In recent years, immune checkpoint inhibitors have significantly changed the field of oncology, emerging as first-line treatment, either alone or in combination with other regimens, for numerous malignancies, improving overall survival and progression-free survival in these patients. However, immune checkpoint inhibitors might also cause severe or fatal immune-related adverse events, including adverse cardiovascular events. Initially, myocarditis was recognized as the main immune checkpoint inhibitor-related cardiac event, but our knowledge of other potential immune-related cardiovascular adverse events continues to broaden. Recently, preclinical and clinical data seem to support an association between immune checkpoint inhibitors and accelerated atherosclerosis as well as atherosclerotic cardiovascular events such as cardiac ischemic disease, stroke, and peripheral artery disease. In this review, by offering a comprehensive overview of the pivotal role of inflammation in atherosclerosis, we focus on the potential molecular pathways underlying the effects of immune checkpoint inhibitors on cardiovascular diseases. Moreover, we provide an overview of therapeutic strategies for cancer patients undergoing immunotherapy to prevent the development of cardiovascular diseases.

Sodium glucose cotransporter-2 inhibitors (SGLT2i), originally developed for type II diabetes mellitus, have recently been approved for the treatment of heart failure in both diabetic and non-diabetic patients due to their significant cardiovascular benefits. Beyond their established role in diabetes and heart failure management, current research is exploring the potential applications of SGLT2 inhibitors in the field of cardio-oncology. This interest is driven by dual possible benefits: cardioprotection against the adverse effects of antitumor therapies and inherent antitumor properties. Patients affected by cancer often face the challenge of managing cardiovascular toxicity induced by antineoplastic treatments. SGLT2 inhibitors have shown promise in mitigating toxicities, thereby enhancing the cardiovascular health of these patients. Additionally, emerging evidence suggests that SGLT2 inhibitors may possess direct antitumor effects, further contributing to their therapeutic potential in oncology. This review aims to provide a comprehensive overview of the molecular mechanisms through which SGLT2 inhibitors exert their cardioprotective and antitumor effects. Furthermore, we will examine the current body of evidence supporting the use of these inhibitors in a cardio-oncology setting.

Introduction Right ventricular–pulmonary artery (RV-PA) coupling evaluates the relationship between right ventricular contractility and afterload. It is normal when both are well-matched. A reduction in RV contractility or an increase in RV afterload leads to RV-PA uncoupling, decreasing left ventricular filling, stroke volume, and causing peripheral hypoperfusion and congestion. The TAPSE/PASP ratio is a reliable non-invasive method to assess this coupling. An impaired TAPSE/PASP ratio is associated with poor prognosis in conditions of elevated RV afterload, but its role in acute coronary syndrome (ACS) is unclear. Aim The aim of this study is to investigate the in-hospital prognostic value of the TAPSE/PASP ratio and the predictors of a low TAPSE/PASP ratio. Methods This retrospective, pilot study included 152 patients admitted for ACS (77.6% STEMI, 22.4% NSTEMI) between November 2023 and March 2025, with available TAPSE/PASP data from echocardiography performed at admission. The primary objective was to assess whether the TAPSE/PASP ratio predicts in-hospital major adverse cardiovascular events (MACE). Secondary objectives included evaluating whether TAPSE/PASP predicts in-hospital ventricular arrhythmias, intraventricular thrombosis, prolonged hospital stay, and identifying predictors of a low TAPSE/PASP ratio. Results TAPSE/PASP < 0.55 was significantly associated with MACE and prolonged hospital stay in univariate analysis, but not in multivariate analysis. TAPSE/PASP < 0.55 was largely explained by E/e′ >14 (OR 6.600; p = 0.0008), RV involvement (OR 9.430; p = 0.0007), and age >75 years (OR 3.243; p = 0.0389). Conclusions Low RV-PA coupling (TAPSE/PASP < 0.55) is associated with MACE and prolonged hospital stay in ACS, but lacks independent prognostic value in multivariate analysis. Graphical abstract In-hospital prognostic value of TAPSE/PASP ratio in patients admitted for ACS. TAPSE: tricuspid anular peak systolic excursion. PASP: pulmonary artery systolic pressure; ACS: acute coronary syndromes

Background: Breast cancer patients are exposed to cardiovascular complications related to both pre-existing cardiovascular risk factors and cardiotoxic cancer therapies. Heart failure with preserved ejection fraction (HFpEF) is an emerging and often under-recognized condition in this population, potentially present before treatment initiation and further influenced by oncologic therapies. This study aimed to characterize baseline HFpEF probability and its longitudinal evolution using validated scoring systems in a real-world cardio-oncology cohort. Methods: We retrospectively evaluated 145 women with breast cancer undergoing baseline cardio-oncology assessment before initiation of potentially cardiotoxic therapies. HFpEF probability was estimated using three validated algorithms (H₂FPEF, ABA, and HFA-PEFF). A subgroup of 89 patients underwent exploratory reassessment after 12 ± 3 months to investigate longitudinal changes in HFpEF probability according to treatment. Results: At baseline, HFpEF probability varied substantially according to the scoring system applied, with 14.8–41.5% of patients classified as having intermediate-to-high probability. Agreement among the three algorithms was limited, particularly between HFA-PEFF and H₂FPEF/ABA scores. Exploratory longitudinal analyses showed no significant changes in HFpEF probability categories during follow-up. Conclusions: HFpEF probability assessment in breast cancer patients showed substantial baseline heterogeneity across validated scoring systems, with clinically relevant differences in risk classification and limited inter-score agreement. These findings provide novel insights into an underexplored cardio-oncology phenotype and suggest that currently available HFpEF scoring systems may not be directly interchangeable in this clinical setting. Prospective studies including provocative testing are needed to determine the clinical relevance of HFpEF probability scores in breast cancer patients.