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1. Flecainide Is Associated With a Lower Incidence of Arrhythmic Events in a Large Cohort of Patients With Catecholaminergic Polymorphic Ventricular Tachycardia.

Author

Bergeman, Auke, Lieve, Krystien, Kallas, Dania, Bos, J, Rosés I Noguer, Ferran, Denjoy, Isabelle, Zorio, Esther, Kammeraad, Janneke, Peltenburg, Puck, Tobert, Katie, Aiba, Takeshi, Atallah, Joseph, Drago, Fabrizio, Batra, Anjan, Brugada, Ramon, Borggrefe, Martin, Clur, Sally-Ann, Cox, Moniek, Davis, Andrew, Dhillon, Santokh, Etheridge, Susan, Fischbach, Peter, Franciosi, Sonia, Haugaa, Kristina, Horie, Minoru, Johnsrude, Christopher, Kane, Austin, Krause, Ulrich, Kwok, Sit-Yee, LaPage, Martin, Ohno, Seiko, Probst, Vincent, Roberts, Jason, Robyns, Tomas, Sacher, Frederic, Semsarian, Christopher, Skinner, Jonathan, Swan, Heikki, Tavacova, Terezia, Tisma-Dupanovic, Svjetlana, Tfelt-Hansen, Jacob, Yap, Sing-Chien, Kannankeril, Prince, Leenhardt, Antoine, Till, Janice, Sanatani, Shubhayan, Tanck, Michael, Ackerman, Michael, Wilde, Arthur, and van der Werf, Christian

Subjects
catecholaminergic polymorphic ventricular tachycardia, sudden cardiac death, ventricular arrhythmias, Female, Humans, Adolescent, Male, Flecainide, Incidence, Cross-Over Studies, Tachycardia, Ventricular, Adrenergic beta-Antagonists, Defibrillators, Implantable, Death, Sudden, Cardiac
Abstract

BACKGROUND: In severely affected patients with catecholaminergic polymorphic ventricular tachycardia, beta-blockers are often insufficiently protective. The purpose of this study was to evaluate whether flecainide is associated with a lower incidence of arrhythmic events (AEs) when added to beta-blockers in a large cohort of patients with catecholaminergic polymorphic ventricular tachycardia. METHODS: From 2 international registries, this multicenter case cross-over study included patients with a clinical or genetic diagnosis of catecholaminergic polymorphic ventricular tachycardia in whom flecainide was added to beta-blocker therapy. The study period was defined as the period in which background therapy (ie, beta-blocker type [beta1-selective or nonselective]), left cardiac sympathetic denervation, and implantable cardioverter defibrillator treatment status, remained unchanged within individual patients and was divided into pre-flecainide and on-flecainide periods. The primary end point was AEs, defined as sudden cardiac death, sudden cardiac arrest, appropriate implantable cardioverter defibrillator shock, and arrhythmic syncope. The association of flecainide with AE rates was assessed using a generalized linear mixed model assuming negative binomial distribution and random effects for patients. RESULTS: A total of 247 patients (123 [50%] females; median age at start of flecainide, 18 years [interquartile range, 14-29]; median flecainide dose, 2.2 mg/kg per day [interquartile range, 1.7-3.1]) were included. At baseline, all patients used a beta-blocker, 70 (28%) had an implantable cardioverter defibrillator, and 21 (9%) had a left cardiac sympathetic denervation. During a median pre-flecainide follow-up of 2.1 years (interquartile range, 0.4-7.2), 41 patients (17%) experienced 58 AEs (annual event rate, 5.6%). During a median on-flecainide follow-up of 2.9 years (interquartile range, 1.0-6.0), 23 patients (9%) experienced 38 AEs (annual event rate, 4.0%). There were significantly fewer AEs after initiation of flecainide (incidence rate ratio, 0.55 [95% CI, 0.38-0.83]; P=0.007). Among patients who were symptomatic before diagnosis or during the pre-flecainide period (n=167), flecainide was associated with significantly fewer AEs (incidence rate ratio, 0.49 [95% CI, 0.31-0.77]; P=0.002). Among patients with ≥1 AE on beta-blocker therapy (n=41), adding flecainide was also associated with significantly fewer AEs (incidence rate ratio, 0.25 [95% CI, 0.14-0.45]; P

Published
2023

2. An International Multicenter Evaluation of Inheritance Patterns, Arrhythmic Risks, and Underlying Mechanisms of CASQ2-Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Ng, Kevin, Titus, Erron W, Lieve, Krystien V, Roston, Thomas M, Mazzanti, Andrea, Deiter, Frederick H, Denjoy, Isabelle, Ingles, Jodie, Till, Jan, Robyns, Tomas, Connors, Sean P, Steinberg, Christian, Abrams, Dominic J, Pang, Benjamin, Scheinman, Melvin M, Bos, J Martijn, Duffett, Stephen A, van der Werf, Christian, Maltret, Alice, Green, Martin S, Rutberg, Julie, Balaji, Seshadri, Cadrin-Tourigny, Julia, Orland, Kate M, Knight, Linda M, Brateng, Caitlin, Wu, Jeremy, Tang, Anthony S, Skanes, Allan C, Manlucu, Jaimie, Healey, Jeff S, January, Craig T, Krahn, Andrew D, Collins, Kathryn K, Maginot, Kathleen R, Fischbach, Peter, Etheridge, Susan P, Eckhardt, Lee L, Hamilton, Robert M, Ackerman, Michael J, Noguer, Ferran Rosés I, Semsarian, Christopher, Jura, Natalia, Leenhardt, Antoine, Gollob, Michael H, Priori, Silvia G, Sanatani, Shubhayan, Wilde, Arthur AM, Deo, Rahul C, and Roberts, Jason D

Subjects
Clinical Research, Cardiovascular, Genetics, Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Calsequestrin, Female, Heterozygote, Homozygote, Humans, Male, Mutation, Missense, Risk Factors, Tachycardia, Ventricular, arrhythmias, cardiac, catecholaminergic polymorphic ventricular tachycardia, death, sudden, genetics, arrhythmias, cardiac, death, sudden, cardiac, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

BackgroundGenetic variants in calsequestrin-2 (CASQ2) cause an autosomal recessive form of catecholaminergic polymorphic ventricular tachycardia (CPVT), although isolated reports have identified arrhythmic phenotypes among heterozygotes. Improved insight into the inheritance patterns, arrhythmic risks, and molecular mechanisms of CASQ2-CPVT was sought through an international multicenter collaboration.MethodsGenotype-phenotype segregation in CASQ2-CPVT families was assessed, and the impact of genotype on arrhythmic risk was evaluated using Cox regression models. Putative dominant CASQ2 missense variants and the established recessive CASQ2-p.R33Q variant were evaluated using oligomerization assays and their locations mapped to a recent CASQ2 filament structure.ResultsA total of 112 individuals, including 36 CPVT probands (24 homozygotes/compound heterozygotes and 12 heterozygotes) and 76 family members possessing at least 1 presumed pathogenic CASQ2 variant, were identified. Among CASQ2 homozygotes and compound heterozygotes, clinical penetrance was 97.1% and 26 of 34 (76.5%) individuals had experienced a potentially fatal arrhythmic event with a median age of onset of 7 years (95% CI, 6-11). Fifty-one of 66 CASQ2 heterozygous family members had undergone clinical evaluation, and 17 of 51 (33.3%) met diagnostic criteria for CPVT. Relative to CASQ2 heterozygotes, CASQ2 homozygote/compound heterozygote genotype status in probands was associated with a 3.2-fold (95% CI, 1.3-8.0; P=0.013) increased hazard of a composite of cardiac syncope, aborted cardiac arrest, and sudden cardiac death, but a 38.8-fold (95% CI, 5.6-269.1; P

Published
2020

4. Transethnic Genome-Wide Association Study Provides Insights in the Genetic Architecture and Heritability of Long QT Syndrome

Author

Lahrouchi, Najim, Tadros, Rafik, Crotti, Lia, Mizusawa, Yuka, Postema, Pieter G., Beekman, Leander, Walsh, Roddy, Hasegawa, Kanae, Barc, Julien, Ernsting, Marko, Turkowski, Kari L., Mazzanti, Andrea, Beckmann, Britt M., Shimamoto, Keiko, Diamant, Ulla-Britt, Wijeyeratne, Yanushi D., Kucho, Yu, Robyns, Tomas, Ishikawa, Taisuke, Arbelo, Elena, Christiansen, Michael, Winbo, Annika, Jabbari, Reza, Lubitz, Steven A., Steinfurt, Johannes, Rudic, Boris, Loeys, Bart, Shoemaker, M. Ben, Weeke, Peter E., Pfeiffer, Ryan, Davies, Brianna, Andorin, Antoine, Hofman, Nynke, Dagradi, Federica, Pedrazzini, Matteo, Tester, David J., Bos, J. Martijn, Sarquella-Brugada, Georgia, Campuzano, Óscar, Platonov, Pyotr G., Stallmeyer, Birgit, Zumhagen, Sven, Nannenberg, Eline A., Veldink, Jan H., van den Berg, Leonard H., Al-Chalabi, Ammar, Shaw, Christopher E., Shaw, Pamela J., Morrison, Karen E., Andersen, Peter M., Müller-Nurasyid, Martina, Cusi, Daniele, Barlassina, Cristina, Galan, Pilar, Lathrop, Mark, Munter, Markus, Werge, Thomas, Ribasés, Marta, Aung, Tin, Khor, Chiea C., Ozaki, Mineo, Lichtner, Peter, Meitinger, Thomas, van Tintelen, J. Peter, Hoedemaekers, Yvonne, Denjoy, Isabelle, Leenhardt, Antoine, Napolitano, Carlo, Shimizu, Wataru, Schott, Jean-Jacques, Gourraud, Jean-Baptiste, Makiyama, Takeru, Ohno, Seiko, Itoh, Hideki, Krahn, Andrew D., Antzelevitch, Charles, Roden, Dan M., Saenen, Johan, Borggrefe, Martin, Odening, Katja E., Ellinor, Patrick T., Tfelt-Hansen, Jacob, Skinner, Jonathan R., van den Berg, Maarten P., Olesen, Morten Salling, Brugada, Josep, Brugada, Ramón, Makita, Naomasa, Breckpot, Jeroen, Yoshinaga, Masao, Behr, Elijah R., Rydberg, Annika, Aiba, Takeshi, Kääb, Stefan, Priori, Silvia G., Guicheney, Pascale, Tan, Hanno L., Newton-Cheh, Christopher, Ackerman, Michael J., Schwartz, Peter J., Schulze-Bahr, Eric, Probst, Vincent, Horie, Minoru, Wilde, Arthur A., Tanck, Michael W.T., and Bezzina, Connie R.

Published
2020
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5. Comprehensive Assessment of Coronary Artery Disease in Sports-Related Sudden Cardiac Arrest

Author

Karam, Nicole, Pechmajou, Louis, Dumas, Florence, Bougouin, Wulfran, Sharifzadehgan, Ardalan, Beganton, Frankie, Bonnet, Guillaume, Jost, Daniel, Lamhaut, Lionel, Varenne, Olivier, Aubry, Pierre, Sideris, Georgios, Spaulding, Christian, Cariou, Alain, Marijon, Eloi, Jouven, Xavier, Adnet, F, Agostinucci, JM, Aissaoui-Balanant, N, Algalarrondo, V, Alla, F, Alonso, C, Amara, W, Annane, D, Antoine, C, Aubry, P, Azoulay, E, Beganton, F, Benhamou, D, Bougouin, W, Bruel, C, Brun Buisson, C, Bruneval, P, Cariou, A, Carli, P, Cerf, C, Chaib, A, Chastre, J, Cholley, B, Cohen, Y, Combes, A, Cornaglia, C, Coulaud, JM, Da Silva, D, Das, V, Deye, N, Dhonneur, G, Diehl, JL, Dinanian, S, Domanski, L, Dreyfuss, D, Duboc, D, Dubois-Rande, JL, Mansencal, N, Duchateau, FX, Duguet, A, Dumas, F, Empana, JP, Extramiana, F, Fartoukh, M, Fenioux, C, Fraisse, F, Gabbas, M, Gandjbakhch, E, Guidet, B, Halimi, F, Henry, P, Hidden Lucet, F, Jabre, P, Jacob, L, Joseph, L, Jost, D, Journois, D, Jouven, X, Karam, N, Lacotte, J, Lahlou-Laforet, K, Lamhaut, L, Lanceleur, A, Langeron, O, Lanoe, V, Lavergne, T, Lecarpentier, E, Leenhardt, A, Lellouche, N, Lemiale, V, Linval, F, Loeb, T, Ludes, B, Mansouri, N, Marijon, E, Marty, J, Maury, E, Maxime, V, Mekontso-Dessaps, A, Mira, JP, Misset, B, Monnet, X, Montalescot, G, Narayanan, K, Nicolas-Robin, A, Perier, MC, Piot, O, Plu, I, Revaux, F, Ricard, JD, Richard, C, Riou, B, Rouby, JJ, Santoli, F, Schortgen, F, Sharshar, T, Sideris, G, Similowski, T, Simon, A, Spaulding, C, Steg, G, Teboul, JL, Timsit, JF, Tourtier, JP, Tuppin, P, Ursat, C, Varenne, O, Vieillard-Baron, A, Voicu, S, Wahbi, K, Waldmann, V, and Wolff, M

Published
2018
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6. Long-Term Follow-Up of Patients With Tetralogy of Fallot and Implantable Cardioverter Defibrillator

Author

Victor Waldmann, Abdeslam Bouzeman, Guillaume Duthoit, Linda Koutbi, Francis Bessiere, Fabien Labombarda, Christelle Marquié, Jean Baptiste Gourraud, Pierre Mondoly, Jean Marc Sellal, Pierre Bordachar, Alexis Hermida, Frédéric Anselme, Anouk Asselin, Caroline Audinet, Yvette Bernard, Serge Boveda, Paul Bru, Sok Sithikun Bun, Gael Clerici, Antoine Da Costa, Maxime de Guillebon, Pascal Defaye, Nathalie Elbaz, Romain Eschalier, Rodrigue Garcia, Charles Guenancia, Benoit Guy-Moyat, Franck Halimi, Didier Irles, Laurence Iserin, François Jourda, Magalie Ladouceur, Philippe Lagrange, Mikael Laredo, Jacques Mansourati, Grégoire Massoulié, Amel Mathiron, Philippe Maury, Anne Messali, Kumar Narayanan, Cédric Nguyen, Sandro Ninni, Marie-Cécile Perier, Bertrand Pierre, Penelope Pujadas, Frédéric Sacher, Pascal Sagnol, Ardalan Sharifzadehgan, Camille Walton, Pierre Winum, Cyril Zakine, Laurent Fauchier, Raphael Martins, Jean Luc Pasquié, Jean Benoit Thambo, Xavier Jouven, Nicolas Combes, Eloi Marijon, Fabien Squara, Guillaume Theodore, Didier Scarlatti, Jérome Hourdain, Jean-Claude Deharo, Pierre Ollitrault, Paul Milliez, Laure Champ-Rigot, Hugues Bader, Cécile Duplantier, Antoine Milhem, Audrey Sagnard, Géraldine Bertaux, Gabriel Laurent, Marc Badoz, Agustin Bortone, Guillaume Laborie, Anne Rollin, Quentin Voglimacci Stephanopoli, Franck Mandel, Alexandre Duparc, Guillaume Domain, Jean-Paul Albenque, Christèle Cardin, Stéphane Combes, Nikita Tanese, Karim Hasni, Christophe Leclercq, Vincent Galand, Dominique Pavin, Philippe Mabo, Nathalie Behar, Nicolas Clementy, Christophe Loose, Akli Otmani, Sandrine Venier, Adrien Carabelli, Peggy Jacon, Mouna Ben Kilani, Jean Bapstist Guichard, Cécile Romeyer-Bouchard, Laurianne Le Gloan, Vincent Probst, Luc Freysz, Hugues Blangy, Christian De Chillou, Nicolas Sadoul, Pierre Khattar, Charlotte Potelle, Frederic Jean, Paul Puie, Ziad Khoueiry, Philippe Chevallier, Arnaud Dulac, Sylvie Di Filippo, Kevin Gardey, Pierre Frey, Chrystelle Akret, Antoine Dompnier, Carole Maupain, Xavier Waintraub, Françoise Hidden-Lucet, Thomas Chastre, Estelle Gandjbakhch, Nicolas Badenco, Fabrice Extramiana, Antoine Leenhardt, Amir Zouaghi, Vincent Algalarrondo, Denis Amet, Emilie Varlet, Tej Chalbia, Séverine Philibert, Jacky Ollitrault, Thomas Lavergne, Pierre Baudinaud, Adrian Mirolo, Arnaud Savouré, Bénédicte Godin, Cathy Bertrand, Pierre Fiorello, Nicolas Johnson, Pierre-Marc Lallemand, Alexis Herminda, Jean-Sylvain Hermida, Bruno Degand, Rim El Bouazzaou, Stéphane Mourot, Samuel Goussot, Gaël Jauvert, Arnaud Lazarus, Caroline Grimard, Christine Alonso, Alexandre Zhao, Olivier Thomas, Bruno Cauchemez, Ghassan Moubarak, Nicolas Lellouche, David Hamon, Bogdan Enache, Gabriel Lactu, Françoise Wiart, Olivier Geoffroy, Damien Poindron, Alice Maltret, Cristine Raimondo, Damien Bonnet, Sébastien Hascoët, Nicolas Derval, Michel Haïssaguerre, Mélèze Hocini, and Clinical sciences

Subjects
Adult, Male, medicine.medical_specialty, Long term follow up, Cyanotic congenital heart disease, medicine.medical_treatment, 030204 cardiovascular system & hematology, Sudden death, Sudden cardiac death, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), Internal medicine, medicine, Humans, Defibrillators, Implantable/trends, Registries, 030212 general & internal medicine, Tetralogy of Fallot, business.industry, medicine.disease, Implantable cardioverter-defibrillator, Tetralogy of Fallot/epidemiology, Defibrillators, Implantable, 3. Good health, Cardiology, Female, Cardiology and Cardiovascular Medicine, business, Follow-Up Studies
Abstract

Background: Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, and sudden cardiac death represents an important mode of death in these patients. Data evaluating the implantable cardioverter defibrillator (ICD) in this patient population remain scarce. Methods: A Nationwide French Registry including all patients with tetralogy of Fallot with an ICD was initiated in 2010 by the French Institute of Health and Medical Research. The primary time to event end point was the time from ICD implantation to first appropriate ICD therapy. Secondary outcomes included ICD-related complications, heart transplantation, and death. Clinical events were centrally adjudicated by a blinded committee. Results: A total of 165 patients (mean age, 42.2±13.3 years, 70.1% males) were included from 40 centers, including 104 (63.0%) in secondary prevention. During a median (interquartile range) follow-up of 6.8 (2.5–11.4) years, 78 (47.3%) patients received at least 1 appropriate ICD therapy. The annual incidence of the primary outcome was 10.5% (7.1% and 12.5% in primary and secondary prevention, respectively; P =0.03). Overall, 71 (43.0%) patients presented with at least 1 ICD complication, including inappropriate shocks in 42 (25.5%) patients and lead dysfunction in 36 (21.8%) patients. Among 61 (37.0%) patients in primary prevention, the annual rate of appropriate ICD therapies was 4.1%, 5.3%, 9.5%, and 13.3% in patients with, respectively, 0, 1, 2, or ≥3 guidelines-recommended risk factors. QRS fragmentation was the only independent predictor of appropriate ICD therapies (hazard ratio, 3.47 [95% CI, 1.19–10.11]), and its integration in a model with current criteria increased the 5-year time-dependent area under the curve from 0.68 to 0.81 ( P =0.006). Patients with congestive heart failure or reduced left ventricular ejection fraction had a higher risk of nonarrhythmic death or heart transplantation (hazard ratio, 11.01 [95% CI, 2.96–40.95]). Conclusions: Patients with tetralogy of Fallot and an ICD experience high rates of appropriate therapies, including those implanted in primary prevention. The considerable long-term burden of ICD-related complications, however, underlines the need for careful candidate selection. A combination of easy-to-use criteria including QRS fragmentation might improve risk stratification. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03837574.

Published
2020
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7. An International Multicenter Cohort Study on β-Blockers for the Treatment of Symptomatic Children With Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Peltenburg, Puck J., primary, Kallas, Dania, additional, Bos, Johan M., additional, Lieve, Krystien V.V., additional, Franciosi, Sonia, additional, Roston, Thomas M., additional, Denjoy, Isabelle, additional, Sorensen, Katrina B., additional, Ohno, Seiko, additional, Roses-Noguer, Ferran, additional, Aiba, Takeshi, additional, Maltret, Alice, additional, LaPage, Martin J., additional, Atallah, Joseph, additional, Giudicessi, John R., additional, Clur, Sally-Ann B., additional, Blom, Nico A., additional, Tanck, Michael, additional, Extramiana, Fabrice, additional, Kato, Koichi, additional, Barc, Julien, additional, Borggrefe, Martin, additional, Behr, Elijah R., additional, Sarquella-Brugada, Georgia, additional, Tfelt-Hansen, Jacob, additional, Zorio, Esther, additional, Swan, Heikki, additional, Kammeraad, Janneke A.E., additional, Krahn, Andrew D., additional, Davis, Andrew, additional, Sacher, Frederic, additional, Schwartz, Peter J., additional, Roberts, Jason D., additional, Skinner, Jonathan R., additional, van den Berg, Maarten P., additional, Kannankeril, Prince J., additional, Drago, Fabrizio, additional, Robyns, Tomas, additional, Haugaa, Kristina, additional, Tavacova, Terezia, additional, Semsarian, Christopher, additional, Till, Jan, additional, Probst, Vincent, additional, Brugada, Ramon, additional, Shimizu, Wataru, additional, Horie, Minoru, additional, Leenhardt, Antoine, additional, Ackerman, Michael J., additional, Sanatani, Shubhayan, additional, van der Werf, Christian, additional, and Wilde, Arthur A.M., additional

Published
2022
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8. Sudden Cardiac Arrest in Young Women

Author

Orianne Weizman, Ardalan Sharifzadehgan, Wulfran Bougouin, Kumar Narayanan, Noémie Tence, Florence Dumas, Victor Waldmann, Lionel Lamhaut, Daniel Jost, Karim Wahbi, Olivier Varenne, Rodrigue Garcia, Nicole Karam, Alain Cariou, Xavier Jouven, Eloi Marijon, JM Agostinucci, V Algalarrondo, F Alla, C Alonso, W Amara, D Annane, C Antoine, P Aubry, E Azoulay, F Beganton, D Benhamou, C Billon, W Bougouin, J Boutet, C Bruel, P Bruneval, A Cariou, P Carli, E Casalino, C Cerf, A Chaib, B Cholley, Y Cohen, A Combes, JM Coulaud, M Crahes, D Da Silva, V Das, A Demoule, I Denjoy, N Deye, G Dhonneur, JL Diehl, S Dinanian, L Domanski, D Dreyfuss, D Duboc, JL Dubois-Rande, F Dumas, JP Empana, F Extramiana, M Fartoukh, F Fieux, M Gabbas, E Gandjbakhch, G Geri, B Guidet, F Halimi, P Henry, F Hidden Lucet, P Jabre, L Jacob, L Joseph, D Jost, X Jouven, N Karam, J Lacotte, F Lapostolle, K Lahlou-Laforet, L Lamhaut, A Lanceleur, O Langeron, T Lavergne, E Lecarpentier, A Leenhardt, N Lellouche, V Lemiale, F Lemoine, F Linval, T Loeb, B Ludes, A Maltret, N Mansencal, N Mansouri, E Marijon, J Marty, E Maury, V Maxime, B Megarbane, A Mekontso-Dessap, JP Mira, X Monnet, K Narayanan, N Ngoyi, MC Perier, O Piot, P Plaisance, I Plu, M Raux, F Revaux, JD Ricard, C Richard, B Riou, F Roussin, F Santoli, F Schortgen, A Sharifzadehgan, G Sideris, C Spaulding, JL Teboul, JF Timsit, P Tuppin, C Ursat, O Varenne, A Vieillard-Baron, S Voicu, K Wahbi, and V Waldmann

Subjects
Adult, medicine.medical_specialty, Adolescent, business.industry, Sudden cardiac arrest, medicine.disease, Sudden cardiac death, Young Adult, Death, Sudden, Cardiac, Physiology (medical), Internal medicine, Cardiology, Medicine, Humans, Female, Prospective Studies, medicine.symptom, Cardiology and Cardiovascular Medicine, business
Published
2021

9. Sudden Cardiac Arrest in Young Women

Author

Weizman, Orianne, primary, Sharifzadehgan, Ardalan, additional, Bougouin, Wulfran, additional, Narayanan, Kumar, additional, Tence, Noémie, additional, Dumas, Florence, additional, Waldmann, Victor, additional, Lamhaut, Lionel, additional, Jost, Daniel, additional, Wahbi, Karim, additional, Varenne, Olivier, additional, Garcia, Rodrigue, additional, Karam, Nicole, additional, Cariou, Alain, additional, Jouven, Xavier, additional, Marijon, Eloi, additional, Agostinucci, JM, additional, Algalarrondo, V, additional, Alla, F, additional, Alonso, C, additional, Amara, W, additional, Annane, D, additional, Antoine, C, additional, Aubry, P, additional, Azoulay, E, additional, Beganton, F, additional, Benhamou, D, additional, Billon, C, additional, Bougouin, W, additional, Boutet, J, additional, Bruel, C, additional, Bruneval, P, additional, Cariou, A, additional, Carli, P, additional, Casalino, E, additional, Cerf, C, additional, Chaib, A, additional, Cholley, B, additional, Cohen, Y, additional, Combes, A, additional, Coulaud, JM, additional, Crahes, M, additional, Da Silva, D, additional, Das, V, additional, Demoule, A, additional, Denjoy, I, additional, Deye, N, additional, Dhonneur, G, additional, Diehl, JL, additional, Dinanian, S, additional, Domanski, L, additional, Dreyfuss, D, additional, Duboc, D, additional, Dubois-Rande, JL, additional, Dumas, F, additional, Empana, JP, additional, Extramiana, F, additional, Fartoukh, M, additional, Fieux, F, additional, Gabbas, M, additional, Gandjbakhch, E, additional, Geri, G, additional, Guidet, B, additional, Halimi, F, additional, Henry, P, additional, Hidden Lucet, F, additional, Jabre, P, additional, Jacob, L, additional, Joseph, L, additional, Jost, D, additional, Jouven, X, additional, Karam, N, additional, Lacotte, J, additional, Lapostolle, F, additional, Lahlou-Laforet, K, additional, Lamhaut, L, additional, Lanceleur, A, additional, Langeron, O, additional, Lavergne, T, additional, Lecarpentier, E, additional, Leenhardt, A, additional, Lellouche, N, additional, Lemiale, V, additional, Lemoine, F, additional, Linval, F, additional, Loeb, T, additional, Ludes, B, additional, Maltret, A, additional, Mansencal, N, additional, Mansouri, N, additional, Marijon, E, additional, Marty, J, additional, Maury, E, additional, Maxime, V, additional, Megarbane, B, additional, Mekontso-Dessap, A, additional, Mira, JP, additional, Monnet, X, additional, Narayanan, K, additional, Ngoyi, N, additional, Perier, MC, additional, Piot, O, additional, Plaisance, P, additional, Plu, I, additional, Raux, M, additional, Revaux, F, additional, Ricard, JD, additional, Richard, C, additional, Riou, B, additional, Roussin, F, additional, Santoli, F, additional, Schortgen, F, additional, Sharifzadehgan, A, additional, Sideris, G, additional, Spaulding, C, additional, Teboul, JL, additional, Timsit, JF, additional, Tuppin, P, additional, Ursat, C, additional, Varenne, O, additional, Vieillard-Baron, A, additional, Voicu, S, additional, Wahbi, K, additional, and Waldmann, V, additional

Published
2021
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10. Long-Term Follow-Up of Patients With Tetralogy of Fallot and Implantable Cardioverter Defibrillator

Author

Waldmann, Victor, primary, Bouzeman, Abdeslam, additional, Duthoit, Guillaume, additional, Koutbi, Linda, additional, Bessiere, Francis, additional, Labombarda, Fabien, additional, Marquié, Christelle, additional, Gourraud, Jean Baptiste, additional, Mondoly, Pierre, additional, Sellal, Jean Marc, additional, Bordachar, Pierre, additional, Hermida, Alexis, additional, Anselme, Frédéric, additional, Asselin, Anouk, additional, Audinet, Caroline, additional, Bernard, Yvette, additional, Boveda, Serge, additional, Bru, Paul, additional, Bun, Sok Sithikun, additional, Clerici, Gael, additional, Da Costa, Antoine, additional, de Guillebon, Maxime, additional, Defaye, Pascal, additional, Elbaz, Nathalie, additional, Eschalier, Romain, additional, Garcia, Rodrigue, additional, Guenancia, Charles, additional, Guy-Moyat, Benoit, additional, Halimi, Franck, additional, Irles, Didier, additional, Iserin, Laurence, additional, Jourda, François, additional, Ladouceur, Magalie, additional, Lagrange, Philippe, additional, Laredo, Mikael, additional, Mansourati, Jacques, additional, Massoulié, Grégoire, additional, Mathiron, Amel, additional, Maury, Philippe, additional, Messali, Anne, additional, Narayanan, Kumar, additional, Nguyen, Cédric, additional, Ninni, Sandro, additional, Perier, Marie-Cécile, additional, Pierre, Bertrand, additional, Pujadas, Penelope, additional, Sacher, Frédéric, additional, Sagnol, Pascal, additional, Sharifzadehgan, Ardalan, additional, Walton, Camille, additional, Winum, Pierre, additional, Zakine, Cyril, additional, Fauchier, Laurent, additional, Martins, Raphael, additional, Pasquié, Jean Luc, additional, Thambo, Jean Benoit, additional, Jouven, Xavier, additional, Combes, Nicolas, additional, Marijon, Eloi, additional, Squara, Fabien, additional, Theodore, Guillaume, additional, Scarlatti, Didier, additional, Hourdain, Jérome, additional, Deharo, Jean-Claude, additional, Ollitrault, Pierre, additional, Milliez, Paul, additional, Champ-Rigot, Laure, additional, Bader, Hugues, additional, Duplantier, Cécile, additional, Milhem, Antoine, additional, Sagnard, Audrey, additional, Bertaux, Géraldine, additional, Laurent, Gabriel, additional, Badoz, Marc, additional, Bortone, Agustin, additional, Laborie, Guillaume, additional, Rollin, Anne, additional, Stephanopoli, Quentin Voglimacci, additional, Mandel, Franck, additional, Duparc, Alexandre, additional, Domain, Guillaume, additional, Albenque, Jean-Paul, additional, Cardin, Christèle, additional, Combes, Stéphane, additional, Tanese, Nikita, additional, Hasni, Karim, additional, Leclercq, Christophe, additional, Galand, Vincent, additional, Pavin, Dominique, additional, Mabo, Philippe, additional, Behar, Nathalie, additional, Clementy, Nicolas, additional, Loose, Christophe, additional, Otmani, Akli, additional, Venier, Sandrine, additional, Carabelli, Adrien, additional, Jacon, Peggy, additional, Kilani, Mouna Ben, additional, Guichard, Jean Bapstist, additional, Romeyer-Bouchard, Cécile, additional, Le Gloan, Laurianne, additional, Probst, Vincent, additional, Freysz, Luc, additional, Blangy, Hugues, additional, Chillou, Christian De, additional, Sadoul, Nicolas, additional, Khattar, Pierre, additional, Potelle, Charlotte, additional, Jean, Frederic, additional, Puie, Paul, additional, Khoueiry, Ziad, additional, Chevallier, Philippe, additional, Dulac, Arnaud, additional, Filippo, Sylvie Di, additional, Gardey, Kevin, additional, Frey, Pierre, additional, Akret, Chrystelle, additional, Dompnier, Antoine, additional, Maupain, Carole, additional, Waintraub, Xavier, additional, Hidden-Lucet, Françoise, additional, Chastre, Thomas, additional, Gandjbakhch, Estelle, additional, Badenco, Nicolas, additional, Extramiana, Fabrice, additional, Leenhardt, Antoine, additional, Zouaghi, Amir, additional, Algalarrondo, Vincent, additional, Amet, Denis, additional, Varlet, Emilie, additional, Chalbia, Tej, additional, Philibert, Séverine, additional, Ollitrault, Jacky, additional, Lavergne, Thomas, additional, Baudinaud, Pierre, additional, Mirolo, Adrian, additional, Savouré, Arnaud, additional, Godin, Bénédicte, additional, Bertrand, Cathy, additional, Fiorello, Pierre, additional, Johnson, Nicolas, additional, Lallemand, Pierre-Marc, additional, Herminda, Alexis, additional, Hermida, Jean-Sylvain, additional, Degand, Bruno, additional, Bouazzaou, Rim El, additional, Mourot, Stéphane, additional, Goussot, Samuel, additional, Jauvert, Gaël, additional, Lazarus, Arnaud, additional, Grimard, Caroline, additional, Alonso, Christine, additional, Zhao, Alexandre, additional, Thomas, Olivier, additional, Cauchemez, Bruno, additional, Moubarak, Ghassan, additional, Lellouche, Nicolas, additional, Hamon, David, additional, Enache, Bogdan, additional, Lactu, Gabriel, additional, Wiart, Françoise, additional, Geoffroy, Olivier, additional, Poindron, Damien, additional, Maltret, Alice, additional, Raimondo, Cristine, additional, Bonnet, Damien, additional, Hascoët, Sébastien, additional, Derval, Nicolas, additional, Haïssaguerre, Michel, additional, and Hocini, Mélèze, additional

Published
2020
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11. An International Multicenter Evaluation of Inheritance Patterns, Arrhythmic Risks, and Underlying Mechanisms ofCASQ2-Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Ng, Kevin, primary, Titus, Erron W., additional, Lieve, Krystien V., additional, Roston, Thomas M., additional, Mazzanti, Andrea, additional, Deiter, Frederick H., additional, Denjoy, Isabelle, additional, Ingles, Jodie, additional, Till, Jan, additional, Robyns, Tomas, additional, Connors, Sean P., additional, Steinberg, Christian, additional, Abrams, Dominic J., additional, Pang, Benjamin, additional, Scheinman, Melvin M., additional, Bos, J. Martijn, additional, Duffett, Stephen A., additional, van der Werf, Christian, additional, Maltret, Alice, additional, Green, Martin S., additional, Rutberg, Julie, additional, Balaji, Seshadri, additional, Cadrin-Tourigny, Julia, additional, Orland, Kate M., additional, Knight, Linda M., additional, Brateng, Caitlin, additional, Wu, Jeremy, additional, Tang, Anthony S., additional, Skanes, Allan C., additional, Manlucu, Jaimie, additional, Healey, Jeff S., additional, January, Craig T., additional, Krahn, Andrew D., additional, Collins, Kathryn K., additional, Maginot, Kathleen R., additional, Fischbach, Peter, additional, Etheridge, Susan P., additional, Eckhardt, Lee L., additional, Hamilton, Robert M., additional, Ackerman, Michael J., additional, Noguer, Ferran Rosés I., additional, Semsarian, Christopher, additional, Jura, Natalia, additional, Leenhardt, Antoine, additional, Gollob, Michael H., additional, Priori, Silvia G., additional, Sanatani, Shubhayan, additional, Wilde, Arthur A.M., additional, Deo, Rahul C., additional, and Roberts, Jason D., additional

Published
2020
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12. Clinical Management of Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Gaetano M. De Ferrari, Peter J. Schwartz, Antoine Leenhardt, Maria Shkolnikova, Attilio Odero, Lia Crotti, Veronica Dusi, Michael Eldar, Maria Kharlap, J. Martijn Bos, Asaad Khoury, Carla Spazzolini, Jan Till, Ferran Rosés I. Noguer, Andrew D. Krahn, Dominic Abrams, Thomas Paul, Louise R.A. Olde Nordkamp, Andrew M. Davis, Charles I. Berul, Michael J. Ackerman, Christopher R. Moir, Arthur A.M. Wilde, Graduate School, Cardiology, ACS - Amsterdam Cardiovascular Sciences, De Ferrari, G, Dusi, V, Spazzolini, C, Bos, J, Abrams, D, Berul, C, Crotti, L, Davis, A, Eldar, M, Kharlap, M, Khoury, A, Krahn, A, Leenhardt, A, Moir, C, Odero, A, Olde Nordkamp, L, Paul, T, Rosés I Noguer, F, Shkolnikova, M, Till, J, Wilde, A, Ackerman, M, and Schwartz, P

Subjects
Tachycardia, Male, Sympathetic nervous system, Adrenergic beta-antagonists, Arrhythmias, Cardiac, Death, Genetics, Sudden, Adolescent, Child, Female, Follow-Up Studies, Humans, Ventricular, Treatment Outcome, Disease Management, Sympathectomy, Cardiology and Cardiovascular Medicine, Physiology (medical), medicine.medical_treatment, Ventricular tachycardia, Adrenergic beta-Antagonists, Tachycardia, Ventricular/diagnosis, Arrhythmia, Beta-blocker, Death, Sudden, Nervous System, Sympathetic, 3. Good health, medicine.anatomical_structure, Anesthesia, Cardiology, medicine.symptom, Ventricular/diagnosis, Human, medicine.drug, medicine.medical_specialty, Catecholaminergic polymorphic ventricular tachycardia, Asymptomatic, Follow-Up Studie, Genetic, Internal medicine, medicine, Flecainide, business.industry, MED/11 - MALATTIE DELL'APPARATO CARDIOVASCOLARE, medicine.disease, Adrenergic beta-antagonist, Sympathectomy/methods, business
Abstract

Background— Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic disorder causing life-threatening arrhythmias whenever sympathetic activity increases. β-Βlockers are the mainstay of therapy; when they fail, implantable cardioverter-defibrillators (ICDs) are used but often cause multiple shocks. Preliminary results with flecainide appear encouraging. We proposed left cardiac sympathetic denervation (LCSD) as useful additional therapy, but evidence remains anecdotal. Methods and Results— We report 63 patients with CPVT who underwent LCSD as secondary (n=54) or primary (n=9) prevention. The median post-LCSD follow-up was 37 months. The 9 asymptomatic patients remained free of major cardiac events. Of the 54 patients with prior major cardiac events either on (n=38) or off (n=16) optimal medical therapy, 13 (24%) had at least 1 recurrence: 0 patients had an aborted cardiac arrest, 2 patients had syncope only, 10 patients had ≥1 appropriate ICD discharges, and 1 patient died suddenly. The 1- and 2-year cumulative event-free survival rates were 87% and 81%. The percentage of patients with major cardiac events despite optimal medical therapy (n=38) was reduced from 100% to 32% ( P P P Conclusions— LCSD is an effective antifibrillatory intervention for patients with CPVT. Whenever syncope occurs despite optimal medical therapy, LCSD could be considered the next step rather than an ICD and could complement ICDs in patients with recurrent shocks.

Published
2015
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13. Defining the Cellular Phenotype of 'Ankyrin-B Syndrome' Variants

Author

Pascale Guicheney, Antoine Leenhardt, Jean-Jacques Schott, Iwona Driskell, Dan M. Roden, Solena Le Scouarnec, Richard B. Kim, Isabelle Denjoy, Peter J. Mohler, Denis Escande, Kris Norris, John S. Lowe, and Lise Caron

Subjects
Ankyrins, Male, Nonsynonymous substitution, Genotype, Mutant, Black People, Biology, Sudden death, Ion Channels, White People, Mice, Asian People, Torsades de Pointes, Physiology (medical), ANK2, Mexican Americans, Genetic variation, Animals, Humans, Myocytes, Cardiac, Gene, Cytoskeleton, Aged, Genetics, Genetic Variation, Arrhythmias, Cardiac, Middle Aged, Phenotype, Mice, Inbred C57BL, Long QT Syndrome, Tachycardia, Ventricular, Female, Cardiology and Cardiovascular Medicine
Abstract

Background— Mutations in the ankyrin-B gene ( ANK2 ) cause type 4 long-QT syndrome and have been described in kindreds with other arrhythmias. The frequency of ANK2 variants in large populations and molecular mechanisms underlying the variability in the clinical phenotypes are not established. More importantly, there is no cellular explanation for the range of severity of cardiac phenotypes associated with specific ANK2 variants. Methods and Results— We performed a comprehensive screen of ANK2 in populations (control, congenital arrhythmia, drug-induced long-QT syndrome) of different ethnicities to discover unidentified ANK2 variants. We identified 7 novel nonsynonymous ANK2 variants; 4 displayed abnormal activity in cardiomyocytes. Including the 4 new variants, 9 human ANK2 loss-of-function variants have been identified. However, the clinical phenotypes associated with these variants vary strikingly, from no obvious phenotype to manifest long-QT syndrome and sudden death, suggesting that mutants confer a spectrum of cellular phenotypes. We then characterized the relative severity of loss-of-function properties of all 9 nonsynonymous ANK2 variants identified to date in primary cardiomyocytes and identified a range of in vitro phenotypes, including wild-type, simple loss-of-function, and severe loss-of-function activity, seen with the variants causing severe human phenotypes. Conclusions— We present the first description of differences in cellular phenotypes conferred by specific ANK2 variants. We propose that the various degrees of ankyrin-B loss of function contribute to the range of severity of cardiac dysfunction. These data identify ANK2 variants as modulators of human arrhythmias, provide the first insight into the clinical spectrum of “ankyrin-B syndrome,” and reinforce the role of ankyrin-B–dependent protein interactions in regulating cardiac electrogenesis.

Published
2007
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14. Prognostic Value of Radionuclide Angiography in Patients With Right Ventricular Arrhythmias

Author

Michel Slama, Thomas Lavergne, Marc Faraggi, Doumit Daou, Antoine Leenhardt, Raphaël Porcher, Hélène Gauthier, Dominique Le Guludec, Salah Benelhadj, and Robert Frank

Subjects
Adult, Male, medicine.medical_specialty, Erythrocytes, Adolescent, Heart disease, Ventricular Dysfunction, Right, Cardiomyopathy, Scintigraphy, Risk Assessment, Sudden death, Electrocardiography, Text mining, Radionuclide angiography, Predictive Value of Tests, Physiology (medical), Internal medicine, medicine, Humans, Prospective Studies, Radionuclide Angiography, Aged, Aged, 80 and over, Likelihood Functions, Fourier Analysis, medicine.diagnostic_test, business.industry, Technetium, Arrhythmias, Cardiac, Stroke Volume, Middle Aged, Prognosis, medicine.disease, Survival Rate, Death, Sudden, Cardiac, Localized disease, Angiography, Cardiology, Female, Cardiology and Cardiovascular Medicine, business, Follow-Up Studies
Abstract

Background —The prognosis of patients with right ventricular (RV) arrhythmias remains uncertain. This study prospectively evaluated the prognostic value of RV and left ventricular (LV) involvement assessed by radionuclide angiography (RNA) as predictors for sudden death. Methods and Results —Patients (n=188) with severe arrhythmias originating from the RV were followed up for a mean of 45±34 months. Data on clinical presentation, resting and stress ECG, signal-averaged ECG, 24-hour Holter monitoring, and programmed stimulation were collected along with RNA. Patients were classified as group I (n=82) with normal RNA or group II (n=106) with an abnormal RV suggestive of arrhythmogenic RV cardiomyopathy, classified as diffuse or localized disease, with or without associated LV abnormalities. During follow-up, 14 patients died suddenly, all in group II. None of the clinical and electrical data were predictive of death. An abnormal RNA study was a highly predictive factor for death ( P P Conclusions —The present study confirms that arrhythmogenic RV cardiomyopathy is a severe disease with a high risk for cardiac death. Evidence of RV abnormalities in patients presenting with RV arrhythmias is highly predictive for sudden death, as is its association with LV involvement.

Published
2001
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15. Notched T Waves on Holter Recordings Enhance Detection of Patients With LQT2 ( HERG ) Mutations

Author

Guy Vaksmann, G. Maillard, Didier Klug, P. Richard, J. M. Lupoglazoff, Philippe Coumel, Isabelle Denjoy, Myriam Berthet, Pascale Guicheney, Antoine Leenhardt, Nathalie Neyroud, Bernard Hainque, and L. Demay

Subjects
Adult, Male, ERG1 Potassium Channel, medicine.medical_specialty, Potassium Channels, Heart block, Long QT syndrome, hERG, QT interval, NOTCHED T WAVES, Electrocardiography, Transcriptional Regulator ERG, Physiology (medical), Internal medicine, medicine, Humans, Cation Transport Proteins, KCNQ Potassium Channels, biology, medicine.diagnostic_test, business.industry, medicine.disease, Ether-A-Go-Go Potassium Channels, Potassium channel, Surgery, DNA-Binding Proteins, Long QT Syndrome, Potassium Channels, Voltage-Gated, KCNQ1 Potassium Channel, Mutation, Electrocardiography, Ambulatory, Trans-Activators, biology.protein, Cardiology, Female, Cardiology and Cardiovascular Medicine, business
Abstract

Background —The 2 genes KCNQ1 (LQT1) and HERG (LQT2), encoding cardiac potassium channels, are the most common cause of the dominant long-QT syndrome (LQTS). In addition to QT-interval prolongation, notched T waves have been proposed as a phenotypic marker of LQTS patients. Methods and Results —The T-wave morphology of carriers of mutations in KCNQ1 (n=133) or HERG (n=57) and of 100 control subjects was analyzed from Holter ECG recordings. Averaged T-wave templates were obtained at different cycle lengths, and potential notched T waves were classified as grade 1 (G1) in case of a bulge at or below the horizontal, whatever the amplitude, and as grade 2 (G2) in case of a protuberance above the horizontal. The highest grade obtained from a template defined the notch category of the subject. T-wave morphology was normal in the majority of LQT1 and control subjects compared with LQT2 (92%, 96%, and 19%, respectively, P P HERG . Conclusions —This study provides novel evidence that Holter recording analysis is superior to the 12-lead ECG in detecting G1 and G2 T-wave notches. These repolarization abnormalities are more indicative of LQT2 versus LQT1, with G2 notches being most specific and often reflecting HERG core domain missense mutations.

Published
2001
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16. Response to Letters Regarding Article, “Clinical Management of Catecholaminergic Polymorphic Ventricular Tachycardia: The Role of Left Cardiac Sympathetic Denervation”

Author

De Ferrari, Gaetano M., primary, Dusi, Veronica, additional, Spazzolini, Carla, additional, Bos, J. Martijn, additional, Abrams, Dominic J., additional, Berul, Charles I., additional, Crotti, Lia, additional, Eldar, Michael, additional, Kharlap, Maria, additional, Khoury, Asaad, additional, Krahn, Andrew D., additional, Leenhardt, Antoine, additional, Moir, Christopher R., additional, Odero, Attilio, additional, Nordkamp, Louise Olde, additional, Paul, Thomas, additional, i Noguer, Ferran Rosés, additional, Shkolnikova, Maria, additional, Till, Jan, additional, Wilde, Arthur A.M., additional, Ackerman, Michael J., additional, and Schwartz, Peter J., additional

Published
2016
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17. Short-coupled variant of torsade de pointes. A new electrocardiographic entity in the spectrum of idiopathic ventricular tachyarrhythmias

Author

Antoine Leenhardt, M Nurnberg, Pierre Maison-Blanche, E Glaser, M Burguera, and Philippe Coumel

Subjects
Adult, Male, medicine.medical_specialty, Time Factors, Heart disease, Ventricular Tachyarrhythmias, Long QT syndrome, Sudden death, Syncope, Electrocardiography, Heart Conduction System, Risk Factors, Torsades de Pointes, Physiology (medical), Internal medicine, medicine, Humans, Heart rate variability, medicine.diagnostic_test, business.industry, Cardiac Pacing, Artificial, medicine.disease, Defibrillators, Implantable, Autonomic nervous system, Death, Sudden, Cardiac, Verapamil, Anesthesia, Ventricular fibrillation, Electrocardiography, Ambulatory, Cardiology, Female, Cardiology and Cardiovascular Medicine, business, Follow-Up Studies
Abstract

BACKGROUND Torsade de pointes is characterized not only by its particular ECG pattern but by its context of congenital or acquired long QT syndrome and the long coupling interval of the initial premature beat. METHODS AND RESULTS We observed 14 patients aged 34.6 +/- 10 years (mean +/- SD) with no structural heart disease who presented with syncope related to a typical ECG aspect of torsade de pointes. However, there was no evidence of long QT syndrome, and the torsade had the unusual particularity of an extremely short coupling interval of the first beat or of the isolated premature beats (245 +/- 28 milliseconds). In 10 cases they deteriorated into ventricular fibrillation. Four patients had a familial history of sudden death. Only 2 patients had a tachyarrhythmia inducible by programmed stimulation. At Holter recordings the heart rate variability was globally and significantly depressed, the vagal limb of the autonomic nervous system being predominantly affected. During a mean follow-up of 7 years there were 5 deaths (4 sudden). Nine patients are alive, 3 with implanted defibrillators and 6 treated with verapamil alone. Unlike the other types of antiarrhythmic agents including beta-blockers and amiodarone, verapamil is in our experience the only drug apparently active on the arrhythmias; however, it does not prevent sudden death. CONCLUSIONS The short-coupled variant of torsade de pointes should be identified because of their ECG pattern and the risk of sudden death in young adults with no structural heart disease.

Published
1994
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18. Clinical Management of Catecholaminergic Polymorphic Ventricular Tachycardia

Author

De Ferrari, Gaetano M., primary, Dusi, Veronica, additional, Spazzolini, Carla, additional, Bos, J. Martijn, additional, Abrams, Dominic J., additional, Berul, Charles I., additional, Crotti, Lia, additional, Davis, Andrew M., additional, Eldar, Michael, additional, Kharlap, Maria, additional, Khoury, Asaad, additional, Krahn, Andrew D., additional, Leenhardt, Antoine, additional, Moir, Christopher R., additional, Odero, Attilio, additional, Olde Nordkamp, Louise, additional, Paul, Thomas, additional, Rosés i Noguer, Ferran, additional, Shkolnikova, Maria, additional, Till, Jan, additional, Wilde, Arthur A.M., additional, Ackerman, Michael J., additional, and Schwartz, Peter J., additional

Published
2015
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19. Catecholaminergic polymorphic ventricular tachycardia in children. A 7-year follow-up of 21 patients

Author

Francis Grau, V. Lucet, Antoine Leenhardt, Philippe Coumel, Isabelle Denjoy, and Dien Do Ngoc

Subjects
Tachycardia, Male, medicine.medical_specialty, Time Factors, Long QT syndrome, Adrenergic beta-Antagonists, Catecholaminergic polymorphic ventricular tachycardia, Sudden death, QT interval, Syncope, Electrocardiography, Risk Factors, Physiology (medical), Internal medicine, medicine, Humans, Child, medicine.diagnostic_test, business.industry, medicine.disease, Signal-averaged electrocardiogram, Long QT Syndrome, Nadolol, Death, Sudden, Cardiac, Anesthesia, Ventricular fibrillation, Cardiology, Exercise Test, Tachycardia, Ventricular, Female, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Follow-Up Studies
Abstract

Background Primary ventricular tachyarrhythmias are rarely seen in children. Among them, catecholaminergic polymorphic ventricular tachycardia has a poor spontaneous outcome. Its diagnosis is often delayed after the first symptoms, which is unacceptable because treatment with the appropriate β-blocker prevents sudden death. Methods and Results We observed 21 children (mean±SD age, 9.9±4 years) at the time of the diagnosis who had no structural heart disease and a normal QT interval on routine ECG. They were referred for stress- or emotion-induced syncope related to ventricular polymorphic tachyarrhythmias. The arrhythmia, consisting of isolated polymorphic ventricular extrasystoles followed by salvoes of bidirectional and polymorphic tachycardia susceptible to degeneration into ventricular fibrillation, was reproducibly induced by any form of increasing adrenergic stimulation. There was a familial history of syncope or sudden death in 30% of our patients. On receiving therapy with the appropriate β-blocker, the patients’ symptoms and polymorphic tachyarrhythmias disappeared. During a mean follow-up period of 7 years, three syncopal events and two sudden deaths occurred, probably due to treatment interruption. Conclusions The entity of adrenergic-dependent, potentially lethal tachyarrhythmia with no structural heart disease deserves to be individualized. It may form a variant of the congenital long QT syndrome in which the ECG marker is lacking; this primary ventricular arrhythmia must be looked for in a pediatric patient with stress- or emotion-induced syncope because only β-blocking therapy can prevent sudden death and therefore must be given for the patient’s lifetime.

Published
1995

20. Incidence and Risk Factors of Arrhythmic Events in Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Hayashi, Meiso, primary, Denjoy, Isabelle, additional, Extramiana, Fabrice, additional, Maltret, Alice, additional, Buisson, Nathalie Roux, additional, Lupoglazoff, Jean-Marc, additional, Klug, Didier, additional, Hayashi, Miyuki, additional, Takatsuki, Seiji, additional, Villain, Elisabeth, additional, Kamblock, Joël, additional, Messali, Anne, additional, Guicheney, Pascale, additional, Lunardi, Joël, additional, and Leenhardt, Antoine, additional

Published
2009
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21. Defining the Cellular Phenotype of “Ankyrin-B Syndrome” Variants

Author

Mohler, Peter J., primary, Le Scouarnec, Solena, additional, Denjoy, Isabelle, additional, Lowe, John S., additional, Guicheney, Pascale, additional, Caron, Lise, additional, Driskell, Iwona M., additional, Schott, Jean-Jacques, additional, Norris, Kris, additional, Leenhardt, Antoine, additional, Kim, Richard B., additional, Escande, Denis, additional, and Roden, Dan M., additional

Published
2007
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22. Mental activity, adrenergic modulation, and cardiac arrhythmias in patients with heart disease

Author

P, Coumel and A, Leenhardt

Subjects
Sympathetic Nervous System, Heart Diseases, Cardiac Pacing, Artificial, Electrocardiography, Ambulatory, Exercise Test, Humans, Arrhythmias, Cardiac, Stress, Psychological
Abstract

All of the electrophysiological mechanisms of arrhythmias are sensitive to the influences of the autonomic nervous system, particularly to its adrenergic limb. Arrhythmogenic areas may also be dependent on the inhomogeneity of these influences because of their pathophysiological structure and/or the neurogenic or humoral nature of the vector of modulation. The complexity of the various possible scenarios, combined with the role of the rate dependence, explains why standardized protocols exploring the autonomic nervous system in clinical arrhythmias are difficult to define. Invasive electrophysiology is not adapted to address the problem. Isoprenaline infusion only reproduces the humoral adrenergic stimulation to which only a few types of arrhythmias are sensitive. The exercise test is a very complex investigation if the multiple parameters involved are considered. Only a part of its limitations are obviated by the mental stress. Under natural conditions, the neurogenic origin, the intensity of the sympathetic stimulation, and its suddenness are all critical factors responsible for severe tachyarrhythmias. Arrhythmias of the long QT syndrome are particularly demonstrative of the importance of the autonomic nervous system, but this evidence can also be documented in more trivial circumstances of diseased or apparently undiseased hearts. Exploring the autonomic nervous system behavior through heart rate variability in ambulatory recordings is the most recent and fruitful method of investigation. This nonprovocative approach has technical obstacles and practical and theoretical limitations related to the fundamental nature of the autonomic nervous system, which is both a marker of the cardiac status and a determinant of arrhythmias.

Published
1991

23. Mapping and Ablation of Ventricular Fibrillation Associated With Long-QT and Brugada Syndromes

Author

Haïssaguerre, Michel, primary, Extramiana, Fabrice, additional, Hocini, Mélèze, additional, Cauchemez, Bruno, additional, Jaïs, Pierre, additional, Cabrera, Jose Angel, additional, Farre, Geronimo, additional, Leenhardt, Antoine, additional, Sanders, Prashanthan, additional, Scavée, Christophe, additional, Hsu, Li-Fern, additional, Weerasooriya, Rukshen, additional, Shah, Dipen C., additional, Frank, Robert, additional, Maury, Philippe, additional, Delay, Marc, additional, Garrigue, Stéphane, additional, and Clémenty, Jacques, additional

Published
2003
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28. Mental activity, adrenergic modulation, and cardiac arrhythmias in patients with heart disease.

Author

Coumel P and Leenhardt A

Subjects
Cardiac Pacing, Artificial, Electrocardiography, Ambulatory, Exercise Test, Humans, Arrhythmias, Cardiac physiopathology, Heart Diseases physiopathology, Stress, Psychological physiopathology, Sympathetic Nervous System physiopathology
Abstract

All of the electrophysiological mechanisms of arrhythmias are sensitive to the influences of the autonomic nervous system, particularly to its adrenergic limb. Arrhythmogenic areas may also be dependent on the inhomogeneity of these influences because of their pathophysiological structure and/or the neurogenic or humoral nature of the vector of modulation. The complexity of the various possible scenarios, combined with the role of the rate dependence, explains why standardized protocols exploring the autonomic nervous system in clinical arrhythmias are difficult to define. Invasive electrophysiology is not adapted to address the problem. Isoprenaline infusion only reproduces the humoral adrenergic stimulation to which only a few types of arrhythmias are sensitive. The exercise test is a very complex investigation if the multiple parameters involved are considered. Only a part of its limitations are obviated by the mental stress. Under natural conditions, the neurogenic origin, the intensity of the sympathetic stimulation, and its suddenness are all critical factors responsible for severe tachyarrhythmias. Arrhythmias of the long QT syndrome are particularly demonstrative of the importance of the autonomic nervous system, but this evidence can also be documented in more trivial circumstances of diseased or apparently undiseased hearts. Exploring the autonomic nervous system behavior through heart rate variability in ambulatory recordings is the most recent and fruitful method of investigation. This nonprovocative approach has technical obstacles and practical and theoretical limitations related to the fundamental nature of the autonomic nervous system, which is both a marker of the cardiac status and a determinant of arrhythmias.

Published
1991

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