Why the study?
To elucidate the biomechanical effects of abnormal active relaxation and increased ventricular diastolic stiffness, and how they interact to create the phenotypes of diastolic dysfunction.
A computational model successfully replicated the three phenotypes of diastolic dysfunction, elucidating the biomechanical effects of abnormal relaxation and increased stiffness.
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Should not yet inform clinical phenotyping of diastolic dysfunction; extends computational models but leaves translation open.
This study uses a complete and validated computational model of the cardiovascular system to simulate the two main pathologies involved in diastolic dysfunction (DD), i.e., abnormal active relaxation and increased ventricular diastolic stiffness. The three phenotypes of DD were successfully replicated according to literature data. We elucidate the biomechanical effect of the relaxation pathologies involved and how these pathologies interact to create the various phenotypes of DD.
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Kadry et al. (2020) studied this question.
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