Mechanical characterization of infarcted porcine hearts using left anterior descending and left circumflex coronary artery models.

Abstract

This study comprehensively analyzes passive mechanical and structural changes of cardiac tissue 6 weeks after myocardial infarction (MI) by biaxial, simple triaxial shear, and confined compression characterization. We considered a porcine model, comparing two MI types: Left Anterior Descending (LAD) artery and Left Circumflex (LCX) artery occlusions. LAD model generated apical transmurally infarcted hearts, while the LCX model generated medial heterogeneous infarctions ranging from mild locally infarcted tissue to transmurally infarcted tissue. Infarcted tissue exhibited significantly higher stiffness than healthy tissue. When peak equibiaxial stretch increases up to 20%, the stress increase is 2.19 for medial locally infarcted tissue, 4.49 for medial fully infarcted tissue, and 6.26 for apical fully infarcted tissue. Fully infarcted animals showed significant macroscopic geometrical remodeling, with thickness reductions in the infarcted area of 45%-60%, while locally infarcted tissue showed no thinning. The anisotropy of healthy myocardium was also altered post-MI: medial infarcts exhibited preferentially circumferential anisotropy, while apical infarctions increased isotropy. Histological analysis validated these mechanical alterations, revealing a substantial increase in collagen content in infarcted regions. In LCX infarctions, collagen distribution was uniformly aligned, whereas in LAD ones, its distribution was spatially heterogeneous. Non-infarcted tissue far from the infarction did not exhibit changes in mechanical properties or collagen content, suggesting a localized effect at least 6 weeks post-MI. These findings highlight the importance of considering the extent and location of MI when developing personalized therapeutic strategies. Statement of Significance This work provides a comprehensive mechanical and histological assessment of post-infarct porcine myocardium using advanced multimodal testing. Unlike previous studies, we compare two infarct types (LAD and LCX) under identical conditions and examine regional and severity-dependent differences in stiffness, compressibility, and anisotropy. We show that infarction induces local rather than global changes in tissue passive mechanics, modulated by infarct geometry and scar distribution. These insights support more accurate cardiac modeling and may guide personalized therapeutic strategies after myocardial infarction.