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Chloroquine-induced cardiomyopathy

Insights

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.
  • 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.

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