Myocardial infarction, caused by coronary artery blockage, results in cardiomyocyte death and the formation of scar tissue. Scar tissue affects the contractile behavior of the left ventricular myocardium, resulting in alterations in intracardiac hemodynamics. In this study, we investigated the effect of scar stiffening on the alteration of intracardiac hemodynamics using in-silico simulation of cardiac motion in a rat heart with and without scar. The in-silico model was used to estimate the changes in endocardial wall motion due to the presence of a non-contractile scar. We used the endocardial wall motion as a moving boundary in computational fluid dynamics simulations of the intracardiac flow in the left ventricle for both healthy and infarcted cases. The fluid dynamics simulations indicated increased wall shear stress in the scar region as well as increased flow oscillations in the presence of the infarct. Further, scar passive stiffness was observed to influence the intensity of the flow oscillation. The method presented in this study can be used to monitor cardiac flow non-invasively and longitudinally using standard cardiac imaging modalities in patients with myocardial infarction. In particular, a feasible estimation of high-fidelity myocardial flow will allow us to study the effect of flow alteration on developing left ventricular thrombosis and aneurysm in myocardial infarction patients.

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Intracardiac Hemodynamics Alteration in Myocardial Infarction

  • Sunder Neelakantan,
  • Dalton Pinto,
  • Rana Raza Mehdi,
  • Seyed Babak Peighambari,
  • Kyle J. Myers,
  • Reza Avazmohammadi

摘要

Myocardial infarction, caused by coronary artery blockage, results in cardiomyocyte death and the formation of scar tissue. Scar tissue affects the contractile behavior of the left ventricular myocardium, resulting in alterations in intracardiac hemodynamics. In this study, we investigated the effect of scar stiffening on the alteration of intracardiac hemodynamics using in-silico simulation of cardiac motion in a rat heart with and without scar. The in-silico model was used to estimate the changes in endocardial wall motion due to the presence of a non-contractile scar. We used the endocardial wall motion as a moving boundary in computational fluid dynamics simulations of the intracardiac flow in the left ventricle for both healthy and infarcted cases. The fluid dynamics simulations indicated increased wall shear stress in the scar region as well as increased flow oscillations in the presence of the infarct. Further, scar passive stiffness was observed to influence the intensity of the flow oscillation. The method presented in this study can be used to monitor cardiac flow non-invasively and longitudinally using standard cardiac imaging modalities in patients with myocardial infarction. In particular, a feasible estimation of high-fidelity myocardial flow will allow us to study the effect of flow alteration on developing left ventricular thrombosis and aneurysm in myocardial infarction patients.