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3. 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

5. Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy

Author

Roberts, Jason D, Murphy, Nathaniel P, Hamilton, Robert M, Lubbers, Ellen R, James, Cynthia A, Kline, Crystal F, Gollob, Michael H, Krahn, Andrew D, Sturm, Amy C, Musa, Hassan, El-Refaey, Mona, Koenig, Sara, Aneq, Meriam Åström, Hoorntje, Edgar T, Graw, Sharon L, Davies, Robert W, Rafiq, Muhammad Arshad, Koopmann, Tamara T, Aafaqi, Shabana, Fatah, Meena, Chiasson, David A, Taylor, Matthew RG, Simmons, Samantha L, Han, Mei, van Opbergen, Chantal JM, Wold, Loren E, Sinagra, Gianfranco, Mittal, Kirti, Tichnell, Crystal, Murray, Brittney, Codima, Alberto, Nazer, Babak, Nguyen, Duy T, Marcus, Frank I, Sobriera, Nara, Lodder, Elisabeth M, van den Berg, Maarten P, Spears, Danna A, Robinson, John F, Ursell, Philip C, Green, Anna K, Skanes, Allan C, Tang, Anthony S, Gardner, Martin J, Hegele, Robert A, van Veen, Toon AB, Wilde, Arthur AM, Healey, Jeff S, Janssen, Paul ML, Mestroni, Luisa, van Tintelen, J Peter, Calkins, Hugh, Judge, Daniel P, Hund, Thomas J, Scheinman, Melvin M, and Mohler, Peter J

Subjects
Heart Disease, Cardiovascular, Clinical Research, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Animals, Ankyrins, Arrhythmogenic Right Ventricular Dysplasia, Disease Models, Animal, Female, Humans, Indoles, Male, Maleimides, Mice, Mice, Knockout, Myocardium, Wnt Signaling Pathway, beta Catenin, Arrhythmias, Cardiology, Cardiovascular disease, Cell Biology, Genetic diseases, Medical and Health Sciences, Immunology
Abstract

Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal β-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and β-catenin. A pharmacological activator of the WNT/β-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and β-catenin, and evidence for targeted activation of the WNT/β-catenin pathway as a potential treatment for this disease.

Published
2019

6. Atrial Fibrillation Ablation in Heart Failure With Reduced vs Preserved Ejection Fraction

Author

Oraii, Alireza, primary, McIntyre, William F., additional, Parkash, Ratika, additional, Kowalik, Krzysztof, additional, Razeghi, Ghazal, additional, Benz, Alexander P., additional, Belley-Côté, Emilie P., additional, Conen, David, additional, Connolly, Stuart J., additional, Tang, Anthony S. L., additional, Healey, Jeff S., additional, and Wong, Jorge A., additional

Published
2024
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8. Long-Term Outcomes of Resynchronization–Defibrillation for Heart Failure

Author

Sapp, John L., primary, Sivakumaran, Soori, additional, Redpath, Calum J., additional, Khan, Habib, additional, Parkash, Ratika, additional, Exner, Derek V., additional, Healey, Jeff S., additional, Thibault, Bernard, additional, Sterns, Laurence D., additional, Lam, Nhat Hung N., additional, Manlucu, Jaimie, additional, Mokhtar, Ahmed, additional, Sumner, Glen, additional, McKinlay, Stuart, additional, Kimber, Shane, additional, Mondesert, Blandine, additional, Talajic, Mario, additional, Rouleau, Jean, additional, McCarron, C. Elizabeth, additional, Wells, George, additional, and Tang, Anthony S. L., additional

Published
2024
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10. PO-05-175 THE TEMPORAL RELATIONSHIP BETWEEN VENTRICULAR ARRHYTHMIAS AND MORTALITY: INSIGHTS FROM THE RESYNCHRONIZATION IN AMBULATORY HEART FAILURE TRIAL (RAFT)

Author

Samuel, Michelle, primary, Tang, Anthony S., additional, Wells, George A., additional, Gardner, Martin, additional, Healey, Jeffrey S., additional, Parkash, Ratika, additional, Beauchamp, Marie-Eve, additional, Thibault, Bernard, additional, Sterns, Laurence D., additional, Birnie, David H., additional, Nery, Pablo B., additional, Sivakumaran, Soori T., additional, Essebag, Vidal, additional, and Sapp, John L., additional

Published
2023
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12. PO-02-027 RELATIONSHIP BETWEEN SEX, BODY SIZE, AND CRT BENEFIT: A PATIENT LEVEL META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS

Author

Friedman, Daniel J., primary, Al-Khatib, Sana M., additional, Cleland, John G., additional, Dalgaard, Frederik, additional, Fudim, Marat, additional, Abraham, William T., additional, Curtis, Anne B., additional, Gold, Michael R., additional, Kutyifa, Valentina, additional, Linde, Cecilia M., additional, Tang, Anthony S., additional, Olivas-Martinez, Antonio, additional, Inoue, Lurdes, additional, and Sanders, Gillian, additional

Published
2023
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14. Bundle Branch Re-Entrant Ventricular Tachycardia: Novel Genetic Mechanisms in a Life-Threatening Arrhythmia

Author

Roberts, Jason D., Gollob, Michael H., Young, Charlie, Connors, Sean P., Gray, Chris, Wilton, Stephen B., Green, Martin S., Zhu, Dennis W., Hodgkinson, Kathleen A., Poon, Annie, Li, Qiuju, Orr, Nathan, Tang, Anthony S., Klein, George J., Wojciak, Julianne, Campagna, Joan, Olgin, Jeffrey E., Badhwar, Nitish, Vedantham, Vasanth, Marcus, Gregory M., Kwok, Pui-Yan, Deo, Rahul C., and Scheinman, Melvin M.

Published
2017
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16. Cardiac Resynchronization Therapy Improves Outcomes in Patients With Intraventricular Conduction Delay But Not Right Bundle Branch Block: A Patient-Level Meta-Analysis of Randomized Controlled Trials

Author

Friedman, Daniel J., primary, Al-Khatib, Sana M., additional, Dalgaard, Frederik, additional, Fudim, Marat, additional, Abraham, William T., additional, Cleland, John G.F., additional, Curtis, Anne B., additional, Gold, Michael R., additional, Kutyifa, Valentina, additional, Linde, Cecilia, additional, Tang, Anthony S., additional, Ali-Ahmed, Fatima, additional, Olivas-Martinez, Antonio, additional, Inoue, Lurdes Y.T., additional, and Sanders, Gillian D., additional

Published
2023
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19. CE-540-01 EFFICACY OF BURST VS RAMP ATP FOR SLOW VT

Author

Hindi, Mathew, primary, Sandhu, Jeslene K., additional, Schwab, Katerina, additional, Singh, Sarah, additional, Tang, Anthony S., additional, Healey, Jeffrey S., additional, Thibault, Bernard, additional, Sapp, John L., additional, Essebag, Vidal, additional, Nery, Pablo B., additional, Sterns, Laurence D., additional, Birnie, David H., additional, and Bennett, Matthew T., additional

Published
2022
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20. CE-522-01 COMPARISON OF THE EFFICACY OF BI-V VS RV BURST ATP IN TERMINATING VT IN PATIENTS WITH NON-ISCHEMIC VS ISCHEMIC CARDIOMYOPATHY

Author

Hindi, Mathew, primary, Schwab, Katerina, additional, Sandhu, Jeslene K., additional, Singh, Sarah, additional, Tang, Anthony S., additional, Healey, Jeffrey S., additional, Thibault, Bernard, additional, Sapp, John L., additional, Essebag, Vidal, additional, Nery, Pablo B., additional, Sterns, Laurence D., additional, Birnie, David H., additional, and Bennett, Matthew T., additional

Published
2022
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22. BS-400-20 COMPARISON OF THE EFFICACY OF BI-V VS RV BURST ATP IN TERMINATING VT IN PATIENTS WITH NON-ISCHEMIC VS ISCHEMIC CARDIOMYOPATHY

Author

Hindi, Mathew, primary, Schwab, Katerina, additional, Sandhu, Jeslene K., additional, Singh, Sarah, additional, Tang, Anthony S., additional, Healey, Jeffrey S., additional, Thibault, Bernard, additional, Sapp, John L., additional, Essebag, Vidal, additional, Nery, Pablo B., additional, Sterns, Laurence D., additional, Birnie, David H., additional, and Bennett, Matthew T., additional

Published
2022
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25. Achieving bi‐directional conduction block during catheter ablation is not enough to prevent recurrence of cavo‐tricuspid isthmus dependant atrial flutter: Role of subclinical conduction.

Author

CLS Di Nubila, Bruna, Divulwewa, Keerthi, Tang, Anthony S. L., and Agarwal, Sharad C.

Subjects
DISEASE relapse prevention, SCIENTIFIC observation, CATHETER ablation, ATRIAL flutter, RETROSPECTIVE studies, HEART block, ELECTROPHYSIOLOGY, DESCRIPTIVE statistics
Abstract

Background: Achieving bi‐directional conduction block, as assessed by differential pacing and change in activation along tricuspid annulus (TA), across the cavo‐tricuspid isthmus (CTI), is considered a satisfactory end point during catheter ablation of atrial flutter (AFL). Aim: To assess role of subclinical conduction by observing polarity reversal of local bipolar signals from RS to QR pattern lateral to the line of ablation, in predicting recurrence of CTI dependant AFL after ablation in patients with bidirectional conduction block. Method and Results: Of 683 patients undergoing ablation of CTI dependent AFL, 73 (10.6%) patients underwent redo flutter ablation and were evaluated further. The mean age was 60.8 years and 51% were males. Evidence of bidirectional block by differential pacing and change is activation along multipolar catheter and reversal of local bipolar signals from RS to QR pattern lateral to the line of ablation, during the 1st and subsequent procedure, were studied. 60% patients had confirmed bidirectional block of which 71% had lack of voltage reversal, at the end of 1st procedure. All patients with bidirectional block with lack of reversal of bipolar signals, after the first procedure had recurrence of AFL whereas only 3/11 (27%) people with bidirectional block and with absence of subclinical conduction had recurrence of AFL. Conclusion: Achieving bidirectional conduction block is not sufficient to prevent recurrence of AFL after CTI ablation. Reversal of local bipolar signals, from RS to QR pattern along with achieving bidirectional conduction delay would reduce recurrence of AFL, post ablation. [ABSTRACT FROM AUTHOR]

Published
2023
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32. Evaluating Polygenic Risk Scores in “Lone” Atrial Fibrillation

Author

Lazarte, Julieta, primary, Dron, Jacqueline S., additional, McIntyre, Adam D., additional, Skanes, Allan C., additional, Gula, Lorne J., additional, Tang, Anthony S., additional, Tadros, Rafik, additional, Laksman, Zachary W., additional, Hegele, Robert A., additional, and Roberts, Jason D., additional

Published
2021
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33. Role of Common Genetic Variation in Lone Atrial Fibrillation

Author

Lazarte, Julieta, primary, Dron, Jacqueline S., additional, McIntyre, Adam D., additional, Skanes, Allan C., additional, Gula, Lorne J., additional, Tang, Anthony S., additional, Tadros, Rafik, additional, Laksman, Zachary W., additional, Hegele, Robert A., additional, and Roberts, Jason D., additional

Published
2021
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39. 2012 EHRA/HRS expert consensus statement on cardiac resynchronization therapy in heart failure: implant and follow-up recommendations and management: A registered branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society; and in collaboration with the Heart Failure Society of America (HFSA), the American Society of Echocardiography (ASE), the American Heart Association (AHA), the European Association of Echocardiography (EAE) of the ESC and the Heart Failure Association of the ESC (HFA).: Endorsed by the governing bodies of AHA, ASE, EAE, HFSA, HFA, EHRA, and HRS

Author

Daubert, Jean-Claude, Saxon, Leslie, Adamson, Philip B., Auricchio, Angelo, Berger, Ronald D., Beshai, John F., Breithard, Ole, Brignole, Michele, Cleland, John, DeLurgio, David B., Dickstein, Kenneth, Exner, Derek V., Gold, Michael, Grimm, Richard A., Hayes, David L., Israel, Carsten, Leclercq, Christophe, Linde, Cecilia, Lindenfeld, JoAnn, Merkely, Bela, Mont, Lluis, Murgatroyd, Francis, Prinzen, Frits, Saba, Samir F., Shinbane, Jerold S., Singh, Jagmeet, Tang, Anthony S., Vardas, Panos E., Wilkoff, Bruce L., Zamorano, Jose Luis, Anand, Inder, Blomström-Lundqvist, Carina, Boehmer, John P., Calkins, Hugh, Cazeau, Serge, Delgado, Victoria, Estes, N.A. Mark, Haines, David, Kusumoto, Fred, Leyva, Paco, Ruschitzka, Frank, Stevenson, Lynne Warner, and Torp-Pedersen, Christian Tobias

Published
2012
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40. Identification of a gene responsible for familial Wolff-Parkinson-White syndrome

Author

Gollob, Michael H., Green, Martin S., Tang, Anthony S.-L., Gollub, Tanya, Karibe, Akihiko, Hassan, Sayegh Al-, Ahmad, Ferhaan, Lozado, Ryan, Shah, Gopi, Fananapazir, Lameh, Bachinski, Linda L., and Roberts, Robert

Subjects
Wolff-Parkinson-White syndrome -- Genetic aspects, Gene mutations -- Health aspects
Abstract

A gene mutation on chromosome seven appears to be one cause of a heart arrhythmia called Wolff-Parkinson-White syndrome, according to a study of two families with 31 members who have the syndrome. The mutation is located at 7q34-q36 and affects the gamma2 regulatory subunit of AMP-activated protein kinase.

Published
2001

41. A simple maneuver to determine if septal accessory pathway ablation requires a left atrial approach

Author

Kanawati, Juliana, primary, Roberts, Jason D., additional, Rowe, Matthew K., additional, Khan, Habib, additional, Chan, William K., additional, Leong‐Sit, Peter, additional, Manlucu, Jaimie, additional, Yee, Raymond, additional, Tang, Anthony S., additional, Gula, Lorne J., additional, Skanes, Allan C., additional, and Klein, George J., additional

Published
2020
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42. 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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48. Ankyrin-B dysfunction predisposes to arrhythmogenic cardiomyopathy and is amenable to therapy

Author

Roberts, Jason D., Murphy, Nathaniel P., Hamilton, Robert M., Lubbers, Ellen R., James, Cynthia A., Kline, Crystal F., Gollob, Michael H., Krahn, Andrew D., Sturm, Amy C., Musa, Hassan, El-Refaey, Mona, Koenig, Sara, Åström, Meriam, Hoorntje, Edgar T., Graw, Sharon L., Davies, Robert W., Rafiq, Muhammad Arshad, Koopmann, Tamara T., Aafaqi, Shabana, Fatah, Meena, Chiasson, David A., Taylor, Matthew R. G., Simmons, Samantha L., Han, Mei, van Opbergen, Chantal J. M., Wold, Loren E., Sinagra, Gianfranco, Mittal, Kirti, Tichnell, Crystal, Murray, Brittney, Codima, Alberto, Nazer, Babak, Nguyen, Duy T., Marcus, Frank I., Sobriera, Nara, Lodder, Elisabeth M., van den Berg, Maarten P., Spears, Danna A., Robinson, John F., Ursell, Philip C., Gréen, Anna, Skanes, Allan C., Tang, Anthony S., Gardner, Martin J., Hegele, Robert A., van Veen, Toon A. B., Wilde, Arthur A. M., Healey, Jeff S., Janssen, Paul M. L., Mestroni, Luisa, van Tintelen, J. Peter, Calkins, Hugh, Judge, Daniel P., Hund, Thomas J., Scheinman, Melvin M., Mohler, Peter J., Roberts, Jason D., Murphy, Nathaniel P., Hamilton, Robert M., Lubbers, Ellen R., James, Cynthia A., Kline, Crystal F., Gollob, Michael H., Krahn, Andrew D., Sturm, Amy C., Musa, Hassan, El-Refaey, Mona, Koenig, Sara, Åström, Meriam, Hoorntje, Edgar T., Graw, Sharon L., Davies, Robert W., Rafiq, Muhammad Arshad, Koopmann, Tamara T., Aafaqi, Shabana, Fatah, Meena, Chiasson, David A., Taylor, Matthew R. G., Simmons, Samantha L., Han, Mei, van Opbergen, Chantal J. M., Wold, Loren E., Sinagra, Gianfranco, Mittal, Kirti, Tichnell, Crystal, Murray, Brittney, Codima, Alberto, Nazer, Babak, Nguyen, Duy T., Marcus, Frank I., Sobriera, Nara, Lodder, Elisabeth M., van den Berg, Maarten P., Spears, Danna A., Robinson, John F., Ursell, Philip C., Gréen, Anna, Skanes, Allan C., Tang, Anthony S., Gardner, Martin J., Hegele, Robert A., van Veen, Toon A. B., Wilde, Arthur A. M., Healey, Jeff S., Janssen, Paul M. L., Mestroni, Luisa, van Tintelen, J. Peter, Calkins, Hugh, Judge, Daniel P., Hund, Thomas J., Scheinman, Melvin M., and Mohler, Peter J.

Abstract

Arrhythmogenic cardiomyopathy (ACM) is an inherited arrhythmia syndrome characterized by severe structural and electrical cardiac phenotypes, including myocardial fibrofatty replacement and sudden cardiac death. Clinical management of ACM is largely palliative, owing to an absence of therapies that target its underlying pathophysiology, which stems partially from our limited insight into the condition. Following identification of deceased ACM probands possessing ANK2 rare variants and evidence of ankyrin-B loss of function on cardiac tissue analysis, an ANK2 mouse model was found to develop dramatic structural abnormalities reflective of human ACM, including biventricular dilation, reduced ejection fraction, cardiac fibrosis, and premature death. Desmosomal structure and function appeared preserved in diseased human and murine specimens in the presence of markedly abnormal beta-catenin expression and patterning, leading to identification of a previously unknown interaction between ankyrin-B and beta-catenin. A pharmacological activator of the WNT/beta-catenin pathway, SB-216763, successfully prevented and partially reversed the murine ACM phenotypes. Our findings introduce what we believe to be a new pathway for ACM, a role of ankyrin-B in cardiac structure and signaling, a molecular link between ankyrin-B and beta-catenin, and evidence for targeted activation of the WNT/beta-catenin pathway as a potential treatment for this disease., Funding Agencies|Marianne Barrie Philanthropic Fund; Canadian Institutes of Health Research [RN332805]; Netherlands CardioVascular Research Initiative: the Dutch Heart Foundation; Dutch Federation of University Medical Centers; Netherlands Organisation for Health Research and Development; Royal Netherlands Academy of Sciences [CVON-PREDICT 2012-10]; Netherlands Cardiovascular Research Initiative - Dutch Heart Foundation [CVON2012-10 PREDICT CVON2018-30 PREDICT2, CVON2015-12 eDETECT]; Netherlands Organization for Scientific Research (NWO) [040.11.586]; Fondation Leducq [16 CVD 02]; Dr. Francis P. Chiramonte Private Foundation; Leyla Erkan Family Fund for ARVD Research; Robin Shah ARVD Fund at Johns Hopkins; Bogle Foundation; Healing Hearts Foundation; Campanella Family; Patrick J. Harrison Family; Peter French Memorial Foundation; Wilmerding Endowments; NIH [HL135754, HL134824, HL139348, HL135096, HL114383, HL114893, HL137331, HL137325, 2UM1HG006542, UL1 TR 001079]; Ohio State Frick Center; JB Project

Published
2019
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