Key result
A computational model demonstrated that increasing left ventricular contractility, preload, wall thickness, or cavity volume increases the myocardial work density-perfusion mismatch ratio at the endocardium.
Why the study?
To investigate the transmural distribution of myocardial demand and supply ratio across the heart wall using a closed-loop computational model.
A computational model demonstrates that increases in LV contractility, preload, wall thickness, or cavity volume can increase the vulnerability of the subendocardial region to ischemia due to work density-perfusion mismatch.
Hypothesis-generating for subendocardial ischemia mechanisms; leaves open clinical translation of computational LV mismatch models.
Myocardial supply changes to accommodate the variation of myocardial demand across the heart wall to maintain normal cardiac function. A computational framework that couples the systemic circulation of a left ventricular (LV) finite element model and coronary perfusion in a closed loop is developed to investigate the transmural distribution of the myocardial demand (work density) and supply (perfusion) ratio. Calibrated and validated against measurements of LV mechanics and coronary perfusion, the model is applied to investigate changes in the transmural distribution of passive coronary perfusion, myocardial work density, and their ratio in response to changes in LV contractility, preload, afterload, wall thickness, and cavity volume. The model predicts the following: (1) Total passive coronary flow varies from a minimum value at the endocardium to a maximum value at the epicardium transmurally that is consistent with the transmural distribution of IMP; (2) Total passive coronary flow at different transmural locations is increased with an increase in either contractility, afterload, or preload of the LV, whereas is reduced with an increase in wall thickness or cavity volume; (3) Myocardial work density at different transmural locations is increased transmurally with an increase in either contractility, afterload, preload or cavity volume of the LV, but is reduced with an increase in wall thickness; (4) Myocardial work density-perfusion mismatch ratio at different transmural locations is increased with an increase in contractility, preload, wall thickness or cavity volume of the LV, and the ratio is higher at the endocardium than the epicardium. These results suggest that an increase in either contractility, preload, wall thickness, or cavity volume of the LV can increase the vulnerability of the subendocardial region to ischemia.
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Fan et al. (2021) studied Myocardial demand-supply mismatch. Alterations in LV contractility, preload, afterload, wall thickness, and cavity volume vs. Baseline calibrated computational model was evaluated on Transmural distribution of passive coronary perfusion, myocardial work density, and their ratio. A computational model demonstrated that increasing left ventricular contractility, preload, wall thickness, or cavity volume increases the myocardial work density-perfusion mismatch ratio at the endocardium.
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