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Chloroquine-induced cardiomyopathy.

H A McAllister, V J Ferrans, R J Hall

    Archives of Pathology & Laboratory Medicine
    |October 1, 1987
    PubMed
    Summary
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    Chloroquine phosphate treatment for systemic lupus erythematosus can cause biventricular hypertrophy and failure. Myocardial deposits in patients indicate chloroquine-induced cardiotoxicity, necessitating clinical awareness and biopsy for diagnosis.

    Area of Science:

    • Cardiology
    • Toxicology
    • Rheumatology

    Background:

    • Systemic lupus erythematosus (SLE) is an autoimmune disease with potential cardiovascular manifestations.
    • Chloroquine phosphate is a medication used to treat SLE and other conditions.
    • Cardiotoxicity is a known potential side effect of certain medications.

    Observation:

    • Two patients with SLE developed biventricular hypertrophy and failure during chloroquine phosphate treatment.
    • Morphologic analysis of cardiac tissue revealed electron-dense lamellar and curvilinear bodies within myocytes.
    • These myocardial deposits resemble those seen in chloroquine-induced skeletal myopathy.

    Findings:

    • The observed myocardial changes are consistent with chloroquine-induced cardiotoxicity.

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  • The findings suggest the cardiac issues were drug-induced rather than a direct manifestation of SLE.
  • Endomyocardial biopsy is crucial for identifying these specific drug-induced cardiac changes.

    • Implications:

    • Clinical awareness of chloroquine cardiotoxicity is essential for patients on this medication.
    • Early diagnosis through endomyocardial biopsy can prevent further cardiac damage.
    • This study highlights the importance of monitoring cardiac function in patients receiving chloroquine phosphate.