The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart

Hao Liu, João S. Soares, John Walmsley, David S. Li, Samarth Raut, Reza Avazmohammadi, Paul Iaizzo, Mark Palmer, Joseph H. Gorman, Robert C. Gorman, Michael S. Sacks

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure. Patient-specific models are a maturing technology for developing and determining therapeutic modalities for MI that require accurate descriptions of myocardial mechanics. While substantial tissue volume reductions of 15–20% during systole have been reported, myocardium is commonly modeled as incompressible. We developed a myocardial model to simulate experimentally-observed systolic volume reductions in an ovine model of MI. Sheep-specific simulations of the cardiac cycle were performed using both incompressible and compressible tissue material models, and with synchronous or measurement-guided contraction. The compressible tissue model with measurement-guided contraction gave best agreement with experimentally measured reductions in tissue volume at peak systole, ventricular kinematics, and wall thickness changes. The incompressible model predicted myofiber peak contractile stresses approximately double the compressible model (182.8 kPa, 107.4 kPa respectively). Compensatory changes in remaining normal myocardium with MI present required less increase of contractile stress in the compressible model than the incompressible model (32.1%, 53.5%, respectively). The compressible model therefore provided more accurate representation of ventricular kinematics and potentially more realistic computed active contraction levels in the simulated infarcted heart. Our findings suggest that myocardial compressibility should be incorporated into future cardiac models for improved accuracy.

Original languageEnglish (US)
Article number13466
JournalScientific reports
Issue number1
StatePublished - Dec 2021

Bibliographical note

Funding Information:
Funding by the National Institutes of Health (R01 HL073021), Moss Heart Foundation, and Medtronic is gratefully acknowledged.

Publisher Copyright:
© 2021, The Author(s).


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