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Adriamycin induced cardiomyopathy

Doxorubicin (Adriamycin). Has been used in oncologic practice since the late 1960s. The tumors most commonly responding to doxorubicin include breast and esophageal carcinomas; osteosarcoma, Kaposi's sarcoma, and soft-tissue sarcomas; and Hodgkin's and non-Hodgkin's lymphomas. However, reports of

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Adriamycin induced cardiomyopathy

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    1. Adriamycin induced cardiomyopathy G.A.Prasad MD Sinai Samaritan Medical Center Milwaukee, WI

    2. Doxorubicin (Adriamycin) Has been used in oncologic practice since the late 1960s. The tumors most commonly responding to doxorubicin include breast and esophageal carcinomas; osteosarcoma, Kaposi's sarcoma, and soft-tissue sarcomas; and Hodgkin's and non-Hodgkin's lymphomas. However, reports of fatal cardiotoxic effects of doxorubicin have subdued enthusiasm for this drug.

    3. Incidence In a retrospective study of 399 patient records, cardiomyopathy and congestive heart failure were dose-dependent. Incidence rose to unacceptably high levels when the cumulative dose of the drug exceeded 550 mg per square meter of body-surface area.

    4. Incidence CHF developed in < 4 % of patients who had received a cumulative dose of 500 to 550 mg of doxorubicin /m2, < 18% at a dose of 551 to 600 mg/m2 and to about 36% at a dose of 601 mg/m2 An empirical dose limit of 500 mg/m2 was suggested as a strategy to minimize the risk of cardiomyopathy. CMP has been reported to develop at a cumulative dose of doxorubicin of less than 500 mg/m2.

    5. Risk-Factors for Doxorubicin Induced Cardiomyopathy Age > 70 yr Combination therapy Mediastinal radiotherapy (previous or concomitant) Previous cardiac disease (coronary, valvular, or myocardial) Hypertension Liver disease Whole-body hyperthermia

    6. Cause ?? The chemical structure of doxorubicin is prone to the generation of free radicals, and the oxidative stress that results correlates with cellular injury. Doxorubicin administration is associated with a decrease in the presence of the endogenous antioxidants responsible for the scavenging of free radicals. A decrease in antioxidants and an increase in oxidants (free radicals) result in increased oxidative stress, leading to myocardial damage.

    7. Diagnosis The standard clinical approach to monitoring for doxorubicin cardiotoxicity : assessment of base-line cardiac performance before doxorubicin therapy begins regular monitoring during treatment, and follow-up after therapy has been completed. The insidious nature of doxorubicin-induced CMP is best observed in the transient improvement in cardiac performance after the completion of therapy, followed by the development of full-blown CMP with CHF after years of latency.

    8. Diagnostic Procedures Characteristics physical examination and history taking lack of specificity electrocardiography: arrhythmias, flattening lack of specificity of T-wave, prolongation of QT interval, decrease in R-wave voltage serial echocardiography and radionuclide high reliability imaging: decrease in left ventricular wide use and ejection fraction availability angiography with radiolabeled anti- high sensitivity myosin antibody for cell necrosis; low specificity angiocardiography with metaiodobenzyl- high sensitivity for guanidine myocardial neural integrity and cardiac function low specificity endomyocardial biopsy greatest reliability high expense

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