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Updated: Jun 25, 2026

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils
09:39

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils

Published on: June 2, 2023

[Neutrophilic intracellular metabolic changes and fatal outcome in coronary heart disease]

A E Kratnov, I V Khabarova

    Klinicheskaia Laboratornaia Diagnostika
    |March 4, 2009
    PubMed

    Insights

    Neutrophil metabolic changes in coronary heart disease (CHD) patients are linked to fatal outcomes. Increased malonic dialdehyde and immune complexes in CHD patients indicate a depleted antioxidant defense, contributing to disease severity.

    Area of Science:

    • Biochemistry
    • Immunology
    • Cardiology

    Context:

    • Coronary heart disease (CHD) is a leading cause of mortality.
    • Neutrophil function plays a role in inflammatory processes associated with cardiovascular disease.
    • Understanding cellular metabolic changes in CHD is crucial for predicting patient outcomes.

    Purpose:

    • To investigate the association between neutrophilic intracellular metabolic alterations and fatal outcomes in coronary heart disease (CHD) patients.
    • To identify specific biomarkers of neutrophilic dysfunction in CHD.
    • To explore the role of oxidative stress and immune complexes in CHD mortality.

    Summary:

    • 121 CHD patients exhibited elevated neutrophils, C-reactive protein, malonic dialdehyde, and neutrophilic lactate on admission compared to controls.
    • Deceased patients were older, had more myocardial infarction history, and lower ejection fraction.
    • Survivors showed higher myeloperoxidase activity, suppressed neutrophilic glutathione reductase, and increased malonic dialdehyde and circulating immune complexes (CIC).

    Impact:

    • Findings suggest that activated lipid peroxidation and CIC-dependent neutrophilic metabolism deplete phagocyte antioxidant defenses in CHD patients with left ventricular systolic dysfunction.
    • This process may lead to neutrophil death, endothelial damage, and hemostatic disorders, contributing to mortality.
    • Identifies potential therapeutic targets for mitigating CHD progression and improving patient survival.

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