Hemodynamics of infarcted hearts

Myocardial infarction occurs when a branch of a coronary artery is occluded by a thrombus (blood clot) and a certain area becomes ischemic. This results in a progressive deterioration of electrical and muscular activity of the injuried area leading to cell death and local failure of muscle contraction [1]. In this work, we employ a high-fidelity numerical heart model to study the hemodynamics after an ischemic event (heart attack). We aim at understanding why after apparently similar infarction events, some patients have a poor prognosis while others perfectly recover [2]. The analysis is based on the fluid-structure-electrophysiology interaction (FSEI2), which can cope with the electrophysiology of the myocardium, including the fibers orientation, its active contraction and passive relaxation, the dynamics of the valves and the hemodynamics within the heart chambers and arteries. All these models are three–way coupled with each other, thus providing a predictive framework for capturing both the healthy and pathologic heart functioning. In particular, the ischemic region perturbs the elastic and electrophysiology properties of the myocardium which, in turn, loses contractility. Importantly, multiple ischemic events will be considered by varying the position and size of the impaired myocardium, depending on which coronary branch gets blocked (e.g anterior, anterior–septal, lateral and inferior). For each case, the hemodynamics effectiveness in terms of transvalvular pressure drops, cardiac output, ventricle washout and wall shear stress will be measured in order to determine what are the sensitive parameters affecting the diseases evolution and detection.