensus opinion of experts, case studies, or standard-of-care) as there are no randomized studies and few nonrandomized studies in Brugada syndrome patients. CONCLUSION Many drugs have been associated with adverse events in Brugada syndrome patients. We have initiated a website (www.brugadadrugs.org) to ensure worldwide availability of information on safe drug use in Brugada syndrome patients.
Nature Genetics | 2013
Connie R. Bezzina; Julien Barc; Yuka Mizusawa; Carol Ann Remme; Jean-Baptiste Gourraud; Floriane Simonet; Arie O. Verkerk; Peter J. Schwartz; Lia Crotti; Federica Dagradi; Pascale Guicheney; Véronique Fressart; Antoine Leenhardt; Charles Antzelevitch; Susan Bartkowiak; Martin Borggrefe; Rainer Schimpf; Eric Schulze-Bahr; Sven Zumhagen; Elijah R. Behr; Rachel Bastiaenen; Jacob Tfelt-Hansen; Morten S. Olesen; Stefan Kääb; Britt M. Beckmann; Peter Weeke; Hiroshi Watanabe; Naoto Endo; Tohru Minamino; Minoru Horie
Brugada syndrome is a rare cardiac arrhythmia disorder, causally related to SCN5A mutations in around 20% of cases. Through a genome-wide association study of 312 individuals with Brugada syndrome and 1,115 controls, we detected 2 significant association signals at the SCN10A locus (rs10428132) and near the HEY2 gene (rs9388451). Independent replication confirmed both signals (meta-analyses: rs10428132, P = 1.0 × 10−68; rs9388451, P = 5.1 × 10−17) and identified one additional signal in SCN5A (at 3p21; rs11708996, P = 1.0 × 10−14). The cumulative effect of the three loci on disease susceptibility was unexpectedly large (Ptrend = 6.1 × 10−81). The association signals at SCN5A-SCN10A demonstrate that genetic polymorphisms modulating cardiac conduction can also influence susceptibility to cardiac arrhythmia. The implication of association with HEY2, supported by new evidence that Hey2 regulates cardiac electrical activity, shows that Brugada syndrome may originate from altered transcriptional programming during cardiac development. Altogether, our findings indicate that common genetic variation can have a strong impact on the predisposition to rare diseases.
Journal of Cardiovascular Electrophysiology | 2009
Michel Haïssaguerre; Stéphanie Chatel; Frederic Sacher; Rukshen Weerasooriya; Vincent Probst; Gildas Loussouarn; Marc Horlitz; Ruedige Liersch M.D.; Eric Schulze-Bahr; Arthur A.M. Wilde; Stefan Kääb; Joseph C. Koster; Yoram Rudy; Hervé Le Marec; Jean-Jacques Schott
Background: Early repolarization in the inferolateral leads has been recently recognized as a frequent syndrome associated with idiopathic ventricular fibrillation (VF). We report the case of a patient presenting dramatic changes in the ECG in association with recurrent VF in whom a novel genetic variant has been identified.
Journal of the American College of Cardiology | 2009
Michel Haïssaguerre; Frederic Sacher; Akihiko Nogami; Nohiriro Komiya; Anne Bernard; Vincent Probst; Sinikka Yli-Mäyry; Pascal Defaye; Yoshifusa Aizawa; Robert Frank; Roberto Mantovan; Riccardo Cappato; Christian Wolpert; Antoine Leenhardt; Lucas de Roy; Hein Heidbuchel; Isabel Deisenhofer; Thomas Arentz; Jean-Luc Pasquié; Rukshen Weerasooriya; Mélèze Hocini; Pierre Jaïs; Nicolas Derval; Pierre Bordachar; Jacques Clémenty
OBJECTIVES Our purpose was to evaluate the efficacy of antiarrhythmic drugs (AADs) in recurrent ventricular fibrillation (VF) associated with inferolateral early repolarization pattern on the electrocardiogram. BACKGROUND Although an implantable cardioverter-defibrillator is the treatment of choice, additional AADs may be necessary to prevent frequent episodes of VF and reduce implantable cardioverter-defibrillator shock burden or as a lifesaving therapy in electrical storms. METHODS From a multicenter cohort of 122 patients (90 male subjects, age 37 +/- 12 years) with idiopathic VF and early repolarization abnormality in the inferolateral leads, we selected all patients with more than 3 episodes of VF (multiple) including those with electrical storms (> or =3 VF in 24 h). The choice of AAD was decided by individual physicians. Follow-up data were obtained for all patients using monitoring with implantable defibrillator. Successful oral AAD was defined as elimination of all recurrences of VF with a minimal follow-up period of 12 months. RESULTS Multiple episodes of VF were observed in 33 (27%) patients. Electrical storms (34 +/- 47 episodes) occurred in 16 and were unresponsive to beta-blockers (11 of 11), lidocaine/mexiletine (9 of 9), and verapamil (3 of 3), while amiodarone was partially effective (3 of 10). In contrast, isoproterenol infusion immediately suppressed electrical storms in 7 of 7 patients. Over a follow-up of 69 +/- 58 months, oral AADs were poorly effective in preventing recurrent VF: beta-blockers (2 of 16), verapamil (0 of 4), mexiletine (0 of 4), amiodarone (1 of 7), and class 1C AADs (2 of 9). Quinidine was successful in 9 of 9 patients, decreasing recurrent VF from 33 +/- 35 episodes to nil for 25 +/- 18 months. In addition, quinidine restored a normal electrocardiogram. CONCLUSIONS Multiple recurrences of VF occurred in 27% of patients with early repolarization abnormality and may be life threatening. Isoproterenol in acute cases and quinidine in chronic cases are effective AADs.
Circulation | 2007
Vincent Probst; Isabelle Denjoy; Paola G. Meregalli; Jean Christophe Amirault; Frederic Sacher; Jacques Mansourati; Dominique Babuty; Elisabeth Villain; Jacques Victor; Jean-Jacques Schott; Jean Marc Lupoglazoff; Philippe Mabo; Christian Veltmann; Laurence Jesel; Philippe Chevalier; S. A. Clur; Michel Haïssaguerre; Christian Wolpert; Hervé Le Marec; Arthur A.M. Wilde
Background— Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and augmented risk of sudden cardiac death. Little is known about the clinical presentation and prognosis of this disease in children. Methods and Results— Thirty children affected by Brugada syndrome who were <16 years of age (mean, 8±4 years) were included. All patients displayed a type I ECG pattern before or after drug provocation challenge. Diagnosis of Brugada syndrome was made under the following circumstances: aborted sudden death (n=1), syncope of unexplained origin (n=10), symptomatic supraventricular tachycardia (n=1), suspicious ECG (n=1), and family screening for Brugada syndrome (n=17). Syncope was precipitated by fever in 5 cases. Ten of 11 symptomatic patients displayed a spontaneous type I ECG. An implantable cardioverter-defibrillator was implanted in 5 children; 4 children were treated with hydroquinidine; and 1 child received a pacemaker because of symptomatic sick sinus syndrome. During a mean follow-up of 37±23 months, 1 child experienced sudden cardiac death, and 2 children received an appropriate implantable cardioverter-defibrillator shock; all of them were symptomatic and had manifested a type I ECG spontaneously. One child had a cardioverter-defibrillator infection that required explantation of the defibrillator. Conclusions— In the largest population of children affected by Brugada syndrome described to date, fever represented the most important precipitating factor for arrhythmic events, and as in the adult population, the risk of arrhythmic events was higher in previously symptomatic patients and in those displaying a spontaneous type I ECG.