This preprint is under consideration at BioMedical Engineering OnLine. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Ekaterina Kovacheva
Karlsruhe Institute of Technology Electrical Engineering and Information Technology: Karlsruher Institut fur Technologie Fakultat fur Elektrotechnik und Informationstechnik
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1574-370X
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Hypertrophic cardiomyopathy is a common heart disease causing alteration in the mechanical behaviour of the left ventricle (LV). Decreased myocardial velocities, reduced strain and strain rates have been reported clinically. These alterations result from underlying pathological mechanisms in the tissue: increased wall thickness, altered active and passive force development and/or fiber disarray, which are cumbersome to measure clinically. With a numerical study, we aim to answer: how the variability in each of these mechanisms contributes to altered mechanics of the LV and if the deformation obtained in in-silico experiments is comparable to values reported from clinical measurements.
Results: We conducted an in-silico sensitivity study on physiological and pathological mechanisms potentially underlying the clinical hypertrophic cardiomyopathy phenotype. Deformation and mechanical behaviour of whole heart models was evaluated globally and regionally. Hypertrophy of the LV affected the course of strain, strain rate and wall thickening—the root mean squared difference of the wall thickening between control (mean thickness 10 mm) and hypertrophic geometries (17 mm) was >10 %. A reduction of active force development by 40 % led to less overall deformation: maximal radial strain reduced from 26 % to 21 %. A five-fold increase in tissue stiffness caused a more homogeneous distribution of the strain values among the 17 AHA segments. Fiber disarray led to minor changes in the circumferential and radial strain. A combination of pathological mechanisms led to reduced and slower deformation of the LV and halved the longitudinal shortening of the left atria.
Conclusions: This study uses a computer model to determine the changes in LV deformation caused by pathological mechanisms that are presumed to underlay hypertrophic cardiomybopathy. This knowledge can complement imaging-derived information to obtain a more accurate diagnosis of hypertrophic cardiomyopathy.
Keywords
hypertrophic cardiomyopathy, in-silico study, altered mechanics, active and passive forces, wall thickness, fiber disarray, strain, strain rate
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
Figure 10
Figure 11
Figure 12
Figure 13
Figure 14
Figure 15
This preprint is available for download as a PDF.
This is a list of supplementary files associated with this preprint. Click to download.
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 22 Mar, 2021
No community comments so far
Editorial decision: Major revision
On 08 Apr, 2021
Review #1 received
Received 31 Mar, 2021
Review #2 received
Received 30 Mar, 2021
Review #3 received
Received 24 Mar, 2021
Review #4 received
Received 24 Mar, 2021
Reviewer #7 agreed
On 21 Mar, 2021
Reviewer #6 agreed
On 21 Mar, 2021
Reviewer #5 agreed
On 20 Mar, 2021
Reviewer #4 agreed
On 20 Mar, 2021
Reviewer #2 agreed
On 19 Mar, 2021
Reviewer #3 agreed
On 19 Mar, 2021
Reviewer #1 agreed
On 19 Mar, 2021
Reviews received
Received 19 Mar, 2021
Editor assigned
On 18 Mar, 2021
Reviewers invited
Invitations sent on 18 Mar, 2021
Submission checks complete
On 18 Mar, 2021
Editor invited
On 18 Mar, 2021
First submitted
On 17 Mar, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cell & Tissue Engineering
Learn more about our company.
This preprint is under consideration at BioMedical Engineering OnLine. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Ekaterina Kovacheva
Karlsruhe Institute of Technology Electrical Engineering and Information Technology: Karlsruher Institut fur Technologie Fakultat fur Elektrotechnik und Informationstechnik
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1574-370X
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 22 Mar, 2021
No community comments so far
Editorial decision: Major revision
On 08 Apr, 2021
Review #1 received
Received 31 Mar, 2021
Review #2 received
Received 30 Mar, 2021
Review #3 received
Received 24 Mar, 2021
Review #4 received
Received 24 Mar, 2021
Reviewer #7 agreed
On 21 Mar, 2021
Reviewer #6 agreed
On 21 Mar, 2021
Reviewer #5 agreed
On 20 Mar, 2021
Reviewer #4 agreed
On 20 Mar, 2021
Reviewer #2 agreed
On 19 Mar, 2021
Reviewer #3 agreed
On 19 Mar, 2021
Reviewer #1 agreed
On 19 Mar, 2021
Reviews received
Received 19 Mar, 2021
Editor assigned
On 18 Mar, 2021
Reviewers invited
Invitations sent on 18 Mar, 2021
Submission checks complete
On 18 Mar, 2021
Editor invited
On 18 Mar, 2021
First submitted
On 17 Mar, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cell & Tissue Engineering
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Hypertrophic cardiomyopathy is a common heart disease causing alteration in the mechanical behaviour of the left ventricle (LV). Decreased myocardial velocities, reduced strain and strain rates have been reported clinically. These alterations result from underlying pathological mechanisms in the tissue: increased wall thickness, altered active and passive force development and/or fiber disarray, which are cumbersome to measure clinically. With a numerical study, we aim to answer: how the variability in each of these mechanisms contributes to altered mechanics of the LV and if the deformation obtained in in-silico experiments is comparable to values reported from clinical measurements.
Results: We conducted an in-silico sensitivity study on physiological and pathological mechanisms potentially underlying the clinical hypertrophic cardiomyopathy phenotype. Deformation and mechanical behaviour of whole heart models was evaluated globally and regionally. Hypertrophy of the LV affected the course of strain, strain rate and wall thickening—the root mean squared difference of the wall thickening between control (mean thickness 10 mm) and hypertrophic geometries (17 mm) was >10 %. A reduction of active force development by 40 % led to less overall deformation: maximal radial strain reduced from 26 % to 21 %. A five-fold increase in tissue stiffness caused a more homogeneous distribution of the strain values among the 17 AHA segments. Fiber disarray led to minor changes in the circumferential and radial strain. A combination of pathological mechanisms led to reduced and slower deformation of the LV and halved the longitudinal shortening of the left atria.
Conclusions: This study uses a computer model to determine the changes in LV deformation caused by pathological mechanisms that are presumed to underlay hypertrophic cardiomybopathy. This knowledge can complement imaging-derived information to obtain a more accurate diagnosis of hypertrophic cardiomyopathy.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
Figure 10
Figure 11
Figure 12
Figure 13
Figure 14
Figure 15
This preprint is available for download as a PDF.
Loading...