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Cardiotoxicity associated with high-dose cyclophosphamide therapy

J S Gottdiener, F R Appelbaum, V J Ferrans

    Archives of Internal Medicine
    |May 1, 1981
    PubMed
    Summary

    High-dose cyclophosphamide chemotherapy can cause severe cardiac toxicity, including fatal heart failure and pericardial tamponade, in patients with hematologic cancers. Early cardiac function decline does not always predict clinical deterioration.

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    Area of Science:

    • Cardiology
    • Oncology
    • Pharmacology

    Background:

    • High-dose cyclophosphamide is a cornerstone chemotherapy for hematologic malignancies.
    • Cyclophosphamide cardiotoxicity is a known but often severe complication.
    • Understanding the specific cardiac effects is crucial for patient management.

    Purpose of the Study:

    • To assess the cardiac effects of high-dose cyclophosphamide in patients with hematologic malignant neoplasms.
    • To characterize the incidence and timing of cardiac dysfunction and failure.
    • To correlate clinical findings with histopathologic evidence of cardiotoxicity.

    Main Methods:

    • Echocardiography was used to evaluate left ventricular systolic function (fractional shortening).
    • Electrocardiogram (ECG) voltage was monitored.

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  • Pericardial effusion and tamponade were assessed.
  • Histopathologic and electron microscopic examination of cardiac tissue was performed.

    • Main Results:

    • Left ventricular systolic function declined significantly 5-16 days post-cyclophosphamide initiation.
    • Pericardial effusion occurred in 33% of patients; ECG voltage decreased in 33% even without effusion.
    • Congestive heart failure developed in 28%, with 19% dying from myocardial failure.
    • Pericardial tamponade occurred in 19%, leading to death in 5 patients.
    • Histopathology revealed endothelial injury and hemorrhagic myopericarditis.

    Conclusions:

    • High-dose cyclophosphamide is associated with a toxic, potentially fatal pericardiomyopathy.
    • Cyclophosphamide-induced cardiotoxicity can manifest as heart failure and pericardial tamponade.
    • Depressed ECG voltage and systolic function do not reliably predict clinical cardiac deterioration.