Why the study?
Understanding the pathophysiological basis and clinical manifestations of trastuzumab-induced cardiotoxicity is paramount for early detection and cardioprotective treatment.
What are the pathophysiological mechanisms and clinical manifestations of trastuzumab-induced cardiotoxicity in patients with HER2-overexpressing breast cancer?
What are the pathophysiological mechanisms and clinical manifestations of trastuzumab-induced cardiotoxicity in patients with HER2-overexpressing breast cancer?
This review outlines the pathophysiology of trastuzumab-induced cardiotoxicity, emphasizing the inhibition of cardioprotective signaling pathways and the need for early detection and cardioprotection.
Trastuzumab is the primary treatment for all stages of HER2-overexpressing breast cancer in patients. Though discovered over 20 years ago, trastuzumab-induced cardiotoxicity (TIC) remains a research topic in cardio-oncology. This review explores the pathophysiological basis of TIC and its clinical manifestations. Their understanding is paramount for early detection and cardioprotective treatment. Trastuzumab renders cardiomyocytes susceptible by inhibiting the cardioprotective NRG-1/HER2/HER4 signaling pathway. The drug acts on HER2-receptor-expressing cardiomyocytes, endothelium, and cardiac progenitor cells (see the Graphical Abstract). The activation of immune cells, fibroblasts, inflammation, and neurohormonal systems all contribute to the evolution of TIC. A substantial amount of research demonstrates that trastuzumab induces overt and subclinical left ventricular (LV) systolic failure. Data suggest the development of right ventricular damage, LV diastolic dysfunction, and heart failure with preserved ejection fraction. Further research is needed to define a chronological sequence of cardiac impairments to guide the proper timing of cardioprotection implementation.
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Slavcheva et al. (2023) conducted a review in Trastuzumab-induced cardiotoxicity. Trastuzumab was evaluated.
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