Anthracyclines and related agents

Source: Late Effects of Treatment for Childhood Cancer (PDQ®)–Health Professional Version, National Cancer Institute.

Source updated: April 14, 2025 · Captured 2026-09-09.

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Context: Late Effects of the Cardiovascular System / Treatment Risk Factors

Anthracyclines (e.g., doxorubicin, daunorubicin, idarubicin, and epirubicin) and anthraquinones (e.g., mitoxantrone) are known to directly injure cardiomyocytes through inhibition of topoisomerase 2-beta in cardiomyocytes and formation of reactive oxygen species, resulting in activation of cell-death pathways and inhibition of mitochondrial apoptosis.[29,30] The downstream results of cell death are changes in heart structure, including wall thinning, which leads to ventricular overload and pathological remodeling that, over time, leads to dysfunction and eventual clinical heart failure.[31,32]

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Risk factors for anthracycline-related cardiomyopathy include the following:[19,33]

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Cumulative dose, particularly greater than 250 to 300 mg/m2.

Younger age at time of exposure, particularly children younger than 5 years.

Increased time from exposure.

While there is no definitive safe lower dose threshold, doses in excess of 250 to 300 mg/m2 have been associated with a substantially increased risk of cardiomyopathy, with cumulative incidences exceeding 5% after 20 years of follow-up, and in some subgroups, reaching or exceeding 10% cumulative incidence by age 40 years.[18,19,32]

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Concurrent chest or heart radiation therapy also further increases risk of cardiomyopathy,[10,28,34] as does the presence of other cardiometabolic traits such as hypertension.[8,35]

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While development of clinical heart failure can occur within a few years after anthracycline exposure, in most survivors—even those who received very high doses—clinical manifestations may not occur for decades.

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Anthracycline dose equivalency →Anthracycline cardioprotection →

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