Search Results (58)

Background: Many risk factors for cancer therapy-related cardiovascular toxicity overlap with risk factors for atherosclerosis. According to the ESC 2022 Cardio-Oncology Guidelines, coronary computed tomography angiography and coronary artery calcium score are not recommended as part of routine risk assessment prior to oncological treatment. The aim of this study was to prospectively assess the influence of coronary artery calcium score (CAC score) on cancer therapy-related cardiac dysfunction in patients with moderate and high risk of cardiovascular toxicity, qualified for anthracycline treatment. Methods: In all patients, risk factors were collected, laboratory tests, echocardiography with global longitudinal strain (GLS) assessment and coronary artery tomography with coronary artery calcium score were performed. A total of 80 patients were included in the study, of which 77 (96.25%) were followed for an average of 11.5 months. The mean age at baseline was 60.5 years and 72 (93.51%) were women. Results: During observation, five patients (6.49%) died, including two due to heart failure and three due to cancer progression. The majority of patients (59, 76.6%) had breast cancer, 11 (14.3%) were diagnosed with sarcoma and seven (9.1%) with lymphoma. According to the HFA-ICOS risk score, 40 patients (51.9%) were classified as moderate risk (MR), and 37 patients (48.1%) as high risk (HR) for cancer therapy-related cardiovascular toxicity. A CAC score greater than 100 was calculated in 17 (22.1%) patients and greater than 400 in three (3.9%) patients. The CAC score above zero was more common in older patients and in patients classified as high risk (p < 0.001). There was also a significant association between CAC score and hypertension, hyperlipidemia, chronic kidney disease, and the level of NT-proBNP. During 12-month follow-up, mild CTRCD occurred in 38 (49.4%) patients, moderate CTRCD was diagnosed in seven (9.1%), and severe in three (3.9%) patients. In the univariable analysis, CTRCD was more common in the high-risk group (p = 0.005) and in patients with a CAC score greater than zero (p = 0.036). In multivariable analysis, the incidence of CTRCD remains higher in the CAC score > 0 group, even after adjusting for age, hypertension, and hyperlipidemia. In this study group, the CTRCD rates increased with the HFA-ICOS risk score. Conclusions: In moderate and high-risk patients, a coronary artery calcium score greater than zero was identified as a significant risk factor for the development of cancer therapy-related cardiac dysfunction during anthracycline-based treatment. Furthermore, the HFA-ICOS risk score demonstrated good correlation with the incidence of CTRCD in this study, supporting its validity as a predictive tool in patients receiving anthracycline therapy. Full article

Sodium–glucose cotransporter-2 inhibitors (SGLT2i), initially developed for the management of type 2 diabetes mellitus, have demonstrated significant nephroprotective and cardioprotective effects. These benefits have led to their inclusion in heart failure (HF) management guidelines, irrespective of glycemic status and left ventricular ejection fraction (LVEF). Various anticancer therapies, particularly anthracyclines, are associated with substantial cardiotoxicity risks, resulting in cancer therapy-related cardiovascular toxicity (CTR-CVT). Promising evidence from preclinical and observational studies indicates that SGLT2i may mitigate cardiotoxic effects of cancer therapy by alleviating LVEF decline, reducing HF incidence and hospitalizations, and lowering overall mortality. Moreover, improved survival has been reported in patients with various malignancies. The current review explores the potential applications of SGLT2i in the prevention of CTR-CVT, highlights their possible mechanisms of cardioprotection, discusses the published evidence, and emphasizes the need for the results from ongoing randomized controlled trials to establish SGLT2i efficacy and safety in cardio-oncology patients. Full article

Patients with active cancer and cancer survivors are at a markedly increased risk for developing cardiovascular comorbidities, including heart failure, coronary artery disease, and renal dysfunction, which are often compounded by the cardiotoxic effects of cancer therapies. This heightened cardiovascular vulnerability underscores the urgent need for effective, safe, and evidence-based cardioprotective strategies to reduce both cardiovascular morbidity and mortality. Sodium-glucose cotransporter 2 inhibitors (SGLT2is), a class of drugs originally developed for the treatment of type 2 diabetes, have demonstrated significant cardiovascular and renal benefits in high-risk populations, independent of glycemic control. Among the currently available SGLT2i, such as empagliflozin, canagliflozin, dapagliflozin, and sotagliflozin, there is growing evidence supporting their role in reducing major adverse cardiovascular events (MACEs), hospitalization for heart failure, and the progression of chronic kidney disease. Recent preclinical and clinical data suggest that SGLT2is exert cardioprotective effects through multiple mechanisms, including the modulation of inflammasome activity, specifically by reducing NLRP3 inflammasome activation and MyD88-dependent signaling, which are critical drivers of cardiac inflammation and fibrosis. Moreover, SGLT2is have been shown to enhance mitochondrial viability in cardiac cells, promoting improved cellular energy metabolism and function, thus mitigating cardiotoxicity. This narrative review critically evaluates the emerging evidence on the cardiorenal protective mechanisms of SGLT2is, with a particular focus on their potential role in cardio-oncology. We explore the common pathophysiological pathways between cardiovascular dysfunction and cancer, the molecular rationale for the use of SGLT2is in cancer patients, and the potential benefits in both primary and secondary prevention of cardiovascular toxicity related to oncological treatments. The aim is to propose a therapeutic paradigm utilizing SGLT2is to reduce cardiovascular mortality, MACE, and the burden of cardiotoxicity in high-risk oncology patients, fostering an integrated approach to cardio-oncology care. Full article

Cancer remains the second leading cause of death worldwide. Doxorubicin (DOX) is a cornerstone of hematologic malignancy treatment, but it is limited by its dose-dependent cardiotoxicity, leading to systolic and diastolic cardiac dysfunction and, ultimately, dilated hypokinetic cardiomyopathy. Cardio-oncology has emerged as a subspecialty addressing cardiovascular complications in cancer patients, highlighting preventive and therapeutic strategies to reduce cancer therapy-related cardiac dysfunction (CTRCD). Current approaches, including beta-blockers, renin–angiotensin system (RAS) inhibitors, and statins, offer partial cardioprotection. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, initially developed for type 2 diabetes mellitus (T2DM), demonstrate pleiotropic cardioprotective effects beyond glycemic control, including reduced oxidative stress, inflammation, and myocardial remodeling. This review explores the interplay between anthracycline therapy, particularly DOX, and cardiotoxicity while evaluating SGLT2 inhibitors as novel agents in cardio-oncology. Preclinical studies suggest SGLT2 inhibitors attenuate CTRCD by preserving mitochondrial function and inhibiting apoptosis, while clinical trials highlight their efficacy in reducing heart failure (HF) hospitalizations and cardiovascular (CV) mortality. Integrating SGLT2 inhibitors into cardio-oncology protocols could revolutionize the management of CTRCD, enhancing patient outcomes in oncology and cardiovascular care. Considering the emerging evidence, SGLT2 inhibitors may provide significant benefits to patients undergoing anthracycline therapy, particularly those with elevated cardiovascular risk profiles. We recommend that future prospective, large-scale clinical trials further evaluate the efficacy and safety of these agents as cardioprotective therapy to optimize individualized treatment strategies. Full article

Interleukin-6, myeloperoxidase, and tumor necrosis factor alpha are proinflammatory cytokines that play a role both in cardiovascular and oncological diseases. The study aimed to prospectively investigate the clinical value of interleukin-6, myeloperoxidase, and tumor necrosis factor alpha as potential biomarkers of cancer therapy-related cardiac dysfunction (CTRCD) in patients receiving anthracycline treatment. A total of 80 patients were included, with 77 (96.25%) followed for an average for 11.5 months. The mean age at baseline was 60.5 years, and 72 (93.51%) were women. Clinical risk factors were documented for all patients, and laboratory assessments, including measurements of IL-6, MPO, and TNF-α, were conducted. All participants also underwent echocardiography with assessment of global longitudinal strain (GLS). In the study group, coronary CT angiography with coronary artery calcium (CAC) score calculation was performed once at the beginning of the study. During observation, any degree of CTRCD was diagnosed in 48 (62.4%) patients. Mild CTRCD occurred in 38 (49.4%) patients, moderate CTRCD was diagnosed in 7 (9.1%), and severe in 3 (3.9%). In patients with high baseline risk, IL-6 levels were significantly elevated compared to those with moderate risk (p = 0.018). Higher levels of IL-6 were found to correlate with an increased grade of CTRCD. In a multivariate repeated measures model of the biomarkers studied, only a higher level of IL-6 was significantly associated with the diagnosis of CTRCD. Among the novel biomarkers studied, we found evidence for IL-6 for its potential use in the detection of cardiac dysfunction related to cancer therapy in patients treated with anthracyclines. Full article

Soft tissue sarcoma (STS) has an 2–8% incidence for all malignant tumors in the adolescent and young adult (AYA) population, which are patients from ages 15 to 39. As most STS tumors are aggressive, they require multimodal management with surgery, radiation and chemotherapy. This article discusses the survivorship considerations in this young population of cancer patients who complete therapy. The lasting side effects include surgical and radiation-related morbidity, chemotherapy toxicity, early and late secondary effects on other organ systems, such as cardiac and endocrine dysfunction, and the development of secondary cancers. The long-term psychologic and practical impacts for those who have received a sarcoma diagnosis in the prime of their life include fertility, mental health, relationship, education and career implications. Although there is a paucity of data in some of these areas, we present existing management guidelines as available. This article serves as a comprehensive review of this wide array of treatment effects intended for all providers participating in the care of AYA sarcoma survivors, to include oncologists, primary care providers and therapists. Full article

The increasing efficacy of cancer therapies has significantly improved survival rates, but it has also highlighted the prevalence of cancer-therapy-related cardiac dysfunction (CTRCD). This review provides a comprehensive overview of the identification, monitoring, and management of CTRCD, a condition resulting from several treatments, such as anthracyclines, HER2-targeted therapies, target therapies, and radiotherapy. The paper includes a discussion of the mechanisms of CTRCD associated with various cancer treatments. Early detection through serum biomarkers and advanced imaging techniques is crucial for effective monitoring and risk stratification. Preventive strategies include pharmacological interventions such as ACE inhibitors/angiotensin receptor blockers, beta-blockers, and statins. Additionally, novel agents like sacubitril/valsartan, sodium-glucose co-transporter type 2 inhibitors, and vericiguat show promise in managing left ventricular dysfunction. Lifestyle modifications, including structured exercise programs and optimized nutritional strategies, further contribute to cardioprotection. The latest treatments for both asymptomatic and symptomatic CTRCD across its various stages are also discussed. Emerging technologies, including genomics, artificial intelligence, novel biomarkers, and gene therapy, are paving the way for personalized approaches to CTRCD prevention and treatment. These advancements hold great promise for improving long-term outcomes in cancer patients by minimizing cardiovascular complications. Full article

Cardiovascular disease is the worldwide leading cause of mortality among survivors of cancer due in part to the cardiotoxicity of anticancer therapies. This paper explores the progress in precision cardio-oncology, particularly in genetic testing and therapeutics, and its impact on cardiovascular diseases in clinical and laboratory settings. These advancements enable clinicians to better assess risk, diagnose conditions, and deliver personalised, cost-effective therapeutics. Through case studies of cancer-therapy-related cardiac dysfunction, clonal haematopoiesis of indeterminate potential, and polygenic risk scoring, we demonstrate the benefits of incorporating precision genomics in individualised care in cardio-oncology. Furthermore, leveraging real-world genomic data in clinical settings can advance our understanding of long noncoding RNAs and microRNAs, which play important regulatory roles in cardio-oncology. Additionally, employing human-induced pluripotent stem cells to stratify risk and guide prevention strategies represents a promising avenue for modelling precision cardio-oncology. While these advancements showcase the significant progress in genetic approaches, they also raise substantial ethical, legal, and societal concerns. Regulatory oversight of genetic and genomic technologies should therefore evolve suitably to keep up with rapid advancements in technology and analysis. Provider education is crucial for the appropriate use of new genetic and genomic applications, including on the existing protection available for patients regarding genetic information. This can provide confidence for diverse study groups to advance genetic studies looking to develop a comprehensive understanding and effective clinical applications for heterogeneous populations. In clinical settings, the implementation of genetic and genomic applications within electronic medical records can offer point-of-care clinical decision support, thus providing timely information to guide clinical management decisions. Full article

Cardiovascular diseases and cancer are the leading causes of morbidity and mortality in modern society. Expanding cancer therapies that have improved prognosis may also be associated with cardiotoxicity, and extended life span after survivorship is associated with the increasing prevalence of cardiovascular disease. As such, the field of cardio-oncology has been rapidly expanding, with an aim to identify cardiotoxicity and cardiac disease early in a patient who is receiving treatment for cancer or is in survivorship. Artificial intelligence is revolutionizing modern medicine with its ability to identify cardiac disease early. This article comprehensively reviews applications of artificial intelligence specifically applied to electrocardiograms, echocardiography, cardiac magnetic resonance imaging, and nuclear imaging to predict cardiac toxicity in the setting of cancer therapies, with a view to reduce early complications and cardiac side effects from cancer therapies such as chemotherapy, radiation therapy, or immunotherapy. Full article

Background: Non-Hodgkin lymphoma (NHL) is associated with significant cardiovascular risks due to treatment-related toxicities, including cancer therapy-related cardiac dysfunction (CTRCD). While multimodality imaging, particularly echocardiography, is pivotal in monitoring cardiac function, the prognostic role of cardiopulmonary exercise testing (CPET) in predicting CTRCD remains underexplored. Methods: The prospective study enrolled 127 NHL patients, 72 men (56.7%) and 55 women (43.3%), with a median age of 62 years (range 34–83 years). The patients were assessed before initiating antitumor treatment and at six months follow-up using echocardiography and cardiopulmonary exercise testing. Results: Asymptomatic CTRCD occurred in 14.2% of NHL patients at six months of treatment. Patients with CTRCD exhibited significantly lower median work rates, volume of oxygen (VO₂) at the anaerobic threshold, and O₂ consumption efficiency, reflecting compromised metabolic and functional performance. Baseline peak oxygen consumption (VO₂ peak) positively correlated with left ventricle ejection fraction (LVEF) at six months, while VO₂ peak < 14 mL/kg/min was negatively associated with LVEF. Conclusions: Asymptomatic CTRCD was identified in 14.2% of NHL patients at six months, with lower work rates, VO₂ at the anaerobic threshold, and O₂ consumption efficiency, indicating impaired performance. Baseline peak oxygen consumption correlated positively with LVEF, highlighting CPET’s potential for early CTRCD risk assessment. Full article

Cardiac involvement in cancer is increasingly important in the diagnosis and follow-up of patients. A thorough cardiovascular evaluation using multimodal imaging is crucial to assess any direct cardiac involvement from oncological disease progression and to determine the cardiovascular risk of patients undergoing oncological therapies. Early detection of cardiac dysfunction, particularly due to cardiotoxicity from chemotherapy or radiotherapy, is essential to establish the disease’s overall prognostic impact. Comprehensive cardiovascular imaging should be integral to the clinical management of cancer patients. Echocardiography remains highly effective for assessing cardiac function, including systolic performance and ventricular filling pressures, with speckle-tracking echocardiography offering early insights into chemotoxicity-related myocardial damage. Cardiac computed tomography (CT) provides precise anatomical detail, especially for cardiac involvement due to metastasis or adjacent mediastinal or lung tumors. Coronary assessment is also important for initial risk stratification and monitoring potential coronary artery disease progression after radiotherapy or chemotherapeutic treatment. Finally, cardiac magnetic resonance (CMR) is the gold standard for myocardial tissue characterization, aiding in the differential diagnosis of cardiac masses. CMR’s mapping techniques allow for early detection of myocardial inflammation caused by cardiotoxicity. This review explores the applicability of echocardiography, cardiac CT, and CMR in cancer patients with extracardiac tumors. Full article

Cancer therapy-related cardiac dysfunction (CTRCD) has emerged as a significant concern with the rise of effective cancer treatments like anthracyclines and targeted therapies such as trastuzumab. While these therapies have improved cancer survival rates, their unintended cardiovascular side effects can lead to heart failure, cardiomyopathy, and arrhythmias. The pathophysiology of CTRCD involves oxidative stress, mitochondrial dysfunction, and calcium dysregulation, resulting in irreversible damage to cardiomyocytes. Inflammatory cytokines, disrupted growth factor signaling, and coronary atherosclerosis further contribute to this dysfunction. Advances in cardio-oncology have led to the early detection of CTRCD using cardiac biomarkers like troponins and imaging techniques such as echocardiography and cardiac magnetic resonance (CMR). These tools help identify asymptomatic patients at risk of cardiac events before the onset of clinical symptoms. Preventive strategies, including the use of cardioprotective agents like beta-blockers, angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors have shown promise in reducing the incidence of CTRCD. This review summarizes the mechanisms, detection methods, and emerging treatments for CTRCD, emphasizing the importance of interdisciplinary collaboration between oncologists and cardiologists to optimize care and improve both cancer and cardiovascular outcomes. Full article

Cardiotoxicity refers to the damage induced by antineoplastic treatments, leading to various cardiovascular conditions. [¹⁸F]FDG PET radiomics analysis could provide relevant information on early onset changes occurring in cardiac metabolism of chemotherapy-induced cardiotoxicity. Patients’ sociodemographic data, cardiovascular risk factors, laboratory parameters, and left ventricle [¹⁸F]FDG PET radiomic features are analyzed. The H_Rad index for the quantification of the heterogeneity of the metabolic uptake patterns is proposed. Statistical analysis is performed by separating patients according to the diagnosis of cancer therapy-related cardiac dysfunction (CTRCD). Baseline, intermediate, and end-of-treatment scans are evaluated as separate groups. Overall, CTRCD+ patients show lower overall mean standardized uptake values (SUV_mean) compared to CTRCD− patients, with statistically significant differences between groups only observed in the intermediate PET study (p = 0.025). A total of 34 radiomic features show statistically significant differences between the CTRCD+ and CTRCD− groups in the intermediate imaging studies. In the CTRCD− group, greater overall heterogeneity of metabolic uptake is observed in the intermediate PET image compared to the CTRCD+ groups (p = 0.025). The assessment of CTRCD through [¹⁸F]FDG PET radiomics analysis could be a potential tool for the identification of a predisposition to the later development of cardiac complications after cardiotoxic treatment. Full article

Background: Hematopoietic stem cell transplantation (HSCT) is a potentially curative procedure that is used in various hematological malignancies. However, among an increasing number of HSCT, the amount of cancer therapy-related cardiac dysfunction (CTRCD) is increasing as well. This study aimed to determine the prevalence of subclinical CTRCD in HSCT patients 12 months after HSCT and to assess the impact of clinical factors on the development of CTRCD. Material and Methods: We included 55 patients who underwent autologous or allogeneic HSCT. The patients were assessed using an echocardiography method before and 12 months after a HSCT procedure. Results: Our study revealed that during the 12-month follow-up period, asymptomatic CTRCD was observed in 15 patients (27.3%), 6 experienced moderate CTRCD, and 9 experienced mild CTRCD. Patients with previous use of anthracyclines tended to have CTRCD more often: nine patients (60%) in the CTRCD group and nine patients (22.5%) in non-CTRCD group. Patients who received the BEAM regimen for conditioning also experienced CTRCD more often: five patients (33.3%) in CTRCD group vs. two patients (5%) in the non-CTRCD group. Conclusions: Our study showed that asymptomatic CTRCD was found in 27.3% of the patients 12 months after HSCT. The BEAM chemotherapy conditioning protocol following prior anthracycline use were identified as factors contributing to the development of CTRCD. Full article

Proteasome inhibitors such as bortezomib and carfilzomib induce apoptosis and are a cornerstone in the treatment of relapsed or refractory multiple myeloma. However, concerns have emerged concerning their link to cancer therapy-related cardiovascular dysfunction (CTRCD). Bortezomib, a reversible first-generation inhibitor, and carfilzomib, a second-generation irreversible inhibitor, are associated with hypertension, heart failure, and cardiac arrhythmias. The current study investigated the effects of bortezomib and carfilzomib on cardiac (left ventricular ejection fraction, LVEF) and vascular (arterial stiffness, vascular reactivity) function. Cardiac function assessment aimed to build upon existing evidence of proteasome inhibitors CTRCD, while arterial stiffness served as an early indicator of potential vascular remodeling. Groups of 12-week-old C57BL/6J male mice (n = 8 per group) were randomly assigned to receive vehicle, carfilzomib (8 mg/kg I.P.), or bortezomib (0.5 mg/kg I.P.). Additionally, proteasome inhibition was assessed in mice treated with L-NAME (0.5 mg/kg) to induce hypertension. Cardiac and vascular parameters were evaluated via echocardiography on days 0 and 3. On day 6, mice were sacrificed for ex vivo analysis of arterial stiffness and vascular reactivity. Overall, no changes in arterial stiffness were detected either in vivo or ex vivo at basal pressures. However, a steeper pressure–stiffness curve was observed for carfilzomib in normotensive (p < 0.01) and hypertensive (p < 0.0001) mice ex vivo. Additionally, in hypertensive mice, carfilzomib decreased LVEF (p = 0.06), with bortezomib exhibiting similar trends. Vascular reactivity remained largely unchanged, but proteasome inhibition tended to enhance endothelial-independent relaxations in both control and hypertensive mice. In conclusion, short-term treatment with carfilzomib and bortezomib is considered relatively safe for the protocols assessed in the study. Full article