Advances in Non-Invasive Myocardial Stiffness Assessment and Clinical Applications in Hypertrophic Cardiomyopathy

Figures

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  Fig. 1.. Mechanisms of increased myocardial stiffness. At the cellular level (left pathway), sarcomere gene mutations serve as the initiating factor, leading to sarcomere hypercontraction, impaired relaxation, and titin dysfunction, which collectively increase intrinsic cardiomyocyte stiffness. At the tissue level (right pathway), these primary cellular issues, compounded by secondary stressors such as altered mechanical stress, energy crisis, and inflammation, result in cardiomyocyte abnormalities and fibroblast activation, ultimately resulting in myocardial disarray and fibrosis. Collectively, the increased intrinsic myocyte stiffness from the cellular pathway and the adverse structural remodeling from the tissue pathway contribute to increased myocardial stiffness. The upward arrow indicates an increase, and the downward arrow indicates a decrease. This figure was created with BioRender.com (BioRender Inc., Toronto, ON, Canada).

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  Fig. 2.. Assessment of contributing factors for myocardial stiffness. Myocardial stiffness arises from intrinsic stiffness, myocyte disarray, and myocardial fibrosis. Various techniques evaluate myocardial stiffness and its contributing factors. Magnetic resonance imaging provides detailed tissue characterization, using late gadolinium enhancement and extracellular volume to quantify myocardial fibrosis, and cardiac diffusion tensor imaging to assess myocyte disarray. Direct quantification of tissue stiffness can be achieved through magnetic resonance elastography, shear wave echocardiography, and intrinsic cardiac elastography. Additionally, artificial intelligence and radiomics analyze image features for characterization of myocardial fibrosis, while finite element analysis creates patient-specific biomechanical models to estimate overall myocardial stiffness. This figure was created with BioRender.com (BioRender Inc., Toronto, ON, Canada).