Key result
A novel computational model of acute myocardial ischemia in human ventricular cardiomyocytes successfully simulated action potential changes and extracellular potassium accumulation consistent with in-vivo human data.
Why the study?
Acute myocardial ischemia causes high mortality worldwide, and existing computational models lacked comprehensive inclusion of ischemia-affected current alterations on the action potential.
A novel computational model of acute myocardial ischemia in human ventricular cardiomyocytes accurately reproduces experimentally observed electrophysiological alterations, including action potential shortening and extracellular potassium accumulation.
Answers are grounded in this paper and cite their sources.
May support ischemia model refinement; leaves open translation to clinical decision-making.
Acute myocardial ischemia is known to be a pathology with a high mortality worldwide. In the last decades, computational simulation has been a widely used tool to study the electrophysiological effects of ischemia. In this work, we present an up-to-date model of the effects of myocardial ischemia in the action potential which includes more ischemia-affected current alterations than any other previously published model. The model was used to simulate action potentials during a 10-minute period of dynamic ischemia, and the main biomarkers of the action potential were monitored, as well as the extracellular potassium elevation. The results agree with those obtained experimentally, suggesting that the model can be useful for 3D simulations of acute myocardial ischemia.
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Girones-Sanguesa et al. (2020) studied Acute myocardial ischemia. Computational simulation of dynamic ischemia vs. Normoxia was evaluated on Action potential duration and extracellular potassium accumulation. A novel computational model of acute myocardial ischemia in human ventricular cardiomyocytes successfully simulated action potential changes and extracellular potassium accumulation consistent with in-vivo human data.
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