Although modern breast cancer therapies have significantly improved long-term survival, reliable tools for the early detection and prediction of Cancer Therapy-Related Cardiac Dysfunction (CTRCD) remain essential. Cardiovascular toxicity encompasses a broad spectrum of manifestations, ranging from asymptomatic myocardial dysfunction to heart failure, ischemic heart disease, valvular abnormalities, arrhythmias, hypertension, and thromboembolic events. Anthracyclines and radiation therapy are the most well-established cardiotoxic treatments. Anthracycline-induced cardiotoxicity demonstrates a dose-dependent and often irreversible pattern (Type I cardiotoxicity), primarily mediated by oxidative stress and mitochondrial injury. In contrast, HER-2 targeted therapies are associated with reversible myocardial dysfunction (Type II cardiotoxicity), mainly through the disruption of the ErbB2 signaling pathway. Newer therapies, including anti-VEGF agents and endocrine therapies combined with CDK4/6 inhibitors, further expand the spectrum of cardiovascular risks. Current guidelines support the use of left ventricular ejection fraction, troponins, and natriuretic peptides for cardiotoxicity monitoring. However, emerging biomarkers, including myeloperoxidase, matrix metalloproteinases, galectin-3, inflammatory markers, and microRNAs, have shown potential for the early detection of myocardial injury. This review summarizes the current evidence regarding the mechanisms, clinical features, and risk factors of cardiotoxicity associated with breast cancer therapy. It further evaluates both established and novel biomarkers and highlights the clinical value of integrating them with advanced imaging modalities to improve the early detection and monitoring of cardiac remodeling. Further research is required to validate these approaches for clinical use (Graphical abstract).

Background: Osteoporotic fractures are a common clinical sign of Cushing syndrome (CS). However, Cushing diagnosis can occur years after this clinical manifestation. Methods: Herein, we present the case of a 45-year-old woman who was referred to our department for further diagnosis and treatment. Results: The patient was already under treatment for arterial hypertension and osteoporosis and was recently diagnosed with dyslipidemia and type 2 diabetes. She reported several previous fractures starting already 8 years before presentation. An adrenal CS was diagnosed, and the patient was treated with laparoscopic adrenalectomy, with a subsequent complete remission of her hypercortisolism. This case report presenting a particularly long time gap between initial osteoporosis signs and the final diagnosis underlines the need for an investigation into secondary osteoporosis in low-energy fractures also in the peripheral skeleton. In this context, we performed a literature review, including case reports with fragility fractures that were attributed to endogenous CS. Conclusions: In summary, a delayed diagnosis of CS in patients with a previous accumulation of such fractures is a worrisome observation and should be considered in everyday clinical practice in order to improve the timely diagnosis and treatment of CS.