Trastuzumab Cardiotoxicity: Mechanism and Management

Abstract

Trastuzumab, a therapeutic drug for patients with breast cancer, is one of the most effective and commonly used anticancer drugs for breast cancer. However, its adverse effects include cardiotoxicity, and there is a risk of developing conditions such as arrhythmia, cardiomyopathy, and heart failure. The adverse cardiac effects associated with trastuzumab are now widely recognized, and their mechanisms are beginning to be partially understood. One of the mechanisms has been suggested to be related to the suppressive action of trastuzumab on the erythroblastic oncogene B2 receptor, which acts protectively on the myocardium. Diagnosis can be made by assessing cardiac function with echocardiography, as well as measuring serum troponin I and N-terminal pro-B-type natriuretic peptide levels as biomarkers, and magnetic resonance imaging diagnosis may be helpful for early detection. As for therapeutic and prophylactic drugs, β-blockers and angiotensin-converting enzyme inhibitors, which are used to treat heart failure, have been shown to be effective, while recently, angiotensin receptor/neprilysin and sodium–glucose cotransporter 2 inhibitors are expected to be effective. Furthermore, the cardioprotective effects of proprotein convertase subtilisin/kexin type 9 inhibitors, which are used to treat lipid disorders, have also been attracting attention. This review will summarize the mechanisms, diagnostic methods, and treatment/preventive methods of cardiotoxicity associated with antihuman epidermal growth factor receptor 2 therapies, including trastuzumab.