Cardiomyopathy due to anthracyclines

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Anthracycline-induced cardiotoxicity is due in large part to the generation of free radicals from doxorubicin through mitochondrial redox cycling of doxorubicin in the cardiomyocyte, which ultimately results in left ventricular dysfunction, and in the most severe cases, congestive heart failure.

Cardiotoxicity[edit | edit source]

Cardiotoxicity is the occurrence of heart electrophysiology dysfunction or muscle damage. The heart becomes weaker and is not as efficient in pumping and therefore circulating blood. Cardiotoxicity may be caused by chemotherapy (an usual example is the class of anthracyclines) treatment, complications from anorexia nervosa, adverse effects of heavy metals intake, or an incorrectly administered drug such as bupivacaine.

Diagnosis[edit | edit source]

One of the ways to detect cardiotoxicity at early stages when there is a subconical dysfunction is by measuring changes in regional function of the heart using strain. A complete examination of the cardiovascular system to detect presence of signs of overt heart failure, such as elevated jugular venous pressure and S3 gallop, is essential. An electrocardiogram should be obtained, which usually demonstrates nonspecific ST-T wave changes and sometimes low-voltage QRS complexes. A chest X-ray is also helpful to assess cardiomegaly and signs of pulmonary venous congestion. It should be emphasized that the presence or absence of the abnormalities by these evaluations are nonspecific and nondiagnostic.

Treatment[edit | edit source]

The medication(s) listed below have been approved by the Food and Drug Administration (FDA) as orphan products for treatment of this condition. Dexrazoxane (Brand name: Zinecard (injection)) Cardiomyopathy associated with doxorubicin administration in women with metastatic breast cancer who have received a cumulative dose of 300mg/m2.

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