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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

730
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Related Experiment Video

Updated: Jan 16, 2026

Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
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A Multi-Scale Finite Element Method for Investigating Fiber Remodeling in Hypertrophic Cardiomyopathy.

Mohammad Mehri, Kenneth S Campbell, Lik Chuan Lee

    Arxiv
    |September 29, 2025
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    Summary
    This summary is machine-generated.

    Hypertrophic cardiomyopathy (HCM) causes significant fiber disarray due to cellular abnormalities, disrupting heart mechanics. This study quantifies how different abnormalities impact disarray and cardiac function.

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    Area of Science:

    • Cardiovascular Research
    • Biomedical Engineering
    • Computational Biology

    Background:

    • Hypertrophic cardiomyopathy (HCM) is characterized by myocardial fiber disarray, a key factor in cardiac dysfunction and heart failure.
    • Understanding the link between cellular abnormalities and fiber disarray is crucial for elucidating HCM pathophysiology.

    Purpose of the Study:

    • To investigate how heterogeneous cellular abnormalities (hypercontractility, hypocontractility, fibrosis) contribute to fiber disarray in HCM.
    • To quantify the impact of these abnormalities on cardiac pumping function using a multiscale finite element model.

    Main Methods:

    • Utilized the MyoFE multiscale finite element cardiac modeling framework.
    • Employed a stress-based law to simulate myofiber and collagen reorientation.
    • Quantified fiber disarray and assessed cardiac performance in models with heterogeneous cellular perturbations.

    Main Results:

    • Heterogeneous cellular abnormalities significantly disrupt myocardial mechanics, leading to substantial fiber disarray.
    • The pattern and severity of fiber disarray varied based on the specific cellular perturbation (hypercontractility, hypocontractility, fibrosis).
    • Higher fiber disarray was consistently observed near the epicardium compared to the endocardium across all perturbed left ventricle (LV) models.

    Conclusions:

    • HCM-induced cellular abnormalities are major drivers of myocardial fiber disarray, impacting cardiac function.
    • Regional differences in fiber disarray (epicardial vs. endocardial) are linked to myocardial mechanics and consistent with experimental findings.
    • Cardiac performance decline is exacerbated by fibrosis and hypocontractility, suggesting therapeutic targets for HCM remodeling.