A Novel Method for Quantifying Smooth Regional Variations in Myocardial Contractility Within an Infarcted XXXX Left Ventricle Based on Delay-Enhanced Magnetic Resonance Imaging.

@entity1 @entity583 @entity712 @entity409
UNASSIGNED: @entity712 is increasing at an alarming rate, making it a worldwide epidemic. As the population ages and life expectancy increases, this trend is not likely to change. @entity583 ( @entity583 )-induced adverse left ventricular (LV) remodeling is responsible for nearly 70% of @entity712 cases. The adverse remodeling process involves an extension of the border zone (BZ) adjacent to an @entity583 , which is normally perfused but shows myofiber @entity409 . To improve @entity1 -specific modeling of cardiac mechanics, we sought to create a finite element model of the @entity1 LV with BZ and @entity583 morphologies integrated directly from delayed-enhancement magnetic resonance (DE-MR) images. Instead of separating the LV into discrete regions (e.g., the @entity583 , BZ, and remote regions) with each having a homogeneous myocardial material property, we assumed a functional relation between the DE-MR image pixel intensity and myocardial stiffness and contractility-we considered a linear variation of material properties as a function of DE-MR image pixel intensity, which is known to improve the accuracy of the model's response. The finite element model was then calibrated using measurements obtained from the same @entity1 -namely, 3D strain measurements-using complementary spatial modulation of magnetization magnetic resonance (CSPAMM-MR) images. This led to an average circumferential strain error of 8.9% across all American Heart Association (AHA) segments. We demonstrate the utility of our method for quantifying smooth regional variations in myocardial contractility using cardiac DE-MR and CSPAMM-MR images acquired from a 78-yr-old @entity1 who experienced an @entity583 approximately 1   yr prior. We found a remote myocardial diastolic stiffness of C0  =0.102   kPa, and a remote myocardial contractility of Tmax  =146.9   kPa, which are both in the range of previously published normal @entity1 values. Moreover, we found a normalized pixel intensity range of 30% for the BZ, which is consistent with the literature. Based on these regional myocardial material properties, we used our finite element model to compute @entity1 -specific diastolic and systolic LV myofiber stress distributions, which cannot be measured directly. One of the main driving forces for adverse LV remodeling is assumed to be an abnormally high level of ventricular wall stress, and many existing and new treatments for @entity712 fundamentally attempt to normalize LV wall stress. Thus, our noninvasive method for estimating smooth regional variations in myocardial contractility should be valuable for optimizing new surgical or medical strategies to limit the chronic evolution from infarction to @entity712 .
