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21 - Cardiovascular Complications

Published online by Cambridge University Press:  23 November 2009

Joseph H. Antin
Affiliation:
Dana-Farber Cancer Institute, Boston
Deborah Yolin Raley
Affiliation:
Dana-Farber Cancer Institute, Boston
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Summary

MYOPERICARDITIS

Cyclophosphamide cardiotoxicity is idiosyncratic and independent of baseline cardiac function. When used in high doses, cyclophosphamide can induce myopericarditis that can be associated with pericardial tamponade or pulseless electrical activity (PEA) arrest and death. Milder forms may lead to congestive heart failure, requiring appropriate therapy. More common is the development of myocardial edema that can result in reduction in electrocardiogram (ECG) voltage but no functional consequences.

Clinical Manifestations

  • Shortness of breath, chest discomfort (often pleuritic and improved with sitting up), cough, fever, tachycardia.

Diagnosis

  • Pericardial rub, ST segment elevation, PR depression.

  • Echocardiogram may show fluid; with impending tamponade, may also have diastolic indentation or collapse of the right ventricle. Aspiration under fluoroscopic guidance may be required for presumed infectious or malignant etiologies.

Treatment

  • If manifestations are mild, supportive care is usually adequate.

  • Nonsteroidal anti-inflammatory drugs (NSAIDS) are not used in patients with thrombocytopenia.

  • If cyclophosphamide is the presumed etiology, there is no specific therapy.

  • If the underlying problem is infectious or malignant it is treated specifically.

  • Pericardiocentesis or a pericardial window if tamponade develops.

ARRHYTHMIAS AND CONDUCTION ABNORMALITIES

Arrhythmias are uncommon during hematopoietic stem cell transplantation (HSCT) except as reflections of preexistent heart disease. New onset rhythm disturbances or conduction delay may be due to dimethyl sulfoxide (DMSO) at the time of stem cell infusion, cyclophosphamide, volume overload, infection, medications, infarction, cardiomyopathy, pulmonary embolus, electrolyte abnormalities, and thyroid disease.

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Publisher: Cambridge University Press
Print publication year: 2009

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