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Myocardial performance and extracellular ionized calcium in a severely failing human heart

R Ginsburg, L J Esserman, M R Bristow

    Annals of Internal Medicine
    |May 1, 1983
    PubMed

    Insights

    In severe heart failure, beta-agonist drugs may fail due to receptor loss. Calcium levels then become critical for heart muscle function, offering a potential treatment target.

    Area of Science:

    • Cardiology
    • Pharmacology
    • Biochemistry

    Background:

    • Investigated a 16-year-old patient with end-stage congestive heart failure unresponsive to beta-agonist therapy.
    • Addressed critically low serum ionized calcium (Ca2+) levels, which were corrected with calcium chloride (CaCl2) infusions.

    Observation:

    • Myocardial performance demonstrated a direct correlation with serum Ca2+ levels.
    • In vitro studies of the explanted heart revealed subsensitivity to isoproterenol and near-complete absence of beta-adrenergic receptors.
    • Papillary muscles responded normally to calcium, and other cellular signaling pathways (adenylate cyclase) were unaffected.

    Findings:

    • Beta-adrenergic receptor down-regulation was identified as the cause of beta-agonist ineffectiveness.
    • Myocardial contractility was found to be dependent on extracellular calcium levels in this specific condition.

    Implications:

    • Suggests that in cases of beta-adrenergic receptor down-regulation, calcium levels are crucial for maintaining cardiac contractility.
    • Highlights a potential therapeutic strategy focusing on calcium modulation when beta-agonists are ineffective in heart failure.

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