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Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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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...
Cellular Adaptation I: Introduction and Atrophy01:23

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Cells can adapt to environmental changes to maintain function and avoid injury, a process called cellular adaptation. Adapted cells exist in a reversible intermediate state with changes in size, number, phenotype, metabolism, or function. These responses help cells meet altered physiological or pathological demands; for example, enlargement of breast and uterine tissues during pregnancy. Early adaptations may enhance function, but persistent stress eventually causes tissue damage.Types of...
Cellular Adaptation II: Hypertrophy01:26

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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
10:21

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Published on: June 14, 2016

Physiologic or pathologic hypertrophy.

H P Krayenbuehl, O M Hess, J Schneider

    European Heart Journal
    |January 1, 1983
    PubMed
    Summary
    This summary is machine-generated.

    Physiologic hypertrophy from exercise has normal function, but abnormal loading causes pathologic changes. Excessive muscle fiber growth, not fibrosis, predicts poor heart function after surgery.

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    Area of Science:

    • Cardiology
    • Pathology

    Background:

    • Physiologic hypertrophy from exercise involves reversible changes and normal heart function.
    • Abnormal loading can cause cardiac hypertrophy, but its 'physiologic' nature is debated due to potential in vitro dysfunction.
    • Left ventricular (LV) hypertrophy from aortic valve disease shows preserved ejection fraction (EF) below 180 g/m², but depressed EF above this mass.

    Purpose of the Study:

    • To compare myocardial structure and function in patients with varying degrees of LV hypertrophy.
    • To investigate the relationship between interstitial fibrosis (IF), muscle fiber diameter (MFD), and LV function.
    • To assess the reversibility of structural changes and their impact on postoperative cardiac function.

    Main Methods:

    • Analysis of endomyocardial biopsies to measure IF and MFD in patients with compensated LV function and heart failure.
    • Comparison of preoperative and postoperative LV function (EF, LVEDP, cardiac index) after aortic valve replacement.
    • Correlation of structural parameters (IF, MFD) with functional parameters (EF, postoperative function).

    Main Results:

    • Interstitial fibrosis was similarly increased in compensated and failing hearts (16-18% vs. normal <5%).
    • Muscle fiber diameter was significantly larger in patients with heart failure (30 µm) and those with depressed postoperative function (35 µm) compared to controls.
    • Despite aortic valve replacement, IF remained elevated and MFD decreased but did not normalize, irrespective of postoperative function.

    Conclusions:

    • In secondary hypertrophy, myocardial structure is pathologic even with normal LV function.
    • Depressed cardiac function is likely linked to excessive muscle fiber hypertrophy rather than interstitial fibrosis.
    • Massive fiber hypertrophy predicts unfavorable postoperative LV function, and fibrosis is irreversible after load correction.