The ACC/AHA Guidelines for the Diagnosis and Treatment of Chronic Heart Failure in Adults recommend that most patients with heart failure should be routinely treated with three classes of drugs: angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor antagonists (ARBs), and β-blockers. Because anthracycline-induced heart failure/cardiomyopathy is associated with tachyarrhythmias, β-blockers are commonly used in the treatment of anthracycline-induced heart failure as symptomatic therapy. However, the prevention of cardiotoxicity in cancer chemotherapy patients is often overlooked by clinical oncologists. Strategies to reduce cardiotoxicity of anthracyclines include: Adequate assessment of the risk of cardiotoxicity prior to cardiotoxic drug therapy. Adjustment of dose or regimen, enhanced monitoring of cardiac function, and use of alternative dosage forms (e.g., liposomal dosage forms). Evidence-based medicine shows that dexrazoxane (DEX) is the only drug that can effectively prevent cardiotoxicity caused by anthracyclines and is now widely used clinically in the US and EU. (1) Application of dexamethasone before the first use of anthracyclines for effective prevention of anthracycline cardiotoxicity The drug that is currently proven by research and recommended by authoritative guidelines for cardiotoxicity protection is dexamethasone (DEX), which can effectively prevent the occurrence of anthracycline subclinical cardiotoxicity. DEX is an analogue of the chelating agent EDTA, which readily penetrates cell membranes and undergoes enzymatic and non-enzymatic hydrolysis reactions in cells. The cardiotoxicity of anthracycline drugs was inhibited. In addition, a recent study also showed that DEX has its own free radical (superoxide anion radical, hydroxyl radical, etc.) scavenging and antioxidant effects in the absence of iron and enzymes. A multicenter randomized controlled clinical study showed significant cardioprotective effects of DEX in breast cancer patients treated with anthracycline chemotherapy without affecting the antitumor efficacy of anthracyclines. 2004 study published in the New England Journal of Medicine also confirmed that dexamphetamine can prevent myocardial injury caused by doxorubicin in patients with acute lymphoblastic leukemia (ALL). Domestic multicenter phase II clinical trials have also demonstrated significant protection against doxorubicin-induced cardiotoxicity in combination with doxorubicin for the treatment of breast cancer and lymphoma. The ACC/AHA Guidelines for the Diagnosis and Treatment of Chronic Heart Failure in Adults noted the cardioprotective effect of dexrazoxane in patients receiving anthracycline-based chemotherapy. In addition, the 2010 NCCN Guidelines for Non-Hodgkin’s Lymphoma and the NCCN Guidelines for Geriatric Oncology both specify that cardiac function should be closely monitored if anthracyclines are used for treatment, and that dexrazoxane can be added as a cardioprotective agent. To effectively prevent anthracycline-induced cardiotoxicity, dextropropylenimine should be co-administered before the first anthracycline, with a dose ratio of 10-20:1 between dextropropylenimine and anthracycline (recommended DEX:ADM = 20:1, D E X : D N R = 20:1, D E X : E P I = 10:1, DEX:MIT = 50:1). Dextropropylenimine is prepared with a special solvent, sodium lactate, and then diluted to 200 ml with 0.9% sodium chloride or 5% glucose injection for rapid intravenous infusion and dosed over 30 minutes, with anthracyclines given immediately after the drip. Other cardioprotective agents, including coenzyme Q10 and leucovorin, may have cardioprotective effects but their mechanism and ability to prevent cardiomyopathy need to be further explored. The latest Meta-analysis showed that coenzyme Q10, levocaine, N-acetylcysteine, vitamin C, and vitamin E have no significant cardioprotective effect on anthracycline chemotherapy, while DEX can benefit patients significantly with a significant reduction in the incidence of heart failure. (2) Other measures to reduce anthracycline cardiotoxicity The chronic and delayed cardiotoxicity of anthracyclines is related to their cumulative dose, so limiting the cumulative dose of anthracyclines can reduce the incidence of their cardiotoxicity. Cardiotoxicity of anthracyclines can also be reduced by continuous intravenous dosing of anthracyclines rather than by bullet injection, the mechanism being by reducing the peak concentration of the drug. However, in a randomized trial, a 48-hour continuous infusion was not found to provide better cardioprotection than intravenous pill injection (1-hour injection). Therefore, whether a change in the method of administration is sufficient to prevent anthracycline cardiotoxicity needs to be investigated in depth. In addition, the use of liposomal anthracyclines may reduce the incidence of anthracycline cardiotoxicity. Doxorubicin, a polyethylene glycol liposome, has a longer half-life because it is not phagocytosed by macrophages and monocytes, and its concentration of drug distribution in the myocardium is reduced, which reduces the tendency of toxin accumulation in the myocardial cells, thus reducing cardiotoxicity and improving safety compared with conventional doxorubicin. Anthracyclines are effective antineoplastic agents, but the severe cardiotoxicity they cause affects their widespread clinical use. The cardiotoxicity of anthracyclines is associated with insufficient clinical attention, in addition to patient and drug factors themselves. The American Heart Association (AHA) recommends that cardiac function be closely monitored during anthracycline therapy, and when LVEF decreases by more than 10%, more sensitive methods of monitoring, such as dynamic monitoring of troponin, are recommended. The monitoring and prevention of cardiotoxicity caused by chemotherapy requires close cooperation between oncologists and cardiovascular physicians, and there is an urgent need to develop monitoring norms or guidelines for the prevention and treatment of cardiotoxicity in chemotherapy patients. The pros and cons of anthracycline chemotherapy should be objectively understood to prevent cardiotoxicity. The benefits and potential risks of treatment should be fully evaluated before treatment, with a comprehensive understanding of the patient’s organ function and tumor status, the mechanism of action, metabolism and interactions, and toxic side effects of the drugs, and full communication with the patient so as to weigh the pros and cons and minimize the risk of heart failure. Cardiac function should be closely monitored during and after treatment for early prevention of anthracycline cardiotoxicity.