Doxorubicin and trastuzumab induce cardiotoxicity through distinct mechanisms, with doxorubicin causing irreversible dose-dependent damage and trastuzumab causing reversible dose-independent damage.
This review highlights the distinct mechanisms of cardiotoxicity induced by doxorubicin (irreversible, TOP2B-mediated) and trastuzumab (reversible, HER2-mediated), emphasizing the need for cardio-oncology monitoring and potential preventative strategies.
Anticancer drugs play an important role in reducing mortality rates and increasing life expectancy in cancer patients. Treatments include monotherapy and/or a combination of radiation therapy, chemotherapy, hormone therapy, or immunotherapy. Despite great advances in drug development, some of these treatments have been shown to induce cardiotoxicity directly affecting heart function and structure, as well as accelerating the development of cardiovascular disease. Such side effects restrict treatment options and can negatively affect disease management. Consequently, when managing cancer patients, it is vital to understand the mechanisms causing cardiotoxicity to better monitor heart function, develop preventative measures against cardiotoxicity, and treat heart failure when it occurs in this patient population. This review discusses the role and mechanism of major chemotherapy agents with principal cardiovascular complications in cancer patients.
Gabani et al. (Wed,) conducted a review in Chemotherapy-induced cardiotoxicity. Doxorubicin and Trastuzumab was evaluated. Doxorubicin and trastuzumab induce cardiotoxicity through distinct mechanisms, with doxorubicin causing irreversible dose-dependent damage and trastuzumab causing reversible dose-independent damage.