Background/Objectives: Cardiovascular involvement drives morbidity and mortality in systemic lupus erythematosus (SLE). Echocardiography has limited predictive value for long-term outcomes, and subclinical right ventricular (RV) remodeling is poorly characterized. Metabolic dysregulation may influence immune activation and myocardial injury. This study investigates whether baseline metabolomic profiles are associated with longitudinal RV changes and disease progression in SLE. Methods: In this prospective, single-center study, patients with established SLE and no known cardiac disease underwent baseline clinical assessment, plasma metabolomic profiling, and advanced echocardiography, including 3D RV analysis. Echocardiography was repeated after 6 years. Metabolomics was performed using NMR spectroscopy and GC–MS. Disease progression was assessed via the SLICC/ACR damage index (SDI), defining clinical stability as ΔSDI = 0 and worsening as ΔSDI ≥ 1. Results: Twenty-five patients completed the follow-up (88% female; mean age 51 ± 13 years). Despite normal echocardiographic values, subtle but significant RV changes were observed, remaining within reference ranges, including mild declines in fractional area change and septal longitudinal strain (p < 0.05). Clinically worsened patients showed reduced TAPSE, while stable patients had slight increases (p < 0.05). Multivariate metabolomic analysis distinguished stable from worsened patients (R2Y = 0.772; Q2 = 0.483), primarily driven by higher 2-aminoheptanedioic acid values in those with progression (p < 0.05), along with trends toward higher fumarate and lower fructose and glucopyranose. Conclusions: Baseline metabolomic and advanced echocardiographic profiling may identify SLE patients at risk of disease progression. Longitudinal echocardiography enables monitoring of subtle RV changes, supporting personalized surveillance to detect early subclinical trajectories before overt dysfunction develops.

Cancer therapy-related cardiac dysfunction (CTRCD) represents a major cause of morbidity among cancer survivors, even in the absence of overt left ventricular (LV) systolic impairment. Current cardio-oncology surveillance strategies predominantly focus on LV ejection fraction and global longitudinal strain, potentially overlooking early alterations in diastolic function and atrial remodeling. The atria, particularly the left atrium, play a pivotal role in modulating ventricular filling pressures and serve as sensitive integrators of cumulative hemodynamic stress. Increasing evidence supports the prognostic value of left atrial volume index and left atrial strain for the early detection of subclinical cardiotoxicity, refinement of diastolic function assessment, and prediction of heart failure and atrial arrhythmias. Moreover, emerging data suggest that right atrial size and mechanics may provide additional insights into right heart involvement during immunotherapy and thoracic radiotherapy, although evidence remains limited. This narrative review summarizes current evidence on atrial volumetric and functional assessment in cardio-oncology, with a particular focus on strain imaging, diastolic function, and novel indices such as left atrial stiffness and mechanical dispersion. We highlight methodological challenges, gaps in standardization, and future directions, including artificial intelligence-assisted imaging and multimodal risk stratification. Integrating atrial imaging into routine cardio-oncology practice may improve early detection of CTRCD, enhance prognostic stratification, and support personalized surveillance strategies in cancer patients exposed to cardiotoxic therapies.

Chronic myeloid leukemia (CML) is a hematological malignancy driven by the BCR-ABL fusion gene, which has become the target of tyrosine kinase inhibitors (TKIs). These therapies have transformed CML outcomes, significantly improving survival rates. However, TKIs are associated with cardiovascular toxicities that represent a critical challenge in the long-term management of patients. This study aimed to evaluate the prevalence, progression, and clinical impact of cardiovascular toxicities in CML patients undergoing treatment with BCR-ABL TKIs, and to identify early markers for improved surveillance and management strategies. A retrospective analysis was conducted on 60 CML patients treated with TKIs at the Echocardiography and Cardiomyopathies Lab. Baseline and follow-up cardiovascular assessments included advanced echocardiographic techniques such as global longitudinal strain (GLS) and mechanical dispersion (MD). Patients were stratified according to ESC cardio-oncology guidelines into low, moderate, high, and very high cardiovascular risk categories. Statistical analyses assessed associations between TKI use, risk scores, and cardiovascular outcomes. At baseline, 65% of patients had hypertension, and Dasatinib was the most frequently used TKI (41.6%). While most patients had preserved left ventricular function, borderline elevations in E/e’ ratios and isolated cases of pericardial (3.3%) and pleural (5%) effusions were noted. Over a median follow-up of 18 months, the high and very high-risk groups showed significant worsening of GLS and MD, alongside higher rates of arrhythmias and arterial occlusions. A higher incidence of adverse cardiovascular events was observed in patients who treated with second- and third-generation TKIs, particularly Nilotinib and Ponatinib. TKI-induced cardiovascular toxicities are clinically significant in CML patients, particularly among those with pre-existing cardiovascular risks or treated with second- and third-generation inhibitors. Routine use of advanced echocardiographic techniques, combined with strict adherence to cardio-oncology surveillance protocols, is essential for early detection and management of subclinical cardiotoxicity. A multidisciplinary approach involving oncologists and cardiologists is critical to optimizing patient outcomes while minimizing treatment-related morbidity.Clinical results

BackgroundSoluble suppression of tumorigenicity-2 (sST2) is a promising biomarker of cardiovascular disease and heart failure. Data about the changes in sST2 concentrations during cancer treatment and the relationship with cancer treatment-related cardiotoxicity are sparse.MethodsWe conducted a systematic review and meta-analysis to explore longitudinal changes in sST2 levels at three time points (T0 baseline, T1 post-chemotherapy, and T2 follow-up) in cancer patients treated with cardiotoxic therapies and compared these changes to traditional biomarkers of cardiac injury, i.e., troponin and NT-proBNP. Using random-effects models, mean differences (MD), and standardized MD (SMD), we analyzed (i) ST2 longitudinal changes, (ii) the association between ST2 and cardiotoxicity [defined through left ventricular ejection fraction (LVEF)] providing pooled estimates of correlations, and (iii) the SMD variations among biomarkers.ResultsEight studies were included, comprising 433 patients treated with anthracycline and/or HER2-directed antibodies. There was a trend toward increased sST2 levels from T0 to T2 (MD 1.86, 95% CI −0.97 to 4.68, p = 0.200) and decreased levels from T1 to T2 (MD −1.96, 95% CI −4.28 to 0.37, p = 0.100). A pooled analysis showed a negative correlation between sST2 levels and LVEF (r −0.29, 95% CI, −0.49- −0.05, p < 0.010). Comparisons with Troponin and NT-proBNP showed a significantly higher Troponin SMD at T0-T1 (p = 0.027), while no significant differences were observed for NT-proBNP.ConclusionsST2 showed dynamic changes during cardiotoxic therapy correlating with cardiotoxicity. Troponin was demonstrated to have greater longitudinal variations. Further research is needed to evaluate longitudinal sST2 levels in patients who develop cardiotoxicity vs. those who do not.

Emerging evidence indicates that specific genetic variants are associated with an increased risk of toxicity from anticancer treatments and cancer-related cardiovascular complications. These genetic factors influence drug metabolism, efficacy, and susceptibility to adverse effects. For cancer patients, the genetic background can have two major cardiovascular implications, namely therapy-related cardiotoxicity and cancer-related cardiovascular complications. Baseline risk stratification is essential to identify higher-risk individuals and ensure they receive appropriate preventive and therapeutic interventions and more frequent follow-up. Current guidelines recommend stratification based on cardiovascular risk factors, but these factors alone cannot accurately define individual risk. Genetic background has been shown to enhance risk stratification. Beyond rare genetic variants, recent genome-wide association studies have identified single nucleotide polymorphisms implicated in cancer therapy toxicity. Despite their current limitations, polygenic risk scores are expected to play a significant role in risk stratification. This review aims to summarize the current evidence on the role of the genetic background of patients with cancer treated with potentially cardiotoxic drugs who develop cardiotoxicity, aiming to provide insights to refine risk stratification further and tailor the management of these patients.

BackgroundCardiotoxicity is a major concern in cancer survivors, potentially compromising treatment efficacy, quality of life and long-term survival. With increasing survival rates, the need for effective cardioprotective strategies has become paramount.ObjectiveThis narrative review evaluates current pharmacological, non-pharmacological, and emerging strategies for preventing cancer therapy-related cardiac dysfunction (CTR-CD), emphasizing recent advances, their clinical applicability and research gaps.MethodsWe conducted a narrative review based on a non-systematic search of PubMed/MEDLINE, Scopus, and Web of Science up to June 2025, focusing on clinical trials, meta-analyses, guideline recommendations, and key observational studies relevant to CTR-CD prevention.ResultsAmong pharmacological approaches, renin-angiotensin-aldosterone system inhibitors (RAASi) and beta-blockers modestly preserve left ventricular ejection fraction (LVEF), though benefits on hard outcomes remain unproven. Dexrazoxane is the only FDA-approved agent and shows robust protection in anthracycline-treated patients. Statins and metformin demonstrate promising but still investigational cardioprotective effects, while sodium-glucose cotransporter-2 inhibitors (SGLT2i) show encouraging pilot data. Non-pharmacological strategies—including structured exercise, mediterranean diet, nutritional support and aggressive control of risk factors—are guideline-endorsed, although most evidence relies on surrogate endpoints. Emerging tools such as telemedicine, artificial intelligence and omics sciences offer innovative opportunities for personalized prevention but require multicenter validation.ConclusionAn integrated, multidisciplinary approach combining both pharmacological and non-pharmacological strategies is essential to effectively prevent cardiotoxicity in cancer patients. Current evidence supports dexrazoxane, risk factor control and selective use of RAASi or beta-blocker in high-risk patients. Exercise and nutrition provide functional and quality of life benefits, while several novel strategies remain exploratory. Future large-scale, multicenter, randomized trial are needed to harmonize international guidelines and define the most effective, sustainable prevention models across diverse patient populations.

Recently, quality indicators (QIs) for the management of patients with cancer or cancer survivors have been identified in cardio-oncology and the first ESC Guidelines on cardio-oncology have been published in 2022. The management of cancer patients requires dedicated healthcare professionals, a multidisciplinary team which should consist of at least an oncologist, cardiologist and a specialist nurse. to investigate the adherence to QIs in Italian cardio-oncology clinic and the application in clinical practice of ESC Cardio-oncology Guidelines. A cross-sectional survey was developed by members of the Working group of cardiotoxicity and cardioprotection of the Italian Society of Cardiology (SIC). The survey consisted of 19 questions which include demographic information, multiple-choice questions related to organization and quality of cardio-oncology laboratories. 77 answers were received from Italian hospitals (of whom 80% from university hospital). We found that dedicated cardio-oncology clinics were present in 70% of hospitals which answered. 75% of these hospitals had at least one physician dedicated to cardio-oncology. Clinical application of ESC Guidelines on cardio-oncology was performed in 83% of hospitals. Regarding the number of dedicated cardio-oncological visits performed weekly: 54% of centers performed between 0-12 visits, 30% between 13-24, 6% between 25-36, 11% performed > 36 visits. Multi-disciplinary team was present in 65% of hospitals and it included only cardiologist and oncologist in 50% of cases; only 20% conformed the presence of a multi-disciplinary team with cardiologist, oncologist, radiologist, professional nurse, surgeon, palliative care. Baseline cardiovascular risk was assessed in 54% of participants; 65% of participants organized follow-up according to the ESC guidelines. The prevalent tumor referred to the cardio-oncology clinic was : breast cancer (45%), followed by gastro-intestinal (14%), hematological (23%), lung (17%). Regarding hospitalization for cardiovascular complication in 1 year were: 78% had between 0-10 hospitalizations, 17% between 11-22, 6% had > 35 hospitalizations. Heart failure was the most frequent cardiovascular complication (59%). Only 72% of participants routinely performed assessment of global longitudinal strain; only 48% always assessed cardiac biomarkers. Cardio-protection has been started in patients at high and very high risk only in 53% of cardio-oncology clinic. Only 19% of participants thinks that current cardio-oncology clinics have criteria that meet the current ESC Cardio-oncology guidelines. Data emerging from this survey outline that ESC cardio-oncology guidelines have been received by the Italian community however implementation in clinical practice still need to be improved and quality indicators are not fully achieved. Further efforts and resources are needed to meet necessary quality indicators in cardio-oncology

Anthracycline cardiotoxicity is a significant complication of oncological therapy. Cardiovascular risk stratification is crucial to identify vulnerable patients. The HFA-ICOS score offers a standardized tool for categorizing baseline risk, supporting personalized management. While global longitudinal strain (GLS) is the gold standard for detecting subclinical cardiotoxicity, the role of right ventricular strain (RVS) remains unclear. We aim to assess the risk of anthracycline-induced cardiotoxicity in breast cancer patients, emphasizing HFA-ICOS score-based risk stratification for personalized care. Additionally, the HFA-ICOS score and echocardiographic parameters relationship, including GLS and RVS, was explored. The study, conducted in collaboration with a Medical Oncology Department, included patients who underwent clinical and anthropometric evaluations. Cardiovascular risk was classified as low or moderate-to-high using the HFA-ICOS score. Cardiovascular risk factors such as hypertension, diabetes, smoking, hypercholesterolemia, and family history of cardiovascular disease were recorded and compared between risk groups. Baseline echocardiographic assessments with color Doppler imaging measured left ventricular ejection fraction (LVEF), GLS, and RVS. Follow-up echocardiograms were longitudinally performed at after a cumulative anthracycline dose of 180 mg/m², at the end of treatment, and during post-therapy follow-up. Changes in GLS, RVS, and LVEF were analyzed by risk group. We enrolled 67 breast cancer patients undergoing anthracycline chemotherapy, with a mean age of 50.8±11 years. Most patients (60) had a low cardiovascular risk profile, while only seven were classified as moderate-to-high risk. Hypertension was the most common risk factor (present in 9 patients, 6 of whom were high-risk), followed by smoking status. At enrollment, echocardiography showed no anatomical or functional abnormalities, with normal LVEF, GLS, and RVS values across all patients. Patients with moderate-to-high risk showed a significantly lower RVS from the 180 mg/m² to the 6-month follow-up compared to the low-risk group (Figure 1). Additionally, the moderate-to-high risk group showed a significant reduction in RVS at 180 mg/m² (p = 0.04), at the end of treatment (p = 0.02), and at 6-month follow-up (p = 0.01) compared to baseline (Figure 1). This reduction was not observed in low-risk patients. Additionally, 57% of moderate to high-risk patients experienced a GLS reduction >15% during therapy, independent of LVEF, compared to 28% of low-risk patients. The HFA-ICOS score effectively stratified subclinical cardiovascular toxicity patients on anthracycline therapy. Early RVS reduction emerges as a key marker of cardiotoxicity, particularly in high-risk patients. Including RVS analysis in routine monitoring may enable earlier interventions potentially improving management.

Global longitudinal strain (GLS) is the standard of care in cardio-oncology to detect subclinical cardiotoxicity (CTX). However, GLS is load-dependent, and differences in systolic blood pressure represent a limitation for serial comparisons. Myocardial Work (MW) permits GLS adjustments for systolic blood pressure, allowing a left ventricular (LV) performance analysis despite afterload variations. We aimed to investigate the role of MW in the early detection of CTX and the potential role of metabolomics analysis in identifying a metabolic pattern (fingerprint) capable of detecting early adaptive changes suggestive of CTX. Patients with breast cancer treated with cardiotoxic therapies were enrolled.The patients underwent baseline assessment and, upon reaching cumulative doses of anthracycline, were evaluated with echocardiographic examination with image acquisition for GLS and MW analysis. A peripheral blood sampling for metabolomic analysis performed by gas chromatography-mass spectrometry (GC/MS) was collected. We enrolled 47 patients; the mean age was 53±11. Baseline LV ejection fraction (EF) was >55% for the whole population, and GLS values were -21± 3%. During treatment, LVEF showed a progressive slight reduction without any individual values falling into the pathological range (67 ± 6% to 65 ± 6%, p=0.90). Similarly, a progressive decline in GLS values was observed starting at a dose of 180 mg/m², becoming more pronounced at a dose of 360 mg/m². Twelve patients exhibited a significant GLS decline. In these patients, heart failure therapy led to a partial recovery of GLS at the dose of 360 mg/m². A similar trend was observed for MW, with significant differences at both 180 mg/m² (p=<0.02 vs basal), and 360 mg/m² (p<0.02 vs basal). Subsequently, we performed two OPLS models using MW values as the Y variable and the data matrix from GC-MS analysis as the X variables, one for each of the two groups analyzed (patients without and with CTX). In both cases, the analysis produced significant results (p< 0.05), confirming MW as a landmark for cardiac muscle workload. Subsequently, we compared the two patient groups performing an OPLS-DA (Figure 1) on the same data matrix. The analysis showed group clustering with good statistical significance, suggesting metabolic remodeling linked to LV performance changes post-chemotherapy. To identify the involved metabolites, VIP analysis revealed a differential distribution of fatty acids, substrates such as ketone bodies, intermediates in energy production such as citrate, and various amino acids, including branched-chain amino acids. Our data confirm that CTX can be detected effectively using both GLS and MW. The reduction of MW seems to be associated with a specific metabolic fingerprint. If confirmed, these results could enhance understanding of chemotherapy-induced damage and improve early, sensitive screening in patient follow-up.

Numerous studies underscore the benefits of exercise prescription in both cardiology and oncology. Recently, emerging eviAlessandro Navadence has highlighted the value of exercise in cardio-oncology, demonstrating its protective effects against the decline in functional capacity and cardiovascular complications that may arise in oncology patients, either as a result of the disease itself or as a side effect of chemotherapy. The purpose of this review is to elucidate the protective mechanisms and cardiovascular clinical benefits conferred by exercise prescription in cancer patients. Additionally, it aims to delineate the principal current exercise protocols that have been validated or proposed, outlining their respective advantages and limitations. Finally, we will explore future perspectives, particularly the development of precision medicine, supported by advancements in AI, to facilitate the creation of novel, personalized exercise protocols tailored to specific patient populations.

BACKGROUND:There are sex differences in HF patients. It is not clear whether such differences mainly reflect cultural behaviours and clinical inertia, and the role of sex on clinical outcomes is still controversial. We aimed to investigate the association of sex with in-hospital management and outcomes in patients with HF. METHODS:We analyzed data of 4016 adult patients hospitalized for HF in 2020 to 2021 and enrolled in a multicentre national registry. RESULTS:Women (n = 1,818 [45%]) were older than men (83 vs 77 years, P < .0001), with a higher prevalence of arterial hypertension (73% vs 69%, P = .011) and atrial fibrillation. Women presented more frequently with HF and preserved ejection fraction -HFpEF (55% vs 32%, P < .001). They were more often hospitalized in internal medicine departments (71% vs 51%), and men in highly specialized cardiology units (49% vs 29%). When considering HF pharmacological treatments at discharge in the subgroup with reduced ejection fraction -HFrEF (n=1525), there were no significant differences (49% of women treated with GDMT [guideline-directed medical therapy] vs 52% of men, P = .197). Sex was not associated either with hospital readmissions (30-days OR [95% CI] = 0.89 [0.71-1.11], P = .304; 1-year OR [95% CI] = 1.02[0.88-1.19], P = .777) or with mortality (in-hospital OR [95% CI] = 1.14 [0.73-1.78], P = .558; 1-year OR [95% CI] = 1.08 [0.87-1.33], P = .478). Similar results were obtained when considering different HF categories based on left ventricular ejection fraction. CONCLUSIONS:Women and men exhibited distinct clinical profiles. Although this may have had an impact on hospital pathways (noncardiology/cardiology units) and pharmacological prescriptions, sex per se did not appear as an independent determinant of clinical choices. Moreover, when considering homogeneous groups, women were not undertreated. Finally, female sex was not associated with worse clinical outcomes.

In recent years, important advances have been made in the field of Cardio-Oncology. The 2022 ESC Guidelines on Cardio-Oncology proposed a baseline cardiovascular risk stratification for cancer patients and preventive strategies in patients at high and very-high risk of cardiotoxicity. Cardiovascular toxic effects of anti-cancer drugs are being extensively studied; surveillance programs have been proposed, based on the baseline cardiovascular risk. On the other hand, there is little data on Cardio-Oncological management of patients at high and very-high cardiovascular risk with previous cardiovascular diseases. For example, little is known about management of cancer patients with heart failure with reduced ejection fraction (HFrEF), patients with a recent myocardial infarction or other cardiovascular diseases; when to resume anti-cancer drugs after a cardiovascular toxic event. Collaboration between Cardiologists and Oncologists and multidisciplinary team evaluations are certainly essential to decide the best therapeutic strategy for cancer patients, to treat cancer while saving the heart. Therefore, in the present review, we attempt to provide a useful guide to clinicians in treating patients with high and very-high risk of cardiotoxicity by enucleating main questions and answering them based on the evidence available as well as expert opinion and our clinical experience.

Heart failure (HF) is a significant disease affecting 1–2% of the general population. Despite its general aspects, HF, like other cardiovascular diseases, presents various gender-specific aspects in terms of etiology, hemodynamics, clinical characteristics, therapy, and outcomes. As is well known, HF with preserved ejection fraction more frequently affects females, with diabetes and arterial hypertension representing the most critical determinants of HF. On the other hand, women are traditionally underrepresented in clinical trials and are often considered undertreated. However, it is not clear whether such differences reflect cultural behaviors and clinical inertia or if they indicate different clinical profiles and the impact of sex on hard clinical outcomes. We aimed to review the sex-related differences in patients affected by HF.

Serum biomarkers represent a reproducible, sensitive, minimally invasive and inexpensive method to explore possible adverse cardiovascular effects of antineoplastic treatments. They are useful tools in risk stratification, the early detection of cardiotoxicity and the follow-up and prognostic assessment of cancer patients. In this literature review, we aim at describing the current state of knowledge on the meaning and the usefulness of cardiovascular biomarkers in patients with cancer; analyzing the intricate relationship between cancer and cardiovascular disease (especially HF) and how this affects cardiovascular and tumor biomarkers; exploring the role of cardiovascular biomarkers in the risk stratification and in the identification of chemotherapy-induced cardiotoxicity; and providing a summary of the novel potential biomarkers in this clinical setting.

In recent years, important advances have been made in the field of Cardio-Oncology. The 2022 ESC Guidelines on Cardio-Oncology proposed a baseline cardiovascular risk stratification for cancer patients and preventive strategies in patients at high and very-high risk of cardiotoxicity. Cardiovascular toxic effects of anti-cancer drugs are being extensively studied; surveillance programs have been proposed, based on the baseline cardiovascular risk. On the other hand, there is little data on Cardio-Oncological management of patients at high and very-high cardiovascular risk with previous cardiovascular diseases. For example, little is known about management of cancer patients with heart failure with reduced ejection fraction (HFrEF), patients with a recent myocardial infarction or other cardiovascular diseases; when to resume anti-cancer drugs after a cardiovascular toxic event. Collaboration between Cardiologists and Oncologists and multidisciplinary team evaluations are certainly essential to decide the best therapeutic strategy for cancer patients, to treat cancer while saving the heart. Therefore, in the present review, we attempt to provide a useful guide to clinicians in treating patients with high and very-high risk of cardiotoxicity by enucleating main questions and answering them based on the evidence available as well as expert opinion and our clinical experience.

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease, and several studies have suggested possible early RV involvement. Aim of the study was to evaluate the 3D echo parameters of the right ventricle (RV) and the metabolomic profile to correlate both with SLE severity. Forty SLE patients, free of cardiovascular disease, were enrolled and the following 3D parameters were evaluated: the RV ejection fraction (RV-EF), longitudinal strain of the interventricular septum (Septal LS), longitudinal strain of the free wall (Free-LS) and the fractional area change (FAC). In addition, a metabolomic analysis was performed. Direct correlations were observed between TAPSE values and the RV 3D parameters. Then, when splitting the population according to the SDI value, it was found that patients with higher cumulative damage (≥3) had significantly lower FAC, RV-EF, Septal LS, and Free-LS values; the latter three parameters showed a significant correlation with the metabolic profile of the patients. Furthermore, the division based on SDI values identified different metabolic profiles related to the degree of RV dysfunction. The RV dysfunction induced by the chronic inflammatory state present in SLE can be identified early by 3D echocardiography. Its severity seems to be related to systemic organ damage and the results associated with a specific metabolic fingerprint constituted by 2,4-dihydroxybutyric acid, 3,4-dihydroxybutyric acid, citric acid, glucose, glutamine, glycine, linoleic acid, oleic acid, phosphate, urea, and valine.

Metabolic syndrome (Mets) is a clinical condition characterized by a cluster of major risk factors for cardiovascular disease (CVD) and type 2 diabetes: proatherogenic dyslipidemia, elevated blood pressure, dysglycemia, and abdominal obesity. Each risk factor has an independent effect, but, when aggregated, they become synergistic, doubling the risk of developing cardiovascular diseases and causing a 1.5-fold increase in all-cause mortality. We will highlight gender differences in the epidemiology, etiology, pathophysiology, and clinical expression of the aforementioned Mets components. Moreover, we will discuss gender differences in new biochemical markers of metabolic syndrome and cardiovascular risk.

Antiblastic drugs-induced cardiomyopathy remains a relevant cause of morbidity and mortality, during and after chemotherapy, despite the progression in protective therapy against cardiovascular diseases and myocardial function. In the last few decades, many groups of researchers have focused their attention on studying the metabolic profile, first in animals, and, subsequently, in humans, looking for profiles which could be able to predict drug-induced cardiotoxicity and cardiovascular damage. In clinical practice, patients identified as being at risk of developing cardiotoxicity undergo a close follow-up and more tailored therapies. Injury to the heart can be a consequence of both new targeted therapies, such as tyrosine kinase inhibitors, and conventional chemotherapeutic agents, such as anthracyclines. This review aims to describe all of the studies carried on this topic of growing interest.