ArticleBiomedical engineering online2013
A multi-scale cardiovascular system model can account for the load-dependence of the end-systolic pressure-volume relationship.
Article in Biomedical engineering online, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed.
- Elucidating the cellular determinants of the end-systolic pressure-volume relationship of the heart via computational modelling.The Journal of physiology · 2026Article
- Integration of multiple perspectives to understand the left ventricular pressure-volume relationship.Communications medicine · 2026Review
- Isolated cardiac muscle contracting against a real-time model of systemic and pulmonary cardiovascular loads.American journal of physiology. Heart and circulatory physiology · 2023Article
- CARDIOSIMBioengineering (Basel, Switzerland) · 2022Review
- Non-linearity of end-systolic pressure-volume relation in afterload increases is caused by an overlay of shortening deactivation and the Frank-Starling mechanism.Scientific reports · 2021Article
- Multiscale Modeling of Cardiovascular Function Predicts That the End-Systolic Pressure Volume Relationship Can Be Targeted via Multiple Therapeutic Strategies.Frontiers in physiology · 2020Article
- Effects of Mechanical Dyssynchrony on Coronary Flow: Insights From a Computational Model of Coupled Coronary Perfusion With Systemic Circulation.Frontiers in physiology · 2020Article
- Insights From Computational Modeling Into the Contribution of Mechano-Calcium Feedback on the Cardiac End-Systolic Force-Length Relationship.Frontiers in physiology · 2020Article
- Computational analysis of the hemodynamic characteristics under interaction influence of β-blocker and LVAD.Biomedical engineering online · 2018Article
- Simulation as a preoperative planning approach in advanced heart failure patients. A retrospective clinical analysis.Biomedical engineering online · 2018Article
- Next-generation, personalised, model-based critical care medicine: a state-of-the art review of in silico virtual patient models, methods, and cohorts, and how to validation them.Biomedical engineering online · 2018Review
- Application of Patient-Specific Computational Fluid Dynamics in Coronary and Intra-Cardiac Flow Simulations: Challenges and Opportunities.Frontiers in physiology · 2018Review
- Simulation of left atrial function using a multi-scale model of the cardiovascular system.PloS one · 2014Article
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9 authors.
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Abstract
backgroundThe end-systolic pressure-volume relationship is often considered as a load-independent property of the heart and, for this reason, is widely used as an index of ventricular contractility. However, many criticisms have been expressed against this index and the underlying time-varying elastance theory: first, it does not consider the phenomena underlying contraction and second, the end-systolic pressure volume relationship has been experimentally shown to be load-dependent.
methodsIn place of the time-varying elastance theory, a microscopic model of sarcomere contraction is used to infer the pressure generated by the contraction of the left ventricle, considered as a spherical assembling of sarcomere units. The left ventricle model is inserted into a closed-loop model of the cardiovascular system. Finally, parameters of the modified cardiovascular system model are identified to reproduce the hemodynamics of a normal dog.
resultsExperiments that have proven the limitations of the time-varying elastance theory are reproduced with our model: (1) preload reductions, (2) afterload increases, (3) the same experiments with increased ventricular contractility, (4) isovolumic contractions and (5) flow-clamps. All experiments simulated with the model generate different end-systolic pressure-volume relationships, showing that this relationship is actually load-dependent. Furthermore, we show that the results of our simulations are in good agreement with experiments.
conclusionsWe implemented a multi-scale model of the cardiovascular system, in which ventricular contraction is described by a detailed sarcomere model. Using this model, we successfully reproduced a number of experiments that have shown the failing points of the time-varying elastance theory. In particular, the developed multi-scale model of the cardiovascular system can capture the load-dependence of the end-systolic pressure-volume relationship.
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