Infarct border-zone biomechanics after myocardial infarction: linking mechanotransduction, fibrosis, and ventricular dysfunction

Figures

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  FIGURE 1. Multiscale structure–function framework of the infarct border zone after myocardial infarction. The schematic integrates processes across biological scales. (A) Shows the organ-scale infarct–remote interface, where myocardial infarction produces a scar core surrounded by a mechanically heterogeneous border zone that redistributes ventricular wall stress and strain. (B) illustrates ventricular torsion and fiber architecture, emphasizing how altered contraction, twist, and untwist can modify border-zone deformation after MI. (C) Shows tissue-level imaging features of infarction and peri-infarct heterogeneity, including scar, gray zone, and adjacent viable myocardium. (D) Summarizes the translational framework in which multimodal imaging, strain assessment, microstructural characterization, and patient-specific computational modeling are integrated to quantify regional mechanics and support model-informed risk stratification. The figure emphasizes that the border zone is not simply a transition between scar and remote myocardium, but a multiscale biomechanical interface linking tissue structure, cellular mechanotransduction, ventricular function, and clinical outcomes.

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  FIGURE 2. Temporal evolution of the infarct border zone after myocardial infarction. The schematic illustrates the changing spatial extent, tissue composition, and mechanical role of the border zone across three broad phases of healing. In the acute phase, the border zone is dominated by edema, inflammation, microvascular injury, depressed contractility, and mechanically vulnerable matrix disruption. In the subacute phase, granulation tissue, fibroblast activation, myofibroblast differentiation, and early collagen deposition alter local stiffness and begin to stabilize the infarct–remote interface. In the chronic phase, mature scar, collagen cross-linking, anisotropic stiffness gradients, residual stress, and persistent electromechanical heterogeneity define the long-term border-zone phenotype. The figure emphasizes that the border zone is not a fixed geometric ring but a time-dependent interface whose mechanical meaning depends on healing phase, loading conditions, and tissue composition.

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  FIGURE 3. Translational workflow for a clinically deployable border-zone mechanical risk phenotype. Stepwise clinical-to-computational pipeline linking routine imaging to an interpretable, uncertainty-aware border-zone risk output. Imaging inputs include echocardiographic strain and cardiovascular magnetic resonance (CMR) measures such as late gadolinium enhancement (LGE) and mapping (T1, T2, and ECV), alongside microvascular injury markers (MVO and IMH) where available, with optional diffusion-tensor CMR to inform microstructural organisation. The workflow proceeds through segmentation of the infarct core and border zone using a prespecified definition, estimation of loading conditions from brachial (or invasive) pressure, and construction of a patient-specific finite-element model incorporating anisotropic constitutive laws and regionally varying activation. Inverse modelling/data assimilation is then used to estimate border-zone parameters (e.g., effective stiffness and active tension) consistent with the observed deformation. At the same time, uncertainty quantification propagates segmentation and measurement uncertainties into stress, strain-gradient, and shear estimates. The final…