Trastuzumab and cardiotoxicity

Breast cancer survivors face an increased incidence of cardiac toxicities, which heightens their risk for cardiovascular disease compared to individuals without cancer, leading to poorer overall survival rates. Although trastuzumab has notably improved patient outcomes, its potential to induce cardiotoxicity has become a significant clinical concern. HER2 signaling and neuregulins play critical roles in maintaining cardiac function. Although the exact mechanism behind trastuzumab-induced cardiotoxicity remains unclear, it differs from anthracycline-induced cardiomyopathy, as trastuzumab-induced cardiotoxicity (type II) is mostly reversible. This is because it stems from reduced myocyte contractility, rather than permanent damage to the myocytes. Single-nucleotide polymorphisms (SNPs) – the most common form of genetic variation – are associated with differences in both the effectiveness of systemic treatments and the occurrence of treatment-related toxicities. However, findings regarding the relationship between specific SNPs and cardiotoxicity remain inconclusive. Early detection of trastuzumab-induced cardiotoxicity is crucial for minimizing side effects and enabling the customization of therapeutic strategies for patients at high risk of developing cardiac complications.