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154. The yield of postmortem genetic testing in sudden death cases with structural findings at autopsy

Author

Lahrouchi, Najim, primary, Raju, Hariharan, additional, Lodder, Elisabeth M., additional, Papatheodorou, Stathis, additional, Miles, Chris, additional, Ware, James S., additional, Papadakis, Michael, additional, Tadros, Rafik, additional, Cole, Della, additional, Skinner, Jonathan R., additional, Crawford, Jackie, additional, Love, Donald R., additional, Pua, Chee J., additional, Soh, Bee Y., additional, Bhalshankar, Jaydutt D., additional, Govind, Risha, additional, Tfelt-Hansen, Jacob, additional, Winkel, Bo G., additional, van der Werf, Christian, additional, Wijeyeratne, Yanushi D., additional, Mellor, Greg, additional, Till, Janice, additional, Cohen, Marta, additional, Tome-Esteban, Maria, additional, Sharma, Sanjay, additional, Wilde, Arthur A. M., additional, Cook, Stuart A., additional, Sheppard, Mary N., additional, Bezzina, Connie R., additional, and Behr, Elijah R., additional

Published
2019
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157. Retracted and Republished: A new prediction model for ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy

Author

Cadrin-Tourigny, Julia, primary, Bosman, Laurens P, additional, Nozza, Anna, additional, Wang, Weijia, additional, Tadros, Rafik, additional, Bhonsale, Aditya, additional, Bourfiss, Mimount, additional, Fortier, Annik, additional, Lie, Øyvind H, additional, Saguner, Ardan M, additional, Svensson, Anneli, additional, Andorin, Antoine, additional, Tichnell, Crystal, additional, Murray, Brittney, additional, Zeppenfeld, Katja, additional, van den Berg, Maarten P, additional, Asselbergs, Folkert W, additional, Wilde, Arthur A M, additional, Krahn, Andrew D, additional, Talajic, Mario, additional, Rivard, Lena, additional, Chelko, Stephen, additional, Zimmerman, Stefan L, additional, Kamel, Ihab R, additional, Crosson, Jane E, additional, Judge, Daniel P, additional, Yap, Sing-Chien, additional, van der Heijden, Jeroen F, additional, Tandri, Harikrishna, additional, Jongbloed, Jan D H, additional, Guertin, Marie-Claude, additional, van Tintelen, J Peter, additional, Platonov, Pyotr G, additional, Duru, Firat, additional, Haugaa, Kristina H, additional, Khairy, Paul, additional, Hauer, Richard N W, additional, Calkins, Hugh, additional, te Riele, Anneline S J M, additional, and James, Cynthia A, additional

Published
2019
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159. Early Repolarization Pattern Inheritance in the Cardiac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER)

Author

Malhi, Navraj, primary, So, Petsy P., additional, Cheung, Christopher C., additional, Laksman, Zachary W.M., additional, Healey, Jeffrey S., additional, Chauhan, Vijay S., additional, Green, Martin S., additional, Champagne, Jean, additional, Steinberg, Christian, additional, Sanatani, Shubhayan, additional, Angaran, Paul, additional, Duff, Henry, additional, Roberts, Jason D., additional, Arbour, Laura, additional, Leather, Richard, additional, Simpson, Christopher S., additional, Tadros, Rafik, additional, Talajic, Mario, additional, Gardner, Martin, additional, Siefer, Colette, additional, and Krahn, Andrew D., additional

Published
2018
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161. B-PO01-020 MACHINE LEARNING TO PREDICT RECURRENT EVENTS FOLLOWING UNEXPLAINED CARDIAC ARREST

Author

Cheung, Christopher C., Davies, Brianna, Roberts, Jason D., Tadros, Rafik, Green, Martin S., Healey, Jeffrey S., Simpson, Christopher S., Sanatani, Shubhayan, Steinberg, Christian, Gardner, Martin J., MacIntyre, Ciorsti, Angaran, Paul, Duff, Henry J., Talajic, Mario, Hamilton, Robert M., Arbour, Laura, Leather, Richard A., Seifer, Colette M., Anne Fournier, Joza, Jacqueline E., Klein, George J., Laksman, Zachary, and Krahn, Andrew D.

Published
2021
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162. Sudden Cardiac Death Prediction in Arrhythmogenic Right Ventricular Cardiomyopathy: A Multinational Collaboration.

Author

Cadrin-Tourigny, Julia, Bosman, Laurens P., Weijia Wang, Tadros, Rafik, Bhonsale, Aditya, Bourfiss, Mimount, Lie, Øyvind H., Saguner, Ardan M., Svensson, Anneli, Andorin, Antoine, Tichnell, Crystal, Murray, Brittney, Zeppenfeld, Katja, van den Berg, Maarten P., Asselbergs, Folkert W., Wilde, Arthur A. M., Krahn, Andrew D., Talajic, Mario, Rivard, Lena, and Chelko, Stephen

Subjects
RESEARCH, RIGHT heart ventricle, RESEARCH methodology, ARRHYTHMOGENIC right ventricular dysplasia, RETROSPECTIVE studies, DISEASE incidence, WORLD health, IMPLANTABLE cardioverter-defibrillators, MEDICAL cooperation, EVALUATION research, COMPARATIVE studies, CARDIAC arrest, ELECTROCARDIOGRAPHY, RESEARCH funding, HEART physiology, STROKE volume (Cardiac output), LONGITUDINAL method, DISEASE complications
Abstract

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is associated with ventricular arrhythmias (VA) and sudden cardiac death (SCD). A model was recently developed to predict incident sustained VA in patients with ARVC. However, since this outcome may overestimate the risk for SCD, we aimed to specifically predict life-threatening VA (LTVA) as a closer surrogate for SCD.Methods: We assembled a retrospective cohort of definite ARVC cases from 15 centers in North America and Europe. Association of 8 prespecified clinical predictors with LTVA (SCD, aborted SCD, sustained, or implantable cardioverter-defibrillator treated ventricular tachycardia >250 beats per minute) in follow-up was assessed by Cox regression with backward selection. Candidate variables included age, sex, prior sustained VA (≥30s, hemodynamically unstable, or implantable cardioverter-defibrillator treated ventricular tachycardia; or aborted SCD), syncope, 24-hour premature ventricular complexes count, the number of anterior and inferior leads with T-wave inversion, left and right ventricular ejection fraction. The resulting model was internally validated using bootstrapping.Results: A total of 864 patients with definite ARVC (40±16 years; 53% male) were included. Over 5.75 years (interquartile range, 2.77-10.58) of follow-up, 93 (10.8%) patients experienced LTVA including 15 with SCD/aborted SCD (1.7%). Of the 8 prespecified clinical predictors, only 4 (younger age, male sex, premature ventricular complex count, and number of leads with T-wave inversion) were associated with LTVA. Notably, prior sustained VA did not predict subsequent LTVA (P=0.850). A model including only these 4 predictors had an optimism-corrected C-index of 0.74 (95% CI, 0.69-0.80) and calibration slope of 0.95 (95% CI, 0.94-0.98) indicating minimal over-optimism.Conclusions: LTVA events in patients with ARVC can be predicted by a novel simple prediction model using only 4 clinical predictors. Prior sustained VA and the extent of functional heart disease are not associated with subsequent LTVA events. [ABSTRACT FROM AUTHOR]

Published
2021
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163. Yield and pitfalls of ajmaline testing in the evaluation of unexplained cardiac arrest and sudden unexplained death: Single centre experience of 482 families

Author

Tadros, Rafik, Nannenberg, Eline A., Lieve, Krystien V., Skoric-Milosavljevic, Doris, Lahrouchi, Najim, Lekanne Dit Deprez, Ronald H., Vendrik, Jeroen, Reckman, Yolan J., Postema, Pieter G., Amin, Ahmad S., Bezzina, Connie R., Wilde, Arthur A. M., Tan, Hanno L., Human Genetics, ACS - Amsterdam Cardiovascular Sciences, Graduate School, Cardiology, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Other Research, ACS - Heart failure & arrhythmias, ACS - Pulmonary hypertension & thrombosis, ACS - Microcirculation, and ACS - Atherosclerosis & ischemic syndromes

Published
2017

164. A Genotype-phenotype Taxonomy of Hypertrophic Cardiomyopathy

Author

Curran, Lara, Marvao, Antonio De, Inglese, Paolo, McGurk, Kathryn, Clement, Adam, Zheng, Sean, Li, Surui, Pua, Chee Jian, Shah, Mit, Jafari, Mina, Theotokis, Pantazis, Buchan, Rachel, Jurgens, Sean, Raphael, Claire, Baksi, John, Pantazis, Antonis, Halliday, Brian, Pennell, Dudley, Bai, Wenjia, Chin, Calvin, Tadros, Rafik, Bezzina, Connie, Watkins, Hugh, Cook, Stuart, Prasad, Sanjay, Ware, James, and O'Regan, Declan

Published
2024
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165. Missense variants in the spectrin repeat domain of DSP are associated with arrhythmogenic cardiomyopathy: A family report and systematic review.

Author

Grondin, Steffany, Wazirian, Avedis‐Christ, Jorda, Paloma, Terrone, Donato G., Gagnon, Johannie, Robb, Laura, Amyot, Julie, Rivard, Lena, Pagé, Sylvain, Talajic, Mario, Cadrin‐Tourigny, Julia, and Tadros, Rafik

Abstract

Rare loss of function variants in DSP, which codes for the desmosomal protein desmoplakin, have been implicated in dilated and arrhythmogenic right ventricular cardiomyopathies. We present a family with arrhythmogenic cardiomyopathy associated with a novel missense variant in DSP (NM_004415.4): c.877G>A, p.(Glu293Lys). The phenotype is characterized by predominant involvement of the left ventricle with systolic dysfunction, fibrosis, and life‐threatening arrhythmias. We performed a systematic review of literature collecting all cardiomyopathy cases with rare missense variants in DSP. We demonstrate that the distribution of missense variants across the protein domains in cardiomyopathy cases differs from that in gnomAD (p =.04), with a case enrichment of rare missense variants in the spectrin repeat domain (36/78 [46%] in cases vs. 449/1495 [30%] in gnomAD; p =.004). Our findings highlight the predominance of cardiac arrhythmia and left ventricular involvement in desmoplakin cardiomyopathy and pinpoint to a potential mutation hotspot in DSP thereby facilitating missense variant interpretation in the diagnostic setting. [ABSTRACT FROM AUTHOR]

Published
2020
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166. Atrial fibrillation in young patients

Author

Gourraud, Jean-Baptiste, primary, Khairy, Paul, additional, Abadir, Sylvia, additional, Tadros, Rafik, additional, Cadrin-Tourigny, Julia, additional, Macle, Laurent, additional, Dyrda, Katia, additional, Mondesert, Blandine, additional, Dubuc, Marc, additional, Guerra, Peter G., additional, Thibault, Bernard, additional, Roy, Denis, additional, Talajic, Mario, additional, and Rivard, Lena, additional

Published
2018
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168. Yield and Pitfalls of Ajmaline Testing in the Evaluation of Unexplained Cardiac Arrest and Sudden Unexplained Death

Author

Tadros, Rafik, primary, Nannenberg, Eline A., additional, Lieve, Krystien V., additional, Škorić-Milosavljević, Doris, additional, Lahrouchi, Najim, additional, Lekanne Deprez, Ronald H., additional, Vendrik, Jeroen, additional, Reckman, Yolan J., additional, Postema, Pieter G., additional, Amin, Ahmad S., additional, Bezzina, Connie R., additional, Wilde, Arthur A.M., additional, and Tan, Hanno L., additional

Published
2017
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171. Common genetic variants and modifiable risk factors underpin hypertrophic cardiomyopathy susceptibility and expressivity

Author

Harper, Andrew R., Goel, Anuj, Grace, Christopher, Thomson, Kate L., Petersen, Steffen E., Xu, Xiao, Waring, Adam, Ormondroyd, Elizabeth, Kramer, Christopher M., Ho, Carolyn Y., Neubauer, Stefan, Tadros, Rafik, Ware, James S., Bezzina, Connie R., Farrall, Martin, and Watkins, Hugh

Abstract

Hypertrophic cardiomyopathy (HCM) is a common, serious, genetic heart disorder. Rare pathogenic variants in sarcomere genes cause HCM, but with unexplained phenotypic heterogeneity. Moreover, most patients do not carry such variants. We report a genome-wide association study of 2,780 cases and 47,486 controls that identified 12 genome-wide-significant susceptibility loci for HCM. Single-nucleotide polymorphism heritability indicated a strong polygenic influence, especially for sarcomere-negative HCM (64% of cases; h2g?=?0.34?±?0.02). A genetic risk score showed substantial influence on the odds of HCM in a validation study, halving the odds in the lowest quintile and doubling them in the highest quintile, and also influenced phenotypic severity in sarcomere variant carriers. Mendelian randomization identified diastolic blood pressure (DBP) as a key modifiable risk factor for sarcomere-negative HCM, with a one standard deviation increase in DBP increasing the HCM risk fourfold. Common variants and modifiable risk factors have important roles in HCM that we suggest will be clinically actionable.

Published
2021
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172. Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect

Author

Tadros, Rafik, Francis, Catherine, Xu, Xiao, Vermeer, Alexa M. C., Harper, Andrew R., Huurman, Roy, Kelu Bisabu, Ken, Walsh, Roddy, Hoorntje, Edgar T., te Rijdt, Wouter P., Buchan, Rachel J., van Velzen, Hannah G., van Slegtenhorst, Marjon A., Vermeulen, Jentien M., Offerhaus, Joost Allard, Bai, Wenjia, de Marvao, Antonio, Lahrouchi, Najim, Beekman, Leander, Karper, Jacco C., Veldink, Jan H., Kayvanpour, Elham, Pantazis, Antonis, Baksi, A. John, Whiffin, Nicola, Mazzarotto, Francesco, Sloane, Geraldine, Suzuki, Hideaki, Schneider-Luftman, Deborah, Elliott, Paul, Richard, Pascale, Ader, Flavie, Villard, Eric, Lichtner, Peter, Meitinger, Thomas, Tanck, Michael W. T., van Tintelen, J. Peter, Thain, Andrew, McCarty, David, Hegele, Robert A., Roberts, Jason D., Amyot, Julie, Dubé, Marie-Pierre, Cadrin-Tourigny, Julia, Giraldeau, Geneviève, L’Allier, Philippe L., Garceau, Patrick, Tardif, Jean-Claude, Boekholdt, S. Matthijs, Lumbers, R. Thomas, Asselbergs, Folkert W., Barton, Paul J. R., Cook, Stuart A., Prasad, Sanjay K., O’Regan, Declan P., van der Velden, Jolanda, Verweij, Karin J. H., Talajic, Mario, Lettre, Guillaume, Pinto, Yigal M., Meder, Benjamin, Charron, Philippe, de Boer, Rudolf A., Christiaans, Imke, Michels, Michelle, Wilde, Arthur A. M., Watkins, Hugh, Matthews, Paul M., Ware, James S., and Bezzina, Connie R.

Abstract

The heart muscle diseases hypertrophic (HCM) and dilated (DCM) cardiomyopathies are leading causes of sudden death and heart failure in young, otherwise healthy, individuals. We conducted genome-wide association studies and multi-trait analyses in HCM (1,733 cases), DCM (5,521 cases) and nine left ventricular (LV) traits (19,260 UK Biobank participants with structurally normal hearts). We identified 16 loci associated with HCM, 13 with DCM and 23 with LV traits. We show strong genetic correlations between LV traits and cardiomyopathies, with opposing effects in HCM and DCM. Two-sample Mendelian randomization supports a causal association linking increased LV contractility with HCM risk. A polygenic risk score explains a significant portion of phenotypic variability in carriers of HCM-causing rare variants. Our findings thus provide evidence that polygenic risk score may account for variability in Mendelian diseases. More broadly, we provide insights into how genetic pathways may lead to distinct disorders through opposing genetic effects.

Published
2021
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173. Utility of Post-Mortem Genetic Testing in Cases of Sudden Arrhythmic Death Syndrome

Author

Lahrouchi, Najim, Raju, Hariharan, Lodder, Elisabeth M, Papatheodorou, Efstathios, Ware, James S, Papadakis, Michael, Tadros, Rafik, Cole, Della, Skinner, Jonathan R, Crawford, Jackie, Love, Donald R, Pua, Chee J, Soh, Bee Y, Bhalshankar, Jaydutt D, Govind, Risha, Tfelt-Hansen, Jacob, Winkel, Bo G, van der Werf, Christian, Wijeyeratne, Yanushi D, Mellor, Greg, Till, Jan, Cohen, Marta C, Tome-Esteban, Maria, Sharma, Sanjay, Wilde, Arthur A M, Cook, Stuart A, Bezzina, Connie R, Sheppard, Mary N, Behr, Elijah R, Lahrouchi, Najim, Raju, Hariharan, Lodder, Elisabeth M, Papatheodorou, Efstathios, Ware, James S, Papadakis, Michael, Tadros, Rafik, Cole, Della, Skinner, Jonathan R, Crawford, Jackie, Love, Donald R, Pua, Chee J, Soh, Bee Y, Bhalshankar, Jaydutt D, Govind, Risha, Tfelt-Hansen, Jacob, Winkel, Bo G, van der Werf, Christian, Wijeyeratne, Yanushi D, Mellor, Greg, Till, Jan, Cohen, Marta C, Tome-Esteban, Maria, Sharma, Sanjay, Wilde, Arthur A M, Cook, Stuart A, Bezzina, Connie R, Sheppard, Mary N, and Behr, Elijah R

Abstract

BACKGROUND: Sudden arrhythmic death syndrome (SADS) describes a sudden death with negative autopsy and toxicological analysis. Cardiac genetic disease is a likely etiology.OBJECTIVES: This study investigated the clinical utility and combined yield of post-mortem genetic testing (molecular autopsy) in cases of SADS and comprehensive clinical evaluation of surviving relatives.METHODS: We evaluated 302 expertly validated SADS cases with suitable DNA (median age: 24 years; 65% males) who underwent next-generation sequencing using an extended panel of 77 primary electrical disorder and cardiomyopathy genes. Pathogenic and likely pathogenic variants were classified using American College of Medical Genetics (ACMG) consensus guidelines. The yield of combined molecular autopsy and clinical evaluation in 82 surviving families was evaluated. A gene-level rare variant association analysis was conducted in SADS cases versus controls.RESULTS: A clinically actionable pathogenic or likely pathogenic variant was identified in 40 of 302 cases (13%). The main etiologies established were catecholaminergic polymorphic ventricular tachycardia and long QT syndrome (17 [6%] and 11 [4%], respectively). Gene-based rare variants association analysis showed enrichment of rare predicted deleterious variants in RYR2 (p = 5 × 10-5). Combining molecular autopsy with clinical evaluation in surviving families increased diagnostic yield from 26% to 39%.CONCLUSIONS: Molecular autopsy for electrical disorder and cardiomyopathy genes, using ACMG guidelines for variant classification, identified a modest but realistic yield in SADS. Our data highlighted the predominant role of catecholaminergic polymorphic ventricular tachycardia and long QT syndrome, especially the RYR2 gene, as well as the minimal yield from other genes. Furthermore, we showed the enhanced utility of combined clinical and genetic evaluation.

Published
2017

174. Pulmonary Vein Stenosis After Atrial Fibrillation Ablation: Insights From the ADVICE Trial

Author

Samuel, Michelle, Khairy, Paul, Mongeon, François-Pierre, Andrade, Jason G., Gomes, Sophie, Galvan, Zurine, Weerasooriya, Rukshen, Novak, Paul, Nault, Isabelle, Arentz, Thomas, Deisenhofer, Isabel, Veenhuyzen, George D., Jaïs, Pierre, Parkash, Ratika, Verma, Atul, Menon, Syamkumar, Puererfellner, Helmut, Scavée, Christophe, Talajic, Mario, Guerra, Peter G., Rivard, Lena, Dubuc, Marc, Dyrda, Katia, Thibault, Bernard, Mondesert, Blandine, Tadros, Rafik, Cadrin-Tourigny, Julia, Aguilar, Martin, Tardif, Jean-Claude, Levesque, Sylvie, Roy, Denis, Nattel, Stanley, and Macle, Laurent

Abstract

Pulmonary vein (PV) stenosis is a complication of atrial fibrillation (AF) ablation. The incidence of PV stenosis after routine post-ablation imaging remains unclear and is limited to single-centre studies. Our objective was to determine the incidence and predictors of PV stenosis following circumferential radiofrequency ablation in the multicentre Adenosine Following Pulmonary Vein Isolation to Target Dormant Conduction Elimination (ADVICE) trial.

Published
2020
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177. The Brugada Syndrome Susceptibility Gene HEY2 Modulates Cardiac Transmural Ion Channel Patterning and Electrical Heterogeneity

Author

Veerman, Christiaan C., primary, Podliesna, Svitlana, additional, Tadros, Rafik, additional, Lodder, Elisabeth M., additional, Mengarelli, Isabella, additional, de Jonge, Berend, additional, Beekman, Leander, additional, Barc, Julien, additional, Wilders, Ronald, additional, Wilde, Arthur A.M., additional, Boukens, Bastiaan J., additional, Coronel, Ruben, additional, Verkerk, Arie O., additional, Remme, Carol Ann, additional, and Bezzina, Connie R., additional

Published
2017
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179. Loss-of-Function KCNE2 Variants

Author

Roberts, Jason D., primary, Krahn, Andrew D., additional, Ackerman, Michael J., additional, Rohatgi, Ram K., additional, Moss, Arthur J., additional, Nazer, Babak, additional, Tadros, Rafik, additional, Gerull, Brenda, additional, Sanatani, Shubhayan, additional, Wijeyeratne, Yanushi D., additional, Baruteau, Alban-Elouen, additional, Muir, Alison R., additional, Pang, Benjamin, additional, Cadrin-Tourigny, Julia, additional, Talajic, Mario, additional, Rivard, Lena, additional, Tester, David J., additional, Liu, Taylor, additional, Whitman, Isaac R., additional, Wojciak, Julianne, additional, Conacher, Susan, additional, Gula, Lorne J., additional, Leong-Sit, Peter, additional, Manlucu, Jaimie, additional, Green, Martin S., additional, Hamilton, Robert, additional, Healey, Jeff S., additional, Lopes, Coeli M., additional, Behr, Elijah R., additional, Wilde, Arthur A., additional, Gollob, Michael H., additional, and Scheinman, Melvin M., additional

Published
2017
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180. Genetic Testing in the Evaluation of Unexplained Cardiac Arrest

Author

Mellor, Greg, primary, Laksman, Zachary W.M., additional, Tadros, Rafik, additional, Roberts, Jason D., additional, Gerull, Brenda, additional, Simpson, Christopher S., additional, Klein, George J., additional, Champagne, Jean, additional, Talajic, Mario, additional, Gardner, Martin, additional, Steinberg, Christian, additional, Arbour, Laura, additional, Birnie, David H., additional, Angaran, Paul, additional, Leather, Richard, additional, Sanatani, Shubhayan, additional, Chauhan, Vijay S., additional, Seifer, Colette, additional, Healey, Jeffrey S., additional, and Krahn, Andrew D., additional

Published
2017
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181. Utility of Post-Mortem Genetic Testing in Cases of Sudden Arrhythmic Death Syndrome

Author

Lahrouchi, Najim, primary, Raju, Hariharan, additional, Lodder, Elisabeth M., additional, Papatheodorou, Efstathios, additional, Ware, James S., additional, Papadakis, Michael, additional, Tadros, Rafik, additional, Cole, Della, additional, Skinner, Jonathan R., additional, Crawford, Jackie, additional, Love, Donald R., additional, Pua, Chee J., additional, Soh, Bee Y., additional, Bhalshankar, Jaydutt D., additional, Govind, Risha, additional, Tfelt-Hansen, Jacob, additional, Winkel, Bo G., additional, van der Werf, Christian, additional, Wijeyeratne, Yanushi D., additional, Mellor, Greg, additional, Till, Jan, additional, Cohen, Marta C., additional, Tome-Esteban, Maria, additional, Sharma, Sanjay, additional, Wilde, Arthur A.M., additional, Cook, Stuart A., additional, Bezzina, Connie R., additional, Sheppard, Mary N., additional, and Behr, Elijah R., additional

Published
2017
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183. Exome sequencing identifies primary carnitine deficiency in a family with cardiomyopathy and sudden death

Author

Lahrouchi, Najim, primary, Lodder, Elisabeth M, additional, Mansouri, Maria, additional, Tadros, Rafik, additional, Zniber, Layla, additional, Adadi, Najlae, additional, Clur, Sally-Ann B, additional, van Spaendonck-Zwarts, Karin Y, additional, Postma, Alex V, additional, Sefiani, Abdelaziz, additional, Ratbi, Ilham, additional, and Bezzina, Connie R, additional

Published
2017
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184. An International Multicenter Evaluation of Type 5 Long QT Syndrome

Author

Roberts, Jason D., Asaki, S. Yukiko, Mazzanti, Andrea, Bos, J. Martijn, Tuleta, Izabela, Muir, Alison R., Crotti, Lia, Krahn, Andrew D., Kutyifa, Valentina, Shoemaker, M. Benjamin, Johnsrude, Christopher L., Aiba, Takeshi, Marcondes, Luciana, Baban, Anwar, Udupa, Sharmila, Dechert, Brynn, Fischbach, Peter, Knight, Linda M., Vittinghoff, Eric, Kukavica, Deni, Stallmeyer, Birgit, Giudicessi, John R., Spazzolini, Carla, Shimamoto, Keiko, Tadros, Rafik, Cadrin-Tourigny, Julia, Duff, Henry J., Simpson, Christopher S., Roston, Thomas M., Wijeyeratne, Yanushi D., El Hajjaji, Imane, Yousif, Maisoon D., Gula, Lorne J., Leong-Sit, Peter, Chavali, Nikhil, Landstrom, Andrew P., Marcus, Gregory M., Dittmann, Sven, Wilde, Arthur A. M., Behr, Elijah R., Tfelt-Hansen, Jacob, Scheinman, Melvin M., Perez, Marco V., Kaski, Juan Pablo, Gow, Robert M., Drago, Fabrizio, Aziz, Peter F., Abrams, Dominic J., Gollob, Michael H., Skinner, Jonathan R., Shimizu, Wataru, Kaufman, Elizabeth S., Roden, Dan M., Zareba, Wojciech, Schwartz, Peter J., Schulze-Bahr, Eric, Etheridge, Susan P., Priori, Silvia G., and Ackerman, Michael J.

Abstract

Supplemental Digital Content is available in the text.

Published
2020
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185. The yield of postmortem genetic testing in sudden death cases with structural findings at autopsy

Author

Lahrouchi, Najim, Raju, Hariharan, Lodder, Elisabeth M., Papatheodorou, Stathis, Miles, Chris, Ware, James S., Papadakis, Michael, Tadros, Rafik, Cole, Della, Skinner, Jonathan R., Crawford, Jackie, Love, Donald R., Pua, Chee J., Soh, Bee Y., Bhalshankar, Jaydutt D., Govind, Risha, Tfelt-Hansen, Jacob, Winkel, Bo G., van der Werf, Christian, Wijeyeratne, Yanushi D., Mellor, Greg, Till, Janice, Cohen, Marta, Tome-Esteban, Maria, Sharma, Sanjay, Wilde, Arthur A. M., Cook, Stuart A., Sheppard, Mary N., Bezzina, Connie R., and Behr, Elijah R.

Abstract

Sudden cardiac death (SCD) is often associated with structural abnormalities of the heart during autopsy. This study sought to compare the diagnostic yield of postmortem genetic testing in (1) cases with structural findings of uncertain significance at autopsy to (2) cases with autopsy findings diagnostic of cardiomyopathy. We evaluated 57 SCD cases with structural findings at cardiac autopsy. Next-generation sequencing using a panel of 77 primary electrical disorder and cardiomyopathy genes was performed. Pathogenic and likely pathogenic variants were classified using American College of Medical Genetics (ACMG) consensus guidelines. In 29 cases (51%) autopsy findings of uncertain significance were identified whereas in 28 cases (49%) a diagnosis of cardiomyopathy was established. We identified a pathogenic or likely pathogenic variant in 10 cases (18%); in 1 (3%) case with non-specific autopsy findings compared with 9 (32%) cases with autopsy findings diagnostic of cardiomyopathy (p= 0.0054). The yield of genetic testing in SCD cases with autopsy findings consistent with cardiomyopathy is comparable with the yield in cardiomyopathy patients that are alive. Genetic testing in cases with findings of uncertain significance offers lower clinical utility than in cardiomyopathy, with lower yields than detected previously. This highlights the need for stringent evaluation of variant pathogenicity.

Published
2020
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186. new prediction model for ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy.

Author

Cadrin-Tourigny, Julia, Bosman, Laurens P, Nozza, Anna, Wang, Weijia, Tadros, Rafik, Bhonsale, Aditya, Bourfiss, Mimount, Fortier, Annik, Lie, Øyvind H, Saguner, Ardan M, Svensson, Anneli, Andorin, Antoine, Tichnell, Crystal, Murray, Brittney, Zeppenfeld, Katja, Berg, Maarten P van den, Asselbergs, Folkert W, Wilde, Arthur A M, Krahn, Andrew D, and Talajic, Mario

Published
2019
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188. Canadian Cardiovascular Society Clinical Practice Update on Contemporary Management of the Patient With Hypertrophic Cardiomyopathy

Author

Crean, Andrew M., Adler, Arnon, Arbour, Laura, Chan, Joyce, Christian, Susan, Cooper, Robert M., Garceau, Patrick, Giraldeau, Genevieve, Heydari, Bobak, Laksman, Zachary, Mital, Seema, Ong, Kevin, Overgaard, Christopher, Ruel, Marc, Seifer, Colette M., Ward, Michael R., and Tadros, Rafik

Abstract

Numerous guidelines on the diagnosis and management of hypertrophic cardiomyopathy (HCM) have been published, by learned societies, over the past decade. Although helpful they are often long and less adapted to nonexperts. This writing panel was challenged to produce a document that grew as much from years of practical experience as it did from the peer-reviewed literature. As such, rather than produce yet another set of guidelines, we aim herein to deliver a concentrate of our own experiential learning and distill for the reader the essence of effective and appropriate HCM care. This Clinical Practice Update on HCM is therefore aimed at general cardiologists and other cardiovascular practitioners rather than for HCM specialists. We set the stage with a description of the condition and its clinical presentation, discuss the central importance of “obstruction” and how to look for it, review the role of cardiac magnetic resonance imaging, reflect on the appropriate use of genetic testing, review the treatment options for symptomatic HCM—crucially including cardiac myosin inhibitors, and deal concisely with practical issues surrounding risk assessment for sudden cardiac death, and management of the end-stage HCM patient. Uniquely, we have captured the pediatric experience on our panel to discuss appropriate differences in the management of younger patients with HCM. We ask the reader to remember that this document represents expert consensus opinion rather than dogma and to use their best judgement when dealing with the HCM patient in front of them.

Published
2024
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189. TECRL, a new life‐threatening inherited arrhythmia gene associated with overlapping clinical features of both LQTS and CPVT

Author

Devalla, Harsha D, primary, Gélinas, Roselle, additional, Aburawi, Elhadi H, additional, Beqqali, Abdelaziz, additional, Goyette, Philippe, additional, Freund, Christian, additional, Chaix, Marie‐A, additional, Tadros, Rafik, additional, Jiang, Hui, additional, Le Béchec, Antony, additional, Monshouwer‐Kloots, Jantine J, additional, Zwetsloot, Tom, additional, Kosmidis, Georgios, additional, Latour, Frédéric, additional, Alikashani, Azadeh, additional, Hoekstra, Maaike, additional, Schlaepfer, Jurg, additional, Mummery, Christine L, additional, Stevenson, Brian, additional, Kutalik, Zoltan, additional, de Vries, Antoine AF, additional, Rivard, Léna, additional, Wilde, Arthur AM, additional, Talajic, Mario, additional, Verkerk, Arie O, additional, Al‐Gazali, Lihadh, additional, Rioux, John D, additional, Bhuiyan, Zahurul A, additional, and Passier, Robert, additional

Published
2016
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191. Dronedarone

Author

Tadros, Rafik, primary, Nattel, Stanley, additional, and Andrade, Jason G., additional

Published
2016
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192. Abstract 17352: Predictors of Ventricular Arrhythmias and Sudden Death in a Quebec Cohort With Brugada Syndrome

Author

Rivard, Lena, primary, Roux, Antoine, additional, Nault, Isabelle, additional, Champagne, Jean, additional, Roux, Jean-Francois, additional, Talajic, Mario, additional, Tadros, Rafik, additional, Cadrin-Tourigny, Julia, additional, Shohoudi, Azadeh, additional, Mondesert, Blandine, additional, Roy, Denis, additional, Macle, Laurent, additional, Andrade, Jason, additional, Dyrda, Katia, additional, Dubuc, Marc, additional, Guerra, Peter G, additional, Sarrazin, Jean-Francois, additional, Thibault, Bernard, additional, and Khairy, Paul, additional

Published
2015
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193. Blinded Randomized Trial of Anticoagulation to Prevent Ischemic Stroke and Neurocognitive Impairment in Atrial Fibrillation (BRAIN-AF): Methods and Design

Author

Rivard, Lena, Khairy, Paul, Talajic, Mario, Tardif, Jean-Claude, Nattel, Stanley, Bherer, Louis, Black, Sandra, Healey, Jeffrey, Lanthier, Sylvain, Andrade, Jason, Massoud, Fadi, Nault, Isabelle, Guertin, Marie-Claude, Dorian, Paul, Kouz, Simon, Essebag, Vidal, Ellenbogen, Kenneth A., Wyse, George, Racine, Normand, Macle, Laurent, Mondesert, Blandine, Dyrda, Katia, Tadros, Rafik, Guerra, Peter, Thibault, Bernard, Cadrin-Tourigny, Julia, Dubuc, Marc, Roux, Jean-Francois, Mayrand, Helene, Greiss, Isabelle, and Roy, Denis

Abstract

Compelling evidence showing a link between atrial fibrillation (AF) and cognitive decline and dementia is accumulating.

Published
2019
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194. Pregnancy in Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Cheung, Christopher C., Lieve, Krystien V., Roston, Thomas M., van der Ree, Martijn H., Deyell, Marc W., Andrade, Jason G., Laksman, Zachary W., Nannenberg, Eline A., Tadros, Rafik, Pang, Benjamin, Rutberg, Julie, Green, Martin S., Conacher, Susan, Seifer, Colette M., Roberts, Jason D., Steinberg, Christian, Sanatani, Shubhayan, Wilde, Arthur A., and Krahn, Andrew D.

Abstract

This investigation was a retrospective study of catecholaminergic polymorphic ventricular tachycardia (CPVT) patients in Canada and the Netherlands to compare pregnancy, postpartum, and nonpregnant event rates.

Published
2019
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195. Challenge and Impact of Quinidine Access in Sudden Death Syndromes

Author

Malhi, Navraj, Cheung, Christopher C., Deif, Bishoy, Roberts, Jason D., Gula, Lorne J., Green, Martin S., Pang, Benjamin, Sultan, Omar, Konieczny, Kaja M., Angaran, Paul, Dorian, Paul, Lashevsky, Ilan, Healey, Jeff S., Alak, Aiman, Tadros, Rafik, Andorin, Antoine, Steinberg, Christian, Ayala-Paredes, Felix, Simpson, Christopher S., Atallah, Joseph, and Krahn, Andrew D.

Abstract

This study sought to determine the nature of quinidine use and accessibility in a national network of inherited arrhythmia clinics.

Published
2019
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196. Caractéristiques et origine fonctionnelle des propriétés fréquentielles du noeud auriculoventriculaire

Author

Tadros, Rafik and Billette, Jacques

Subjects
Période réfractaire, Heart rate, Atrioventricular node, Propriétés fréquentielles, Tachycardie supraventriculaire, Conduction, Refractory period, Electrophysiology, Supraventricular tachycardia, Recovery, Rate-dependent properties, Électrophysiologie, Fréquence cardiaque, Facilitation, Récupération, Noeud auriculoventriculaire, Fatigue
Abstract

Le nœud auriculoventriculaire (AV) joue un rôle vital dans le cœur normal et pathologique. Il connecte les oreillettes aux ventricules et, grâce à sa conduction lente, génère un délai entre les contractions auriculaire et ventriculaire permettant d’optimiser le pompage sanguin. Sa conduction lente et sa longue période réfractaire font du nœud AV un filtre d’impulsions auriculaires lors de tachyarythmies assurant ainsi une fréquence ventriculaire plus lente favorable au débit cardiaque. L’optimisation de ce filtrage est une cible dans le traitement de ces arythmies. Malgré ce rôle vital et de nombreuses études, le nœud AV demeure l’objet de plusieurs controverses qui en rendent la compréhension laborieuse. Nos études expérimentales sur des préparations isolées de cœurs de lapin visent à apporter des solutions à certains des problèmes qui limitent la compréhension des propriétés fréquentielles du nœud AV. Le premier problème concerne la définition de la propriété de récupération nodale. On s’accorde généralement sur la dépendance du temps de conduction nodale (intervalle auriculo-Hissien, AH) du temps de récupération qui le précède mais un débat presque centenaire persiste sur la façon de mesurer ce temps de récupération. Selon que l’on utilise à cette fin la longueur du cycle auriculaire (AA) ou l’intervalle His-auriculaire précédent (HA), la même réponse nodale montre des caractéristiques différentes, un paradoxe à ce jour inexpliqué. Le temps de conduction nodale augmente aussi avec le degré et la durée d'une fréquence rapide, un phénomène appelé fatigue. Or, les caractéristiques de la fatigue mesurée varient avec l’indice de récupération utilisé (AA vs. HA). De plus, une troisième propriété appelée facilitation qui entraîne un raccourcissement du temps de conduction diffère aussi avec l’indice de récupération utilisé. Pour établir l’origine de ce problème, nous avons déterminé les différences entre les courbes de récupération (AH compilé en fonction du AA ou HA) pour 30 états fonctionnels nodaux différents. Ces conditions étaient obtenues à l’aide de protocoles permettant la variation du cycle de base (BCL) et du cycle prétest (PTCL), deux paramètres connus pour altérer la fonction nodale. Nous avons pu établir que pour chaque état fonctionnel, la forme de la courbe de récupération et le niveau de fatigue étaient les mêmes pour les deux indices de récupération. Ceci s’applique aussi aux données obtenues à des BCL et PTCL égaux comme dans les protocoles de stimulation prématurée conventionnels couramment utilisés. Nos résultats ont établi pour la première fois que les propriétés nodales de récupération et de fatigue sont indépendantes de l’indice de récupération utilisé. Nos données montrent aussi que les différences entre les courbes de récupération en fonction de l’indice utilisé proviennent d’effets associés aux variations du PTCL. Notre deuxième étude établit à partir des mêmes données pourquoi les variations du PTCL altèrent différemment les courbes de récupération selon l’indice utilisé. Nous avons démontré que ces différences augmentaient en proportion directe avec l’augmentation du temps de conduction au battement prétest. Cette augmentation cause un déplacement systématique de la courbe construite avec l’intervalle AA vers la droite et de celle construite avec l’intervalle HA vers la gauche. Ce résultat met en évidence l’importance de tenir compte des changements du temps de conduction prétest dans l’évaluation de la fonction nodale, un paramètre négligé dans la plupart des études. Ce résultat montre aussi que chacun des deux indices a des limites dans sa capacité d’évaluer le temps de récupération nodale réel lorsque le temps de conduction prétest varie. Lorsque ces limites sont ignorées, comme c’est habituellement le cas, elles entraînent un biais dans l’évaluation des effets de fatigue et de facilitation. Une autre grande difficulté dans l’évaluation des propriétés fréquentielles du nœud AV concerne son état réfractaire. Deux indices sont utilisés pour évaluer la durée de la période réfractaire nodale. Le premier est la période réfractaire efficace (ERPN) définie comme l’intervalle AA le plus long qui n’est pas conduit par le nœud. Le deuxième est la période réfractaire fonctionnelle (FRPN) qui correspond à l’intervalle minimum entre deux activations mesurées à la sortie du nœud. Paradoxalement et pour des raisons obscures, l’ERPN augmente alors que la FRPN diminue avec l’augmentation de la fréquence cardiaque. De plus, ces effets varient grandement avec les sujets, les espèces et l’âge. À partir des mêmes données que pour les deux autres études, nous avons cherché dans la troisième étude l’origine des variations fréquentielles de l’ERPN et de la FRPN. Le raccourcissement du BCL prolonge l’ERPN mais n’affecte pas la FRPN. L’allongement de l’ERPN provient principalement d’un allongement du temps de conduction prétest. Un PTCL court en comparaison avec un BCL court allonge encore plus substantiellement le temps de conduction prétest mais raccourcit en même temps l’intervalle His-auriculaire, ces deux effets opposés s’additionnent pour produire un allongement net de l’ERPN. Le raccourcissement de l’intervalle His-auriculaire par le PTCL court est aussi entièrement responsable pour le raccourcissement de la FRPN. Nous avons aussi établi que, lorsque la composante du temps de conduction prétest est retirée de l’ERPN, un lien linéaire existe entre la FRPN et l’ERPN à cause de leur dépendance commune de l’intervalle His-auriculaire. Le raccourcissement combiné du BCL et du PTCL produit des effets nets prévisibles à partir de leurs effets individuels. Ces effets reproduisent ceux obtenus lors de protocoles prématurés conventionnels. Ces observations supportent un nouveau schème fonctionnel des variations fréquentielles de l’ERPN et de la FRPN à partir des effets distincts du BCL et du PTCL. Elles établissent aussi un nouveau lien entre les variations fréquentielles de l’ERPN et de la FRPN. En conclusion, la modulation fréquentielle de la fonction du nœud AV provient de la combinaison d’effets concurrents cumulatifs liés au cycle de base et non-cumulatifs liés au cycle prétest. Ces effets peuvent être interprétés de façon consistante indépendamment de l’indice de récupération en tenant compte des changements du temps de conduction au battement prétest. Les effets fréquentiels disparates sur l’ERPN et la FRPN sont aussi grandement liés aux changements du temps de conduction prétest. Lorsque l’analyse tient compte de ce facteur, l’ERPN et la FRPN montrent des variations parallèles fortement liées à celles de l’intervalle His-auriculaire. Le nouveau schème fonctionnel des propriétés fréquentielles du nœud AV supporté par nos données aidera à mieux cibler les études sur les mécanismes cellulaires contrôlant la modulation fréquentielle nodale. Nos données pourraient aider à l’interprétation et au contrôle des réponses nodales diverses associées aux tachyarythmies supraventriculaires et à leur traitement pharmacologique. En bref, nos travaux supportent une compréhension factuelle améliorée du comportement fréquentiel du nœud AV, un domaine aux applications multiples en rythmologie cardiaque., The atrioventricular (AV) node is the sole electrical connection between atria and ventricles, and is of utmost importance in both normal and perturbed cardiac function. Through slow conduction, it generates a delay between atrial and ventricular systoles, thereby optimising cardiac output. The AV node also has a long refractory period which confers it a filtering role during supraventricular tachyarrhythmias. Because of this ventricular rate watchdog role, the AV node has become a primary therapeutic target in atrial fibrillation, a frequent arrhythmia with major clinical burden. Not withstanding intense research, understanding of AV nodal function remains restrained by many controversies, some of which have persisted for almost a century. Major obstacles concern the definition of nodal recovery time and nodal refractoriness. The objective of our studies is to untangle some of these controversies regarding rate-dependent AV nodal function in an experimental model of superfused rabbit heart preparations. Our first study concerns the definition of AV nodal recovery time used to assess rate-dependent nodal function. The dependence of conduction time through the node (atrio-His interval; AH) on time elapsed since last activation i.e., recovery time (RT), is a well accepted fact but its assessment is controversial for nearly a century. This problem arises from the fact that the nodal recovery function shows different characteristics depending upon whether RT is assessed from the preceding atrial cycle length (AA) or His-atrial (HA) interval. Moreover, the rate- and time-dependent increase in AH, known as fatigue, also shows different characteristics depending on RT index used. Furthermore, the third rate-dependent AV nodal property known as facilitation and that tends to shorten AH with penultimate cycle length, is obviously present or virtually absent when studying it with HA or AA index, respectively. Our first study sought to identify the source of this paradoxical apparent dependence of nodal rate-dependent properties on selected RT index. For this purpose, we varied two known independent modulators of AV nodal function, the basic (BCL) and pretest cycle length (PTCL), in 30 different combinations and assessed how the resulting 30 nodal functional states alter the recovery and the fatigue property as assessed with both recovery indexes. We found that, for each functional state, the shape of the nodal recovery curve and the level of fatigue was identical regardless of selected recovery index. We thus documented for the first time that recovery and fatigue properties are consistent whether assessed with HA or AA. However, we also found that PTCL effects appeared different on the two recovery curve formats. In a second study, using the same data, we investigated the origin of PTCL related variations of nodal recovery curves constructed with different recovery indexes. We found that PTCL shortening induced rightward AA curve shifts and leftward HA curve shifts proportional to the increase in pretest conduction time. Moreover, these curve shifts affected all data points equally. This finding suggests that both AA and HA indexes are biased by increases in pretest conduction time. These increases appeared to delay nodal recovery for an identical AA, and to hasten nodal recovery for an identical HA. Uncontrolled changes in pretest conduction time during fast rates thus produce apparent different effects depending on nodal recovery index. Taking into account changes in pretest conduction time results in unified rate-dependent nodal conduction properties regardless of chosen recovery index. Another major problem in AV nodal physiology relates to rate-dependent changes in nodal refractoriness. Two indexes of nodal refractoriness, effective (ERPN) and functional (FRPN) refractory periods, are commonly determined. ERPN and FRPN correspond to the longest AA resulting in nodal block and shortest interval between successive His bundle activations, respectively. For unclear reasons, increasing rate typically results in ERPN prolongation but FRPN shortening, and these effects vary greatly with individuals, ages and species. In a third study, we assessed the functional origin of rate-induced changes in ERPN and FRPN. BCL shortening prolonged ERPN but did not significantly affect FRPN. This ERPN prolongation mainly arose from an increase in pretest conduction time. PTCL shortening also prolonged the pretest conduction time and hence ERPN, but this prolongation was partly counterbalanced by a decrease in the His-atrial subinterval at ERPN. Similar PTCL-induced His-atrial shortening also fully accounted for FRPN shortening. Notably, we found that when ERPN is corrected for the increase in pretest conduction time, ERPN and FRPN vary in parallel according to their respective His-atrial subintervals. Combined BCL and PTCL shortening, including those corresponding to standard commonly used protocols, result in net changes in refractory measures predictable from the sum of their individual effects. These observations not only support a new functional scheme for rate-dependent AV nodal refractoriness but also establish a relationship between ERPN and FRPN which, for a long time, were thought to reflect different nodal properties. In conclusion, rate-dependent AV nodal function reflect the net sum of concurrent yet independent cumulative and non-cumulative effects arising from BCL and PTCL changes, respectively. Nodal recovery and fatigue properties are independent of recovery index. Rate-induced non-cumulative variations in nodal recovery curves originate from changes in pretest conduction time and reflect current limitations of recovery indexes to precisely measure exact nodal recovery time. Changes in pretest conduction time also explain opposite rate-induced changes in ERPN and FRPN. When these changes are taken into account, FRPN and ERPN vary in parallel with heart rate and largely depend on His-atrial interval. These data support a new functional model of rate-dependent nodal conduction and refractoriness, which may help guide studies on underlying cellular and ionic mechanisms as well as on nodal behaviour during supraventricular tachyarrhythmias.

Published
2011

200. Abstract 14782: Incidence and Characteristics of Pulmonary Vein Stenosis Following Catheter Ablation of Atrial Fibrillation: Insights From the Contemporary Multicenter ADVICE Trial

Author

Gomes, Sophie, primary, Khairy, Paul, additional, Andrade, Jason, additional, Nattel, Stanley, additional, Talajic, Mario, additional, Guerra, Peter G, additional, RIvard, Lena, additional, Dubuc, Marc, additional, Dyrda, Katia, additional, Thibault, Bernard, additional, Montdesert, Blandine, additional, Levesque, Sylvie, additional, Tadros, Rafik, additional, Malliet, Nicolas, additional, Venier, Sandrine, additional, Millette, Catherine, additional, Roy, Denis, additional, and Macle, Laurent, additional

Published
2014
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