Electromechanical substrate characterization in arrhythmogenic cardiomyopathy using imaging-based patient-specific computer simulations
Abstract Aims Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. The aim of this study is to use computer simulations to non-invasively estimate the individual patient’s myocardial tissue...
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| Vydáno v: | Europace (London, England) Ročník 23; číslo Supplement_1; s. i153 - i160 |
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| Hlavní autoři: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
Oxford University Press
04.03.2021
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| ISSN: | 1099-5129, 1532-2092, 1532-2092 |
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| Abstract | Abstract
Aims
Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. The aim of this study is to use computer simulations to non-invasively estimate the individual patient’s myocardial tissue substrates underlying regional right ventricular (RV) deformation abnormalities in a cohort of AC mutation carriers.
Methods and results
In 68 AC mutation carriers and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS), and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects. Using the individual’s deformation data as model input, this protocol automatically estimated regional RVfw and global IVS and LVfw tissue properties. The computational model was able to reproduce clinically measured regional deformation patterns for all subjects, with highly reproducible parameter estimations. Simulations revealed that regional RVfw heterogeneity of both contractile function and compliance were increased in subjects with clinically advanced disease compared to mutation carriers without clinically established disease (17 ± 13% vs. 8 ± 4%, P = 0.01 and 18 ± 11% vs. 10 ± 7%, P < 0.01, respectively). No significant difference in activation delay was found.
Conclusion
Regional RV deformation abnormalities in AC mutation carriers were related to reduced regional contractile function and tissue compliance. In clinically advanced disease stages, a characteristic apex-to-base heterogeneity of tissue abnormalities was present in the majority of the subjects, with most pronounced disease in the basal region of the RVfw. |
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| AbstractList | Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. The aim of this study is to use computer simulations to non-invasively estimate the individual patient's myocardial tissue substrates underlying regional right ventricular (RV) deformation abnormalities in a cohort of AC mutation carriers.
In 68 AC mutation carriers and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS), and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects. Using the individual's deformation data as model input, this protocol automatically estimated regional RVfw and global IVS and LVfw tissue properties. The computational model was able to reproduce clinically measured regional deformation patterns for all subjects, with highly reproducible parameter estimations. Simulations revealed that regional RVfw heterogeneity of both contractile function and compliance were increased in subjects with clinically advanced disease compared to mutation carriers without clinically established disease (17 ± 13% vs. 8 ± 4%, P = 0.01 and 18 ± 11% vs. 10 ± 7%, P < 0.01, respectively). No significant difference in activation delay was found.
Regional RV deformation abnormalities in AC mutation carriers were related to reduced regional contractile function and tissue compliance. In clinically advanced disease stages, a characteristic apex-to-base heterogeneity of tissue abnormalities was present in the majority of the subjects, with most pronounced disease in the basal region of the RVfw. Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. The aim of this study is to use computer simulations to non-invasively estimate the individual patient's myocardial tissue substrates underlying regional right ventricular (RV) deformation abnormalities in a cohort of AC mutation carriers.AIMSArrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. The aim of this study is to use computer simulations to non-invasively estimate the individual patient's myocardial tissue substrates underlying regional right ventricular (RV) deformation abnormalities in a cohort of AC mutation carriers.In 68 AC mutation carriers and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS), and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects. Using the individual's deformation data as model input, this protocol automatically estimated regional RVfw and global IVS and LVfw tissue properties. The computational model was able to reproduce clinically measured regional deformation patterns for all subjects, with highly reproducible parameter estimations. Simulations revealed that regional RVfw heterogeneity of both contractile function and compliance were increased in subjects with clinically advanced disease compared to mutation carriers without clinically established disease (17 ± 13% vs. 8 ± 4%, P = 0.01 and 18 ± 11% vs. 10 ± 7%, P < 0.01, respectively). No significant difference in activation delay was found.METHODS AND RESULTSIn 68 AC mutation carriers and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS), and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects. Using the individual's deformation data as model input, this protocol automatically estimated regional RVfw and global IVS and LVfw tissue properties. The computational model was able to reproduce clinically measured regional deformation patterns for all subjects, with highly reproducible parameter estimations. Simulations revealed that regional RVfw heterogeneity of both contractile function and compliance were increased in subjects with clinically advanced disease compared to mutation carriers without clinically established disease (17 ± 13% vs. 8 ± 4%, P = 0.01 and 18 ± 11% vs. 10 ± 7%, P < 0.01, respectively). No significant difference in activation delay was found.Regional RV deformation abnormalities in AC mutation carriers were related to reduced regional contractile function and tissue compliance. In clinically advanced disease stages, a characteristic apex-to-base heterogeneity of tissue abnormalities was present in the majority of the subjects, with most pronounced disease in the basal region of the RVfw.CONCLUSIONRegional RV deformation abnormalities in AC mutation carriers were related to reduced regional contractile function and tissue compliance. In clinically advanced disease stages, a characteristic apex-to-base heterogeneity of tissue abnormalities was present in the majority of the subjects, with most pronounced disease in the basal region of the RVfw. Abstract Aims Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac dysfunction. The aim of this study is to use computer simulations to non-invasively estimate the individual patient’s myocardial tissue substrates underlying regional right ventricular (RV) deformation abnormalities in a cohort of AC mutation carriers. Methods and results In 68 AC mutation carriers and 20 control subjects, regional longitudinal deformation patterns of the RV free wall (RVfw), interventricular septum (IVS), and left ventricular free wall (LVfw) were obtained using speckle-tracking echocardiography. We developed and used a patient-specific parameter estimation protocol based on the multi-scale CircAdapt cardiovascular system model to create virtual AC subjects. Using the individual’s deformation data as model input, this protocol automatically estimated regional RVfw and global IVS and LVfw tissue properties. The computational model was able to reproduce clinically measured regional deformation patterns for all subjects, with highly reproducible parameter estimations. Simulations revealed that regional RVfw heterogeneity of both contractile function and compliance were increased in subjects with clinically advanced disease compared to mutation carriers without clinically established disease (17 ± 13% vs. 8 ± 4%, P = 0.01 and 18 ± 11% vs. 10 ± 7%, P < 0.01, respectively). No significant difference in activation delay was found. Conclusion Regional RV deformation abnormalities in AC mutation carriers were related to reduced regional contractile function and tissue compliance. In clinically advanced disease stages, a characteristic apex-to-base heterogeneity of tissue abnormalities was present in the majority of the subjects, with most pronounced disease in the basal region of the RVfw. |
| Author | van Osta, Nick Cramer, Maarten-Jan Delhaas, Tammo Lumens, Joost Lyon, Aurore Kirkels, Feddo Koopsen, Tijmen van Loon, Tim Teske, Arco J |
| AuthorAffiliation | 1 Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University , Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands 2 Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht , Utrecht, The Netherlands |
| AuthorAffiliation_xml | – name: 2 Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht , Utrecht, The Netherlands – name: 1 Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University , Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands |
| Author_xml | – sequence: 1 givenname: Nick orcidid: 0000-0002-8927-9110 surname: van Osta fullname: van Osta, Nick email: n.vanosta@maastrichtuniversity.nl organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands – sequence: 2 givenname: Feddo surname: Kirkels fullname: Kirkels, Feddo organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands – sequence: 3 givenname: Aurore orcidid: 0000-0001-6019-7376 surname: Lyon fullname: Lyon, Aurore organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands – sequence: 4 givenname: Tijmen surname: Koopsen fullname: Koopsen, Tijmen organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands – sequence: 5 givenname: Tim surname: van Loon fullname: van Loon, Tim organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands – sequence: 6 givenname: Maarten-Jan surname: Cramer fullname: Cramer, Maarten-Jan organization: Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands – sequence: 7 givenname: Arco J surname: Teske fullname: Teske, Arco J organization: Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands – sequence: 8 givenname: Tammo orcidid: 0000-0001-6897-9700 surname: Delhaas fullname: Delhaas, Tammo organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands – sequence: 9 givenname: Joost orcidid: 0000-0001-8129-7384 surname: Lumens fullname: Lumens, Joost organization: Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Universiteitssingel 50 (UNS50), 6229 ER Maastricht, The Netherlands |
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| CitedBy_id | crossref_primary_10_1016_j_jacc_2023_05_065 crossref_primary_10_3389_fphy_2023_1306210 crossref_primary_10_3389_fphys_2021_738926 crossref_primary_10_3389_fphys_2022_782592 crossref_primary_10_1038_s44161_021_00007_3 crossref_primary_10_1016_j_compbiomed_2024_108986 crossref_primary_10_1186_s12938_024_01232_0 crossref_primary_10_1093_eurheartj_ehac135 crossref_primary_10_1016_j_cma_2021_114092 |
| Cites_doi | 10.1161/01.CIR.41.6.899 10.1016/j.jcmg.2018.01.012 10.1093/ehjci/jew229 10.1016/S0140-6736(09)60256-7 10.1016/j.jacc.2014.04.044 10.1186/s12968-015-0111-7 10.1093/eurheartj/ehq025 10.1056/NEJM198801213180301 10.1186/1476-7120-5-27 10.1016/j.jacc.2008.12.045 10.1038/s41467-017-00127-0 10.1016/j.jcm.2016.02.012 10.1111/jce.12222 10.1161/CIRCGENETICS.114.001003 10.1016/j.jacc.2016.08.061 10.1371/journal.pcbi.1004284 10.1007/s10439-009-9774-2 10.1093/ehjci/jeu184 10.1093/eurheartj/ehr069 10.1152/ajpheart.00444.2004 10.1007/s003950170002 |
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| Keywords | Computer modelling and simulation Arrhythmogenic right ventricular cardiomyopathy Deformation imaging Right ventricle Contractility |
| Language | English |
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Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive... Arrhythmogenic cardiomyopathy (AC) is an inherited cardiac disease, characterized by life-threatening ventricular arrhythmias and progressive cardiac... |
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| SubjectTerms | Cardiomyopathies - diagnostic imaging Cardiomyopathies - genetics Computer Simulation Echocardiography Heart Ventricles - diagnostic imaging Humans Models, Cardiovascular Supplement Papers Ventricular Dysfunction, Right |
| Title | Electromechanical substrate characterization in arrhythmogenic cardiomyopathy using imaging-based patient-specific computer simulations |
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