Key result
In a computational model, acute myocardial infarction decreased stroke work by 25%, and subsequent infarct stiffening altered local work density without further affecting global pump function.
Why the study?
Adverse ventricular remodeling after acute MI can cause HF, and understanding how time-dependent changes in myocardial material properties relate to contractile function may elucidate post-MI HF development and guide novel therapies.
Computational modeling demonstrates that post-MI pump function loss is exacerbated by impaired mechanical function in healthy tissue adjacent to the infarct, while infarct stiffening primarily affects work density distribution rather than overall pump function.
Acute MI impairs global function via contractility loss, not stiffening; leaves open whether targeting border-zone mechanics improves HF outcomes.
Introduction 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. Methods 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 and chronic MI were modeled by reducing active stress generation and subsequent step-wise increase of material stiffness. Results 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. Conclusion 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 did not affect pump function but did affect the distribution of work density in tissue adjacent to the infarct.
No takes yet. Share an insight, caveat, or question.
Janssens et al. (2023) studied Myocardial infarction. Simulated acute and chronic myocardial infarction vs. Simulated healthy left ventricle was evaluated on Stroke work. In a computational model, acute myocardial infarction decreased stroke work by 25%, and subsequent infarct stiffening altered local work density without further affecting global pump function.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: