Indication
Doxorubicin-induced cardiomyopathy
Doxorubicin-induced cardiomyopathy is a toxic myocardial disorder affecting the cardiovascular system in pediatric and adult oncology patients treated with the anthracycline chemotherapeutic agent doxorubicin. Read more about Doxorubicin-induced cardiomyopathy
20 drugs 17 manufacturers
Drugs that treat it
Common Doxorubicin-induced cardiomyopathy therapies.
DEXRAZOXANE (dexrazoxane HCl)
DEXRAZOXANE HCL
TOTECT (dexrazoxane HCl)
TOTECT (dexrazoxane HCl)
DEXRAZOXANE (dexrazoxane HCl)
DEXRAZOXANE (dexrazoxane HCl)
DEXRAZOXANE (dexrazoxane HCl)
DEXRAZOXANE (dexrazoxane HCl)
News & literature
Coming soonRelated codes
Coming soonRelated conditions & guidelines
Coming soonDoxorubicin-induced cardiomyopathy is a toxic myocardial disorder affecting the cardiovascular system in pediatric and adult oncology patients treated with the anthracycline chemotherapeutic agent doxorubicin.
Pathophysiologically, the condition is driven by cumulative, dose-dependent myocardial injury characterized by topoisomerase IIß inhibition, mitochondrial dysfunction, reactive oxygen species generation, and disrupted calcium homeostasis, which culminate in cardiomyocyte death, myofibrillar loss, and myocardial fibrosis.
Clinically, it most frequently manifests as chronic or late-onset dilated cardiomyopathy marked by progressive left ventricular systolic dysfunction, reduced ejection fraction, cardiac remodeling, and congestive heart failure.
- nih.gov
Doxorubicin-induced cardiomyopathy is a toxic myocardial disorder affecting the cardiovascular system in pediatric and adult oncology patients treated with the anthracycline chemotherapeutic agent doxorubicin
- nih.gov
Doxorubicin-induced cardiomyopathy is a toxic myocardial disorder affecting the cardiovascular system in pediatric and adult oncology patients treated with the anthracycline chemotherapeutic agent doxorubicin
- nih.gov
Pathophysiologically, the condition is driven by cumulative, dose-dependent myocardial injury characterized by topoisomerase IIβ inhibition, mitochondrial dysfunction, reactive oxygen species generation, and disrupted calcium homeostasis, which culminate in cardiomyocyte death, myofibrillar loss, and myocardial fibrosis Clinically, it most frequently manifests as chronic or late-onset dilated cardiomyopathy marked by progressive left ventricular systolic dysfunction, reduced ejection fraction, c...
- nih.gov
Pathophysiologically, the condition is driven by cumulative, dose-dependent myocardial injury characterized by topoisomerase IIβ inhibition, mitochondrial dysfunction, reactive oxygen species generation, and disrupted calcium homeostasis, which culminate in cardiomyocyte death, myofibrillar loss, and myocardial fibrosis Clinically, it most frequently manifests as chronic or late-onset dilated cardiomyopathy marked by progressive left ventricular systolic dysfunction, reduced ejection fraction, c...
- ijpsjournal.com
Pathophysiologically, the condition is driven by cumulative, dose-dependent myocardial injury characterized by topoisomerase IIβ inhibition, mitochondrial dysfunction, reactive oxygen species generation, and disrupted calcium homeostasis, which culminate in cardiomyocyte death, myofibrillar loss, and myocardial fibrosis Clinically, it most frequently manifests as chronic or late-onset dilated cardiomyopathy marked by progressive left ventricular systolic dysfunction, reduced ejection fraction, c...
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