Etoposide cardiotoxicity

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Rescuing COX-2 inhibitors from the waste bin. Nature Reviews Drug Discovery. Protecting against anthracycline-induced myocardial damage: Anthracyclines Cytarabine, Cisplatin, 5-fluorouracil, Cytokines, Arsenic trioxide, Radiation therapy.

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However, high-dose rapid administration may induce lethal acute pericarditis and hemorrhagic myocarditis [56]. Patient was discharged and advised to avoid beta-blockers. Use of cardiac troponin T levels as an indicator of doxorubicin-induced cardiotoxicity. Perez EA, Rodeheffer R: Coronary artery spasm induced by capecitabine.

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Rituximab is used to treat a variety of malignant and benign hematologic conditions. Fatal coronary artery fibrosis after treatment with bleomycin, vinblastine, and cis-platinum.

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Extra caution should be given to patients who are already on medications, which may subject them to bradycardia, such as beta blockers. It seems that reduction of capillary permeability causes increased pressure load, leading to hypertrophy of the heart and subsequently congestive HF [71].

Atrial fibrillation AF AF can be induced by various cytostatic agents, such as ifosfamide, gemcitabine, melphalan, cisplatin, docetaxel, 5-FU, or etoposide [42] and [43]. H9c2 cardiomyoblasts treated with increasing concentrations of DOX were also assessed for hypertrophy.

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A baseline and periodic ECG monitoring are recommended, as well as dosage adjustments or discontinuation of therapy that may be necessary in the face of QT prolongation. Jpn J Pharmacol The onset typically occurs within the first week after therapy. Bradycardia is a rare side effect of etoposide, there is only one reported case in the literature.

Acute and chronic pericarditis [ 68 ] and late appearance of chronic pericardial disease [ 6970 ] after mediastinal radiation for Hodgkin lymphoma were reported in echocardiographic studies. ErbB2 is essential in the prevention of dilated cardiomyopathy. Burger AJ, Mannino S: Effects of chemotherapy on the heart, in Kapoor AS ed: Journal of Clinical Investigation.

Serum markers that detect damage of the myofibrils and of the cardiomyocytes, such as the different isoforms of troponin, are useful in detecting the acute cardiotoxicity that is mediated by therapeutic agents that induce cell death [86].

A prospective evaluation of new dosing regimens.