Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation
Abstract Cardiac volume overload from mitral regurgitation (MR) is a trigger for left ventricular dilatation, remodeling, and ultimate failure. While the functional and structural adaptations to this overload are known, the adaptation of myocardial mechanical properties remains unknown. Using a rode...
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| Format: | Article |
| Language: | English |
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Wiley
2022-07-01
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| Series: | Physiological Reports |
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| Online Access: | https://doi.org/10.14814/phy2.15305 |
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| author | Daniella Corporan Maher Saadeh Alessandra Yoldas Jahnavi Mudigonda Brooks Alexander Lane Muralidhar Padala |
| author_facet | Daniella Corporan Maher Saadeh Alessandra Yoldas Jahnavi Mudigonda Brooks Alexander Lane Muralidhar Padala |
| author_sort | Daniella Corporan |
| collection | DOAJ |
| description | Abstract Cardiac volume overload from mitral regurgitation (MR) is a trigger for left ventricular dilatation, remodeling, and ultimate failure. While the functional and structural adaptations to this overload are known, the adaptation of myocardial mechanical properties remains unknown. Using a rodent model of MR, in this study, we discern changes in the passive material properties of the intact and decellularized myocardium. Eighty Sprague‐Dawley rats (350–400 g) were assigned to two groups: (1) MR (n = 40) and (2) control (n = 40). MR was induced in the beating heart by perforating the mitral leaflet with a 23G needle, and rats were terminated at 2, 10, 20, or 40 weeks (n = 10/time‐point). Echocardiography was performed at baseline and termination, and explanted hearts were used for equibiaxial mechanical testing of the intact myocardium and after decellularization. Two weeks after inducing severe MR, the myocardium was more extensible compared to control, however, stiffness and extensibility of the extracellular matrix did not differ from control at this timepoint. By 20 weeks, the myocardium was stiffer with a higher elastic modulus of 1920 ± 246 kPa, and a parallel rise in extracellular matrix stiffness. Despite some matrix stiffening, it only contributed to 31% and 36% of the elastic modulus of the intact tissue in the circumferential and longitudinal directions. At 40 weeks, similar trends of increasing stiffness were observed, but the contribution of extracellular matrix remained relatively low. Chronic MR induces ventricular myocardial stiffening, which seems to be driven by the myocyte compartment of the muscle, and not the extracellular matrix. |
| first_indexed | 2024-03-09T01:05:33Z |
| format | Article |
| id | doaj.art-42557543f44e4408b5b14151f509b01e |
| institution | Directory Open Access Journal |
| issn | 2051-817X |
| language | English |
| last_indexed | 2024-03-09T01:05:33Z |
| publishDate | 2022-07-01 |
| publisher | Wiley |
| record_format | Article |
| series | Physiological Reports |
| spelling | doaj.art-42557543f44e4408b5b14151f509b01e2023-12-11T09:26:21ZengWileyPhysiological Reports2051-817X2022-07-011014n/an/a10.14814/phy2.15305Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitationDaniella Corporan0Maher Saadeh1Alessandra Yoldas2Jahnavi Mudigonda3Brooks Alexander Lane4Muralidhar Padala5Structural Heart Research and Innovation Laboratory Carlyle Fraser Heart Center Emory University Hospital Midtown Atlanta Georgia USAStructural Heart Research and Innovation Laboratory Carlyle Fraser Heart Center Emory University Hospital Midtown Atlanta Georgia USAStructural Heart Research and Innovation Laboratory Carlyle Fraser Heart Center Emory University Hospital Midtown Atlanta Georgia USAStructural Heart Research and Innovation Laboratory Carlyle Fraser Heart Center Emory University Hospital Midtown Atlanta Georgia USAStructural Heart Research and Innovation Laboratory Carlyle Fraser Heart Center Emory University Hospital Midtown Atlanta Georgia USAStructural Heart Research and Innovation Laboratory Carlyle Fraser Heart Center Emory University Hospital Midtown Atlanta Georgia USAAbstract Cardiac volume overload from mitral regurgitation (MR) is a trigger for left ventricular dilatation, remodeling, and ultimate failure. While the functional and structural adaptations to this overload are known, the adaptation of myocardial mechanical properties remains unknown. Using a rodent model of MR, in this study, we discern changes in the passive material properties of the intact and decellularized myocardium. Eighty Sprague‐Dawley rats (350–400 g) were assigned to two groups: (1) MR (n = 40) and (2) control (n = 40). MR was induced in the beating heart by perforating the mitral leaflet with a 23G needle, and rats were terminated at 2, 10, 20, or 40 weeks (n = 10/time‐point). Echocardiography was performed at baseline and termination, and explanted hearts were used for equibiaxial mechanical testing of the intact myocardium and after decellularization. Two weeks after inducing severe MR, the myocardium was more extensible compared to control, however, stiffness and extensibility of the extracellular matrix did not differ from control at this timepoint. By 20 weeks, the myocardium was stiffer with a higher elastic modulus of 1920 ± 246 kPa, and a parallel rise in extracellular matrix stiffness. Despite some matrix stiffening, it only contributed to 31% and 36% of the elastic modulus of the intact tissue in the circumferential and longitudinal directions. At 40 weeks, similar trends of increasing stiffness were observed, but the contribution of extracellular matrix remained relatively low. Chronic MR induces ventricular myocardial stiffening, which seems to be driven by the myocyte compartment of the muscle, and not the extracellular matrix.https://doi.org/10.14814/phy2.15305mitral regurgitationmitral valve prolapsemyocardial mechanicsmyocardial remodelingvalvular heart disease |
| spellingShingle | Daniella Corporan Maher Saadeh Alessandra Yoldas Jahnavi Mudigonda Brooks Alexander Lane Muralidhar Padala Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation Physiological Reports mitral regurgitation mitral valve prolapse myocardial mechanics myocardial remodeling valvular heart disease |
| title | Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation |
| title_full | Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation |
| title_fullStr | Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation |
| title_full_unstemmed | Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation |
| title_short | Passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation |
| title_sort | passive mechanical properties of the left ventricular myocardium and extracellular matrix in hearts with chronic volume overload from mitral regurgitation |
| topic | mitral regurgitation mitral valve prolapse myocardial mechanics myocardial remodeling valvular heart disease |
| url | https://doi.org/10.14814/phy2.15305 |
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