Regional Left Ventricular Myocardial Contractility and Stress in a Finite Element Model of Posterobasal Myocardial Infarction

Abstract

Recently, a non-invasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study sheep with anteroapical infarction [1]. Using the methodology developed in the previous study [1], which incorporates tagged magnetic resonance images (MRI), three-dimensional (3D) myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction was investigated. Active material parameters in the noninfarcted borderzone (BZ) myocardium adjacent to the infarct (Tmax_B), in the myocardium remote from the infarct (Tmax_R), and in the infarct (Tmax_I) were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized Tmax_B was found to be significantly depressed relative to Tmax_R, while Tmax_I was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure.

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

“…When Shimkunas et al [5] studied the effect of doxycycline, an inhibitor of matrix metalloproteinases, rigor stiffness, and essential light-chain phosphorylation was not reduced in BZ myocardium, suggesting that doxycycline had a protective effect on BZ contractility. Fortunately, ex vivo biaxial tissue testing is not required to quantify in vivo regional contractilities for the case of a posterobasal or posterolateral MI because the thickness of the infarcted wall segment is at least 50% of normal [3,6,13]. In the previous studies [3,6,13], we could measure 3D myocardial strain in the MI.…”

“…Fortunately, ex vivo biaxial tissue testing is not required to quantify in vivo regional contractilities for the case of a posterobasal or posterolateral MI because the thickness of the infarcted wall segment is at least 50% of normal [3,6,13]. In the previous studies [3,6,13], we could measure 3D myocardial strain in the MI. In all three of those studies, however, it was not necessary to use a nonzero T max value in the MI for the LV finiteelement models to predict strain fields as measured with tagged MRI.…”

“…Conversely, for high pixel intensities, i.e., infarcted tissues, the local stiffness C 0 corresponds to a much higher stiffness of 10 C 0 , following the infarct to remote stiffness ratio of Ref. [13]. As represented in Fig.…”

“…We start by briefly describing our LV finite-element modeling framework, emphasizing the improvement with regard to the previous work from our group [4,[12][13][14].…”

“…More details on the formulation and the definition and values of the parameters, can be found in Refs. [4,[12][13][14]. The parameter T max scales the tissue contractility and, similar to C 0 for the passive law, needs to be personalized for each patient.…”