Anti-breast cancer therapies induce cardiotoxicity that affects the survival of patients with a nearly 90% 5-year survival rate, which may be prevented by ACE inhibitors, ARBs, and beta-blockers.
What are the mechanisms of anti-breast cancer drug-induced cardiomyopathy and strategies for its prevention?
This review highlights the mechanisms of chemotherapy-induced cardiomyopathy in breast cancer patients and suggests that ACE inhibitors, ARBs, and beta-blockers may offer cardioprotection.
With the progression of tumor treatment, the 5-year survival rate of breast cancer is close to 90%. Cardiovascular toxicity caused by chemotherapy has become a vital factor affecting the survival of patients with breast cancer. Anthracyclines, such as doxorubicin, are still some of the most effective chemotherapeutic agents, but their resulting cardiotoxicity is generally considered to be progressive and irreversible. In addition to anthracyclines, platinum- and alkyl-based antitumor drugs also demonstrate certain cardiotoxic effects. Targeted drugs have always been considered a relatively safe option. However, in recent years, some random clinical trials have observed the occurrence of subclinical cardiotoxicity in targeted antitumor drug users, which may be related to the effects of targeted drugs on the angiotensin converting enzyme, angiotensin receptor and β receptor. The use of angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and beta-blockers may prevent clinical cardiotoxicity. This article reviews the toxicity and mechanisms of current clinical anti-breast cancer drugs and proposes strategies for preventing cardiovascular toxicity to provide recommendations for the clinical prevention and treatment of chemotherapy-related cardiomyopathy.
Liu et al. (Mon,) conducted a review in Breast cancer-induced cardiomyopathy. Anti-breast cancer drugs was evaluated. Anti-breast cancer therapies induce cardiotoxicity that affects the survival of patients with a nearly 90% 5-year survival rate, which may be prevented by ACE inhibitors, ARBs, and beta-blockers.