Key result
A simple feedback model based on the role of the enzyme CaMKII was developed to describe the whole dynamic picture of the force-frequency relationship in cardiac cells.
Why the study?
Previous models could only explain a short period of time after changing pacing frequency in cardiac myocytes.
A new iterated map model incorporating CaMKII feedback was developed to better explain the complex transient contraction force behaviors in cardiac cells following changes in pacing frequency.
Hypothesis-generating for CaMKII-mediated force-frequency dynamics in cells; requires validation before any clinical consideration.
Experiment data on isolated rat hearts shows that the transient behaviors after switching pacing intervals are very complicated with increasing, decreasing, and rebound of the contraction force. The strength of contraction in the heart muscle is strongly related to intracellular free Ca2+ mediated by an action potential. This behavior can be explained by calcium cycling inside the excitable cardiac myocytes coupled with their action potential. The previous and recently proposed models can only explain a short period of time after changing the pacing frequency. Our aim is to develop a simple feedback model based on the role of the enzyme CaMKII to describe the whole dynamic picture captured from experiments.
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Duy et al. (2022) studied Cardiac cell force-frequency relationship. Iterated map model with CaMKII feedback vs. Previous models was evaluated on Modeling the force frequency relationship of a cardiac cell. A simple feedback model based on the role of the enzyme CaMKII was developed to describe the whole dynamic picture of the force-frequency relationship in cardiac cells.
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