Search Results (49)

Background: Immune checkpoint inhibitors (ICIs) improve cancer outcomes but may cause cardiovascular toxicity, including early subclinical myocardial injury. Conventional echocardiography has limited sensitivity, whereas speckle-tracking echocardiography (STE) allows for early detection of myocardial deformation. Data on short-term ICI-related effects on biventricular mechanics are limited, and atrial function remains poorly characterized. This study evaluated the early impact of ICI therapy on biventricular and biatrial mechanics using STE in patients with advanced cancer. Methods: In this prospective, single-center study, 28 consecutive patients with advanced cancer undergoing ICI therapy were followed for 3 months. Clinical, laboratory, electrocardiographic, and echocardiographic assessments were performed at baseline, 1 month, and 3 months. STE was used to assess left ventricular global longitudinal strain (LV-GLS) and circumferential strain; right ventricular GLS (RV-GLS); and left and right atrial reservoir, conduit, and contractile strain parameters. Subclinical LV dysfunction was defined as a relative LV-GLS reduction >15%. Logistic and Cox regression analyses identified predictors of strain impairment and adverse clinical events. Results: Conventional echocardiographic parameters, including left ventricular ejection fraction, remained stable. In contrast, LV-GLS declined progressively from 20.7 ± 2.1% to 17.6 ± 2.7% at 3 months (p = 0.002), with subclinical LV dysfunction observed in 85.7% of patients. RV-GLS also deteriorated despite preserved TAPSE. Both left and right atrial strain and strain-rate parameters showed an early and marked decline, accompanied by increased left atrial stiffness despite unchanged atrial volumes. Older age and higher neutrophil-to-lymphocyte ratio (NLR) were associated with LV-GLS impairment. Over a mean follow-up of 5.4 ± 3 months, baseline LV-GLS independently predicted adverse clinical events and mortality. Optimal cut-off values were 67 years for age, 4 for NLR, and 19.5% for LV-GLS. Conclusions: Short-term ICI therapy is associated with early, diffuse subclinical myocardial dysfunction involving both ventricles and atria, detectable only by STE. Comprehensive biventricular and biatrial strain assessment may enhance early cardio-oncology surveillance and risk stratification in ICI-treated patients. Full article

Background. The aim of this study was to develop a predictive model of anticancer drug therapy toxicity in patients with gastric cancer. Methods. The retrospective study included 100 patients with stage II–IV gastric cancer who underwent 4 chemotherapy cycles. Initial significant toxicity factors included age, gender, height, body mass, body mass index, disease stage, skeletal muscle index (SMI), as well as plasma levels of trace elements (copper, zinc, selenium, manganese) and thyroid-stimulating hormone, cancer histology type and treatment regimen. The CTCAE v5.0 scale was employed to assess the severity of adverse events. Statistical analysis and building of mathematical neural network models were carried out in SPSS Statistics (v19.0). Results. Lower SMI values were associated with higher rates of toxicity-related complications of anticancer drug therapy (p < 0.05): leukopenia, hypoproteinemia, nausea, vomiting, cardiovascular events. Anemia, thrombocytopenia, hepatic cytolysis syndrome, nausea, diarrhea, constipation and stomatitis showed a weaker correlation with SMI. An increase in TSH was associated with higher rates of thrombocytopenia, nausea and vomiting. A decrease in Cu/Zn in plasma correlated with the severity of leukopenia and diarrhea, whereas Se/Mn showed an inverse correlation with the severity of anemia. Conclusions. Sarcopenia, abnormal thyroid status and imbalances in copper, zinc, selenium and manganese in blood plasma of patients with gastric cancer may be used as predictors of increased toxicity of anticancer drug therapy. Full article

Recent advances in oncology have contributed to a steady rise in cancer survivorship. However, many cancer therapies are associated with cardiovascular adverse events, leading to increased rates of cardiovascular morbidity and mortality. As a result, cardio-oncology has emerged as a rapidly advancing discipline that relies on multidisciplinary collaboration. Cardiovascular multimodality imaging (CVMI) is an essential diagnostic and surveillance tool for cardiovascular toxicity, along with clinical evaluation and biomarkers. CVMI plays a central role in diagnosing cancer therapy-related cardiac dysfunction (CTRCD) and myocarditis, while also supporting the assessment of vascular toxicity and arrhythmias. It is essential for baseline cardiac evaluation and continuous monitoring throughout and following cancer therapy. CVMI enables early detection of cardiovascular toxicity, facilitating prompt initiation of cardioprotective therapy and allowing cancer therapy to proceed without compromising safety. Echocardiography is the primary imaging modality for screening, diagnosing, and monitoring CTRCD. Moreover, it is the first-line imaging test for cardiac structural and functional assessment in patients who develop immune checkpoint inhibitor (ICI)-related myocarditis. Advanced imaging techniques, such as cardiac magnetic resonance (CMR), nuclear imaging, and cardiac computed tomography, may help determine the cause and severity of left ventricular dysfunction, as well as assess cardiac masses and vascular toxicity. Not least, CMR is the gold standard imaging modality to diagnose myocarditis. This article is a narrative review that focuses on the various modalities of CVMI and their applications in cardio-oncology. Since the issue addressed is very extensive, this review was designed to be concise. Full article

Mediastinal radiotherapy plays a central role in the treatment of several malignancies, particularly Hodgkin lymphoma and breast cancer. However, exposure to thoracic radiation is associated with long-term cardiovascular complications, among which valvular heart disease (VHD) is increasingly recognized. Radiation-induced VHD typically presents after a latency period of 10–20 years and is characterized by progressive valve fibrosis, thickening, and calcification, most commonly affecting the left-sided valves. Management of radiation-induced VHD generally follows standard guidelines but remains challenging due to extensive calcification and coexisting radiation-related cardiac or pulmonary injury. A history of thoracic radiotherapy is associated with increased perioperative risk and may negatively impact surgical outcomes, which often alters the risk–benefit balance and favors less invasive therapeutic approaches. Advances in the transcatheter approach have expanded treatment options for this high-risk population; however, data on long-term outcomes remain limited. Evolving dose-reduction techniques, such as deep-inspiration breath-hold, intensity-modulated radiotherapy, and proton therapy, together with predictive dosimetric models, aim to minimize future cardiac toxicity. Given the delayed onset and progressive nature of radiation-associated VHD, structured long-term surveillance is essential to enable early detection and timely intervention in cancer survivors at risk. Full article

Numerous studies and international recommendations have investigated risk factors that put childhood cancer survivors (CCSs) at a higher risk of late-onset cancer therapy-related cardiovascular toxicities (CTR-CVTs). While anthracyclines and chest-directed radiotherapy are well-established high-risk treatments, other anticancer therapies, including alkylating agents, antimetabolites, targeted therapies, and hematopoietic stem cell transplantation, also carry potential cardiotoxic effects. The likelihood of developing CTR-CVT is further modulated by the presence of cardiometabolic risk factors, prior occurrence of CTR-CVT during treatment, and certain clinical conditions, which may predispose survivors to long-term cardiovascular complications. This state-of-the-art review summarizes current strategies for stratifying the risk for developing CTR-CVT in CCSs. We then propose a tailored, multimodal approach for guiding cardio-oncological assessments both during treatment and in long-term follow-up, including a structured echocardiographic protocol. Future perspectives include validation of this approach to optimize early detection and personalized management of CTR-CVT. Full article

Background and Objectives: Cardiac injury caused by cancer therapy can be detected early using high-sensitivity cardiac troponins (hs-cTns), and this is crucial for preventing irreversible consequences. Clinically relevant issues regarding hs-cTns in oncologic settings—such as reliable cut-off values, the optimal assessment timeframe, factors influencing their levels, and their prognostic ability in relation to functional echocardiographic parameters—require further investigation. In this study, we aimed to examine the determinants of hs-cTnT variations during cancer therapy and the relationship between the biomarker and functional conventional echocardiographic parameters. Materials and Methods: We prospectively evaluated adult patients scheduled for chemotherapy for either breast or gastrointestinal cancers, excluding those with pulmonary and cardiac disorders. We enrolled 40 patients who underwent a minimum of one cycle of potentially cardiotoxic regimens containing at least one of the following agents: anthracyclines, cyclophosphamide, taxanes, 5-fluorouracil, platinum compounds, trastuzumab, or bevacizumab. We observed two-dimensional and tissue Doppler echocardiographic parameters and hs-cTnT levels for a median of 360 days (IQR 162, 478) following the start of chemotherapy. Results: The generalised estimating equation (GEE) analysis revealed significant elevations in hs-cTnT levels at three months (β = 1.2; p = 0.005) and six months (β = 2.3; p = 0.02) from baseline, influenced by anthracycline treatment (p = 0.009), renal function (p = 0.003), and increased cardiotoxicity risk (high: p = 0.013; medium: p < 0.001). Elevated hs-cTnT levels independently predicted the deterioration of the LV longitudinal myocardial function, measured by the systolic tissue velocities, according to the GEE analysis. The receiver operating characteristic curve-derived hs-cTnT thresholds—of 8.23 ng/L and 8.08 ng/L—had a high negative predictive value for identifying Average and Lateral LVS′ decreases, respectively. Conclusions: Our research supports the use of baseline and continuing hs-cTnT testing in cancer patients, showing the dependence of the biomarker on renal function, cardiovascular toxicity risk level, and anthracycline treatment. The hs-cTnT cut-off value of approximately 8 ng/L may suggest a low probability of longitudinal myocardial function impairment and this observation needs further validation in larger cohorts. Full article

The growing overlap between cardiovascular disease and cancer has made cardio-oncology a key subspecialty in modern oncology care. Improved cancer survival has increased the burden of therapy-related cardiovascular complications, including heart failure, arrhythmias, ischemic events, and vascular toxicity, driven by oxidative stress, endothelial dysfunction, immune-mediated injury, and metabolic vulnerability. Effective management requires a continuum-of-care approach, integrating baseline risk assessment, biomarker- and imaging-guided surveillance, and timely cardioprotective therapy without compromising cancer treatment. Key strategies include validated risk scores (HFA/ICOS, Mayo), early detection of subclinical dysfunction via troponin, natriuretic peptides, and strain imaging, and proactive cardioprotective agents such as ACE inhibitors, beta-blockers, SGLT2 inhibitors, and statins in high-risk patients. This narrative review summarizes risk-stratification models, structured care pathways, and multidisciplinary hub-and-spoke networks linking specialized centers with community oncology services. It emphasizes modifiable cardiometabolic factors, obesity, insulin resistance, NAFLD, sarcopenia, and chronic inflammation, which heighten cardiotoxicity risk and should guide precision prevention and survivorship care. We also address emerging challenges, including the integration of digital health, tele-monitoring, and AI-based decision support, and the shift toward value-based reimbursement models, highlighting persistent barriers such as data privacy, infrastructure gaps, and inequitable access to specialized care. Full article

Background: Anthracycline-based chemotherapy is associated with a risk of cancer therapy-related cardiac dysfunction (CTRCD), particularly in patients with moderate to high cardiovascular risk. Left ventricular global longitudinal strain (GLS) is a sensitive marker for early myocardial dysfunction, but the prognostic value of baseline GLS in this population remains unclear. Objective: We aimed to evaluate whether baseline GLS can predict CTRCD in moderate- to high-risk cancer patients undergoing anthracycline chemotherapy. Methods: In this prospective, single-center observational study, 80 anthracycline-naive cancer patients classified as moderate or high risk were enrolled. Baseline GLS was assessed via speckle-tracking echocardiography, with a threshold of ≥−18% considered decreased. Patients were followed for 12 months, and the primary endpoint was the development of CTRCD per ESC 2022 Cardio-oncology guidelines. Results: Of the 77 patients completing follow-up, 27.3% had decreased baseline GLS. CTRCD occurred in 62.4% of patients, with higher incidence among those with decreased GLS (76.7%) compared to those with normal GLS. In multivariable analysis, GLS ≥−18% was the only significant independent predictor of CTRCD (RR 12.0, 95% CI 2.0–71.9; p = 0.0065). All-cause mortality was also significantly higher in patients with decreased baseline GLS (19.1% vs. 1.8%, p = 0.018). Conclusions: Decreased baseline global longitudinal strain is an independent predictor of cancer therapy-related cardiac dysfunction and all-cause mortality in moderate- to high-risk patients receiving anthracycline therapy. These findings support the inclusion of baseline GLS in pre-treatment cardiovascular risk assessment, particularly in patients with an LVEF above 54%, to more effectively identify those who may benefit from early cardioprotective interventions. Full article

The introduction of novel oncologic therapies, including targeted agents, immunotherapies, and antibody–drug conjugates, has transformed the therapeutic landscape of cancer care. This evolution has resulted in a dual clinical scenario; while survival outcomes have markedly improved, leading to a growing population of long-term cancer survivors, an increasing incidence of previously unrecognized treatment-related toxicities has emerged. Among these, cardiovascular adverse events represent some of the most prevalent and clinically significant complications observed in both conventional chemotherapy and modern therapeutic regimens. Cardiotoxicity has become a major concern, with the potential to adversely affect not only cardiovascular health but also the continuity and efficacy of oncologic treatments, thereby impacting overall survival. This opinion paper synthesizes current evidence, identifies critical gaps in knowledge, and advocates for a multidisciplinary, evidence-based framework to guide the prevention, early detection, and optimal management of cardiotoxicity associated with anticancer therapies. Full article

Aromatase inhibitors (AIs), with or without gonadotropin-releasing hormone analogs, are the cornerstone of adjuvant endocrine therapy for women with hormone receptor-positive early-stage breast cancer, offering significant reductions in recurrence risk and improving long-term survival. Their use is frequently accompanied by treatment-related toxicities that can adversely affect patients’ quality of life (QoL) and adherence to therapy. Commonly reported side effects include vasomotor symptoms, such as hot flashes; musculoskeletal disorders, such as arthralgia and myalgia; mood disorders; and genitourinary discomfort, such as vaginal dryness and dyspareunia. Additionally, AIs are associated with a heightened risk of bone loss, leading to osteoporosis and fractures, and may have implications for cardiovascular health. Effective management of these adverse events is pivotal in maintaining treatment adherence and preserving QoL. Evidence-based strategies to address these toxicities include pharmacological interventions, such as analgesics for joint pain, bisphosphonates or denosumab for bone health, and hormonal or non-hormonal approaches for vasomotor and genitourinary symptoms. Non-pharmacological measures, including physical activity, dietary adjustments, and complementary therapies, can also help mitigate symptoms. This review examines the broad spectrum of AI-associated toxicities, discusses their clinical implications, and provides an overview of evidence-based management strategies. These insights aim to support clinicians in optimizing patient care while minimizing the toxicities of therapy. Full article

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

The knowledge concerning mild-to-moderate renal toxicity of adjuvant chemotherapy (CTH) in colon cancer patients is scarce. We retrospectively evaluated changes in the estimated glomerular filtration rate (eGFR) after three months of adjuvant treatment and the overall renal risk of the 6-month regimen in 145 patients who completed three months of therapy at three oncological centers. A decrease in eGFR of at least 1.5 mL/min/1.73 m² after three months and 3.0 mL/min/1.73 m² after six months was considered relevant in terms of kidney-related cardiovascular risk. Out of 114 patients who completed a 6-month regimen, kidney function deterioration occurred in 62 (54.4%) after 3 months and in 54 (47.4%) after 6 months. Age ≥ 70 years (RR = 2.66; 95% CI: 1.15–6.16) and diabetes (RR = 2.52; 95% CI: 0.98–6.45) were risk factors for kidney outcomes during the first three months of CTH. However, renal function decline during the first three months did not increase the risk of further deterioration on CTH continuation. In conclusion, older age and diabetes are factors increasing the risk of renal function deterioration during adjuvant CTH in colon cancer patients without preexisting chronic kidney disease. However, the decline during the first three months does not allow for predicting further changes under continued adjuvant 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, also known as malignant tumors, is formed due to abnormal mutations and the proliferation of human cells. Cancer cells not only demonstrate accelerated proliferation but also show robust invasive and metastatic potential, disseminating from a primary affected region of the body to multiple areas and potentially culminating in organ dysfunction or failure, thereby jeopardizing the individual’s life. The rapid growth of the biopharmaceutical market has given rise to numerous novel medicines, thereby precipitating a paradigm shift in contemporary drug development methodologies. This modification is focused on identifying methodologies that can effectively target cancerous cells while minimizing damage to normal cells. There is an increasing societal movement that supports the utilization of natural ingredients derived from plants. In recent years, traditional herbal medicine has experienced a surge in popularity within the global cancer market. In comparison with the use of more toxic chemotherapy methods, there has been an increasing focus on advanced therapies that exhibit reduced side effects. Ginsenoside compound K (CK) is derived from the natural components in ginseng through biotransformation. The utilization of CK in cancer research is a practice engaged in by numerous scientists. The underlying rationale is that CK exhibits a multitude of effects within the realm of cancer research, including but not limited to the mitigation of inflammation, the suppression of cancerous cell proliferation, and the safeguarding of cardiovascular, hepatic, and renal functions. This review methodically identifies and organizes CK-related journals according to the following key points of cancer treatment: the effects on cancer cells themselves, angiogenesis inhibition, modulation of immune response to identify cancer cells, and inflammation regulation. The intricate interplay between ginsenoside CK and cells is elucidated through a graphical representation. The present review focuses on the results of CK in in vitro tests. It is our hope that the present article will aid future studies on the results of CK in vivo tests, clarify the correlation between cellular mechanisms in vivo and in vitro tests, and assist in the development of drugs. Full article