Key result
In a computational model of acute myocardial infarction, stroke work decreased by 25% compared to a healthy left ventricle, demonstrating that relative loss in pump function exceeds the loss in healthy tissue.
Why the study?
Understanding the relation between time-dependent changes in myocardial material properties and cardiac contractile function post-MI may clarify the development of HF and guide novel therapies.
Effect estimate: 25% decrease
Absolute Event Rate: 0.74% vs 0.98%
Computational modeling demonstrates that post-MI pump function loss is disproportionately large due to impaired mechanical function in the healthy tissue adjacent to the infarct.
May explain excess pump failure beyond infarct size; extends border-zone models but leaves clinical validation open.
Adverse ventricular remodeling following acute myocardial infarction (MI) may induce ventricular dilation, fibrosis, and loss of global contractile function, possibly resulting in heart failure (HF). Understanding the relation between the time-dependent changes in material properties of the myocardium and the contractile function of the heart may further our understanding of the development of HF post-MI and guide the development of novel therapies. A finite element model of cardiac mechanics was used to model MI in a thick-walled truncated ellipsoidal geometry. Infarct core and border zone comprised 9.6 and 8.1% of the LV wall volume, respectively. Acute MI was modeled by inhibiting active stress generation. Chronic MI was modeled by the additional effect of infarct material stiffening, wall thinning and fiber reorientation. In acute MI, stroke work decreased by 25%. In the infarct core, fiber stress was reduced but fiber strain was increased, depending on the degree of infarct stiffening. Fiber work density was equal to zero. Healthy tissue adjacent to the infarct showed decreased work density depending on the degree of infarct stiffness and the orientation of the myofibers with respect to the infarct region. Thinning of the wall partially restored this loss in work density while the effects of fiber reorientation were minimal. We found that the relative loss in pump function in the infarcted heart exceeds the relative loss in healthy myocardial tissue due to impaired mechanical function in healthy tissue adjacent to the infarct. Infarct stiffening, wall thinning and fiber reorientation did not affect pump function but did affect the distribution of work density in tissue adjacent to the infarct.
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Janssens et al. (2023) studied Myocardial infarction. Simulated acute and chronic myocardial infarction vs. Healthy left ventricular model was evaluated on Stroke work (25% decrease). In a computational model of acute myocardial infarction, stroke work decreased by 25% compared to a healthy left ventricle, demonstrating that relative loss in pump function exceeds the loss in healthy tissue.
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