Risk Of Cardiotoxicity With Lapatinib Treatment In Patients With Or Without Previous Cardiotoxicity Induced By Trastuzumab With Cardiac Disorder Who Were Treated With Lapatinib: A Single Institutional Retrospective Study.

Abstract

Background: Cardiotoxicity is a significant adverse event of trastuzumab, which is used in human epidermal growth factor receptor 2 (HER2)-positive breast cancer patients. Lapatinib (Lap) is a small molecule tyrosine kinase inhibitor of HER1 and HER2, serving as an anti-HER2 treatment. Lap reportedly causes lesser cardiotoxicity than does trastuzumab. In clinical practice, Lap is often administered to patients with cardiac disorder (CD) induced by trastuzumab. However, there are only a few reports on the safety of Lap administration and subsequent evaluation of CDs in such patients. We evaluated whether there was a difference in cardiac toxicity due to Lap administration based on the presence or absence of previous cardiotoxicity induced by trastuzumab.Methods: Ten patients who received Lap for the treatment of metastatic or recurrent and HER2-positive breast cancer at the National Center for Global Health and Medicine, Tokyo, Japan, between April 1, 2016 and August 31, 2020, were included in this study. All patients had a history of trastuzumab administration, and two had developed CD after trastuzumab administration. Lap was carefully administered to these two patients after consultation with a cardiologist. Left ventricular ejection fraction (LVEF) and other clinical information before and after Lap treatment were retrieved from electronic medical records. Results: All patients other than the two with CD after trastuzumab treatment had a baseline LVEF of >55%, and there was no clinically relevant decrease in LVEF after the initiation of Lap. The two patients with CD after trastuzumab treatment exhibited LVEF of 38% and 51% after Lap treatment, respectively.Conclusion: Our data indicate that Lap can be administered without causing further deterioration of cardiac function in patients with CD induced by anti-HER2 monoclonal antibodies. The number of cases must be expanded for further investigation.