Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation
Abstract Background Chronic pulmonary regurgitation often leads to myocardial dysfunction and heart failure. It is not fully known why secondary hypertrophy cannot fully protect against the increase in wall stress brought about by the increased end-diastolic volume in ventricular dilation. It has be...
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Format: | Article |
Language: | English |
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Elsevier
2017-11-01
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Series: | Journal of Cardiovascular Magnetic Resonance |
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Online Access: | http://link.springer.com/article/10.1186/s12968-017-0404-0 |
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author | Peter Agger Christine Ilkjær Christoffer Laustsen Morten Smerup Jesper R. Frandsen Steffen Ringgaard Michael Pedersen John B. Partridge Robert H. Anderson Vibeke Hjortdal |
author_facet | Peter Agger Christine Ilkjær Christoffer Laustsen Morten Smerup Jesper R. Frandsen Steffen Ringgaard Michael Pedersen John B. Partridge Robert H. Anderson Vibeke Hjortdal |
author_sort | Peter Agger |
collection | DOAJ |
description | Abstract Background Chronic pulmonary regurgitation often leads to myocardial dysfunction and heart failure. It is not fully known why secondary hypertrophy cannot fully protect against the increase in wall stress brought about by the increased end-diastolic volume in ventricular dilation. It has been assumed that mural architecture is not deranged in this situation, but we hypothesised that there might be a change in the pattern of orientation of the aggregations of cardiomyocytes, which would contribute to contractile impairment. Methods We created pulmonary valvular regurgitation by open chest, surgical suturing of its leaflets in seven piglets, performing sham operations in seven control animals. Using cardiovascular magnetic resonance imaging after 12 weeks of recovery, we demonstrated significantly increased right ventricular volumes in the test group. After sacrifice, diffusion tensor imaging of their hearts permitted measurement of the orientation of the cardiomyocytes. Results The helical angles in the right ventricle approached a more circumferential orientation in the setting of right ventricular RV dilation (p = 0.007), with an increased proportion of surface-parallel cardiomyocytes. In contrast, this proportion decreased in the left ventricle. Also in the left ventricle a higher proportion of E3 angles with a value around zero was found, and conversely a lower proportion of angles was found with a numerical higher value. In the dilated right ventricle the proportion of E3 angles around −90° is increased, while the proportion around 90° is decreased. Conclusion Contrary to traditional views, there is a change in the orientation of both the left ventricular and right ventricular cardiomyocytes subsequent to right ventricular dilation. This will change their direction of contraction and hinder the achievement of normalisation of cardiomyocytic strain, affecting overall contractility. We suggest that the aetiology of the cardiac failure induced by right vetricular dilation may be partly explained by morphological changes in the myocardium itself. |
first_indexed | 2024-04-24T08:48:20Z |
format | Article |
id | doaj.art-03c7c73989ea4937890fd58ce22ce48e |
institution | Directory Open Access Journal |
issn | 1532-429X |
language | English |
last_indexed | 2024-04-24T08:48:20Z |
publishDate | 2017-11-01 |
publisher | Elsevier |
record_format | Article |
series | Journal of Cardiovascular Magnetic Resonance |
spelling | doaj.art-03c7c73989ea4937890fd58ce22ce48e2024-04-16T12:36:59ZengElsevierJournal of Cardiovascular Magnetic Resonance1532-429X2017-11-0119111610.1186/s12968-017-0404-0Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilationPeter Agger0Christine Ilkjær1Christoffer Laustsen2Morten Smerup3Jesper R. Frandsen4Steffen Ringgaard5Michael Pedersen6John B. Partridge7Robert H. Anderson8Vibeke Hjortdal9Department of Cardiothoracic & Vascular Surgery, Aarhus University HospitalDepartment of Cardiothoracic & Vascular Surgery, Aarhus University HospitalMR Research Center, Aarhus University HospitalDepartment of Cardiothoracic Surgery, RigshospitaletCenter for Functionally Integrative Neuroscience, Aarhus University HospitalMR Research Center, Aarhus University HospitalComparative Medicine Lab, Aarhus University HospitalEurobodalla Unit, Rural Clinical School of the ANU College of Medicine, Biology & EnvironmentInstitute of Genetic Medicine, Newcastle UniversityDepartment of Cardiothoracic & Vascular Surgery, Aarhus University HospitalAbstract Background Chronic pulmonary regurgitation often leads to myocardial dysfunction and heart failure. It is not fully known why secondary hypertrophy cannot fully protect against the increase in wall stress brought about by the increased end-diastolic volume in ventricular dilation. It has been assumed that mural architecture is not deranged in this situation, but we hypothesised that there might be a change in the pattern of orientation of the aggregations of cardiomyocytes, which would contribute to contractile impairment. Methods We created pulmonary valvular regurgitation by open chest, surgical suturing of its leaflets in seven piglets, performing sham operations in seven control animals. Using cardiovascular magnetic resonance imaging after 12 weeks of recovery, we demonstrated significantly increased right ventricular volumes in the test group. After sacrifice, diffusion tensor imaging of their hearts permitted measurement of the orientation of the cardiomyocytes. Results The helical angles in the right ventricle approached a more circumferential orientation in the setting of right ventricular RV dilation (p = 0.007), with an increased proportion of surface-parallel cardiomyocytes. In contrast, this proportion decreased in the left ventricle. Also in the left ventricle a higher proportion of E3 angles with a value around zero was found, and conversely a lower proportion of angles was found with a numerical higher value. In the dilated right ventricle the proportion of E3 angles around −90° is increased, while the proportion around 90° is decreased. Conclusion Contrary to traditional views, there is a change in the orientation of both the left ventricular and right ventricular cardiomyocytes subsequent to right ventricular dilation. This will change their direction of contraction and hinder the achievement of normalisation of cardiomyocytic strain, affecting overall contractility. We suggest that the aetiology of the cardiac failure induced by right vetricular dilation may be partly explained by morphological changes in the myocardium itself.http://link.springer.com/article/10.1186/s12968-017-0404-0Myocardial remodelingDiffusion tensor imagingHeart failureCongenital heart disease |
spellingShingle | Peter Agger Christine Ilkjær Christoffer Laustsen Morten Smerup Jesper R. Frandsen Steffen Ringgaard Michael Pedersen John B. Partridge Robert H. Anderson Vibeke Hjortdal Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation Journal of Cardiovascular Magnetic Resonance Myocardial remodeling Diffusion tensor imaging Heart failure Congenital heart disease |
title | Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation |
title_full | Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation |
title_fullStr | Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation |
title_full_unstemmed | Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation |
title_short | Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation |
title_sort | changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation |
topic | Myocardial remodeling Diffusion tensor imaging Heart failure Congenital heart disease |
url | http://link.springer.com/article/10.1186/s12968-017-0404-0 |
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