Cardio-oncology最新文献

Background: Cancer survivors (CSs) are at increased risk of atrial fibrillation (AF), potentially due to cancer-related inflammation and treatment effects. While inflammation has been implicated in both cancer and AF, the association between C-reactive protein (CRP) and AF risk in CSs remains unclear.

Methods: We analyzed data from 19,677 UK Biobank participants (mean age 60; 34.2% male) with a prior cancer diagnosis. Incident AF was evaluated using competing-risk Cox proportional hazards models, adjusting for sociodemographic, lifestyle, and clinical factors.

Results: Over a median follow-up of 10.4 years, 836 CSs (4.2%) developed AF. Competing risk analysis revealed that the significant association between elevated CRP (> 2 mg/L) and AF risk in CSs, observed in models adjusted for sociodemographic and clinical factors (HR 1.21, 95% CI 1.06-1.37; P = 0.005), progressively attenuated with further adjustment for lifestyle factors (HR 1.14, 95% CI 0.99-1.31; P = 0.076). Despite losing statistical significance in the fully adjusted model, a consistent, suggestive trend was observed. This association was particularly pronounced in individuals not receiving radiotherapy.

Conclusions: Our findings suggest that systemic inflammation is associated with an increased risk of AF among CSs, particularly in individuals without a history of radiotherapy. Further studies are needed to explore underlying mechanisms and therapeutic implications.

Background: Anthracycline-induced cardiotoxicity (CTX) requires close monitoring in lymphoma patients. Increased myocardial uptake of fluorine-18-fluorodeoxyglucose (18F-FDG) via positron emission tomography combined with computed tomography (PET/CT) may reflect early metabolic alterations and serve as a potential marker for CTX.

Objectives: To evaluate changes in cardiac metabolism, myocardial strain, and troponin levels during anthracycline-based chemotherapy.

Methods: This prospective multicenter study included 55 adult lymphoma patients receiving anthracycline therapy. Echocardiography, high-sensitivity troponin, and cardiac 18F-FDG PET/CT were performed at baseline, mid-therapy, and posttreatment. CTX was defined as a ≥ 15% reduction in global longitudinal strain (GLS) from baseline.

Results: The mean age was 42 ± 16.7 years; 60% were female. Subclinical CTX occurred in 34% of patients, with a GLS decline observed after 3 months of follow-up, despite preserved left ventricular ejection fraction (LVEF). CTX was associated with older age, hypertension, diabetes, and dyslipidemia. Troponin levels were elevated in 33% but did not differ between the CTX and non-CTX groups. Myocardial 18F-FDG uptake increased in 49.1% of patients (≥ 30% standardized uptake value increase), without correlation with GLS or LVEF changes.

Conclusions: GLS can detect early myocardial changes in lymphoma patients treated with anthracyclines, whereas increased 18F-FDG uptake on PET/CT did not correlate with ventricular dysfunction. The clinical significance of myocardial metabolic upregulation requires further investigation.

Background: Cardiotoxicity remains a critical barrier to effective cancer treatment, contributing significantly to morbidity and mortality in cancer survivors. Recent advancements (2020-2025) highlight artificial intelligence (AI) as a transformative tool in cardio-oncology, enhancing cardiotoxicity detection, personalized risk assessment, and patient management. Despite rapid technological progress, significant gaps remain in AI integration across different healthcare settings globally.

Methods: This narrative review systematically synthesizes literature published between 2020 and 2025, evaluating key applications of AI in cardio-oncology, including imaging modalities, predictive modeling, wearable technology, and clinical decision-support systems. Comparative analyses between high-income countries (HICs) and low-to-middle-income countries (LMICs), with an emphasis on the Middle East, were performed to illustrate global disparities and unique regional challenges.

Results: AI-enabled imaging technologies, particularly echocardiography and cardiac MRI, significantly improved the early detection and management of cardiotoxicity. Predictive algorithms integrating multimodal data demonstrated superior risk stratification accuracy over traditional methods. Wearable technologies combined with AI enabled real-time cardiac monitoring, demonstrating feasibility in diverse resource settings. Nonetheless, adoption barriers such as dataset biases, inadequate regulatory frameworks, prohibitive costs, ethical dilemmas, and limited digital infrastructure persist, disproportionately affecting LMICs.

Conclusion: To harness the full potential of AI in cardio-oncology, strategic investments in collaborative international research, standardized regulatory frameworks, educational initiatives, and infrastructural support are urgently needed. Future research should prioritize equitable, inclusive AI solutions, validated through prospective trials and adapted specifically to underserved populations.

Objectives: Primary cardiac sarcomas (PCSs) are uncommon malignant tumors with a poor prognosis. This study aims to present the clinical characteristics and treatment outcomes for PCS observed in our centers.

Method: We retrospectively gathered records of patients diagnosed with PCS at Peking University Cancer Hospital and Zhejiang Cancer Hospital between 2016 and 2023. Clinicopathological data, treatments, and outcomes were included in the analysis.

Result: Between January 2016 and October 2023, a total of 26 patients with primary cardiac sarcoma were included in this study, with a majority being female (57.7%). The median age of the patients was 38.5 years, ranging from 15 to 82 years. The median overall survival (OS) for all patients was 18.7 months (95% CI: 16.2-25.4). Patients with normal baseline LDH levels had a significantly longer median OS of 25.4 months compared to 12.9 months for those with elevated LDH levels (p < 0.01). The median OS for patients who underwent R0 resection was 23.7 months, while it was 16.9 months for those who underwent R1/R2 resection, and 11.6 months for those who did not undergo surgery. Patients who received anthracycline-based chemotherapy seem to have better survival outcomes compared to those who received paclitaxel-based chemotherapy (mOS for chemotherapy 11.3 vs. 8.97 months, p = 0.25), but there was no statistical difference. First-line treatment with antiangiogenic agents or immunotherapy may enhance survival, with statistical significance observed.

Conclusion: PCS presents a complex management challenge. Complete surgical resection remains the primary treatment option when feasible. Systemic treatment options, including chemotherapy, targeted therapy, and immunotherapy, may also improve survival outcomes.

Background: CPX-351, a dual-drug liposomal encapsulation of daunorubicin and cytarabine in a synergistic 1:5 molar ratio, has demonstrated significantly improved overall survival in acute myeloid leukemia (AML) compared with 7 + 3, but its impact on cardiac function remains unclear. In a post hoc analysis of the pivotal clinical trial, we sought to determine the relative cardiotoxicity of CPX-351 vs. 7 + 3 in high-risk AML.

Methods: We evaluated cardiotoxicity in 102 patients with AML (CPX-351, n = 57; 7 + 3, n = 45) who had normal baseline left ventricular ejection fraction (LVEF) ≥ 53% and at least one post-baseline echocardiographic assessment. Cardiotoxicity was assessed through reported cardiac adverse events (AEs) and core lab assessment of echocardiograph changes in LVEF and/or left ventricular global longitudinal strain (GLS).

Results: A clinically significant change in LVEF (absolute change from baseline > 10% and LVEF <53%) and GLS (relative change from baseline > 12% and GLS < 18%) was less common with CPX-351 vs. 7 + 3 at follow-up 1 and/or 2 (8.8% vs. 20.0% and 21.1% vs. 44.4%, respectively). No CPX‑351-treated patients evaluated at final follow-up (follow-up 2) had decreased LVEF < 53% at follow-up 2, compared to 17.8% of 7 + 3-treated patients. The frequency of reported cardiac AEs was similar with CPX-351 (40.4%) and 7 + 3 (42.2%); most frequent were tachycardia in CPX-351-treated patients (CPX-351, 21.1%; 7 + 3, 8.9%) and atrial fibrillation/flutter in 7 + 3-treated patients (CPX-351, 7.0%; 7 + 3, 11.1%).  CONCLUSION: In addition to improving overall survival as demonstrated in the pivotal trial, CPX-351 may also be associated with less cardiotoxicity than 7 + 3 in high-risk AML patients.

Background: Cardiac involvement in diffuse large B-cell lymphoma (DLBCL) is rare but often complicated by life-threatening arrhythmias, conduction disturbances, and heart failure. Electrocardiography (ECG) is essential for early recognition and guiding intervention.

Objectives: To characterize ECG manifestations of cardiac-involved DLBCL and evaluate strategies for managing associated cardiac complications.

Methods: This study is a retrospective institutional case series conducted at MacKay Memorial Hospital from 2010 to 2025. We reviewed five patients with histologically confirmed primary or secondary cardiac DLBCL. Data on tumor location, ECG and echocardiographic findings, cardioprotective and anti-arrhythmic therapy, chemotherapy regimens, and outcomes were analyzed to correlate electrical abnormalities with anatomical involvement and therapeutic response.

Results: ECG patterns varied according to tumor distribution. Right atrial involvement was often associated with atrial tachycardia or atrial fibrillation. Pericardial infiltration produced low-voltage QRS complexes and electrical alternans in cases of massive effusion, whereas minimal effusion preserved normal sinus rhythm. Myocardial infiltration appeared to increase the risk of ventricular tachycardia and high-grade atrioventricular block, which is supported by the previous research about the reentry circuits at tumor-myocardium interfaces. Chemotherapy remains the principal therapeutic approach for cardiac DLBCL; however, our limited observations suggest that integrating anti-arrhythmic and cardioprotective therapy may improve chemotherapy tolerance. Successful arrhythmia control frequently correlated with improved clinical outcomes. However, the optimal use of anthracycline-based regimens in cardiac DLBCL remains uncertain and warrants further investigation.

Conclusions: Our findings highlight the importance of early recognition and multidisciplinary management for cardiac complications in the patients with cardiac-involved DLBCL. Cardioprotective strategies, anti-arrhythmic management, and careful chemotherapy selection are crucial to balance oncologic efficacy with cardiovascular safety.

Immune checkpoint inhibitors (ICIs) have significantly advanced cancer therapy. However, these therapies can disrupt immune self-tolerance, leading to immune-related adverse events, among which immune checkpoint inhibitor-related myocarditis (ICIrM) is associated with the highest mortality rates. Clinical presentation of ICIrM varies widely, ranging from asymptomatic cardiac biomarker elevation to fulminant heart failure. As such, uniform treatment guidelines may not be appropriate, and a personalized approach is essential. There is no universal consensus on routine screening; however, baseline ECG and echocardiography are recommended by most cardio-oncology guidelines. Serial cardiac biomarker monitoring may aid in early detection and intervention. Both cardiac troponin T and cardiac troponin I are sensitive for the diagnosis of ICIrM and prognosis of increased risk of major adverse cardiovascular events. Two diagnostic frameworks for ICIrM help clinicians in establishing diagnosis. Echocardiographic global longitudinal strain measurement provides a more sensitive risk assessment than traditional measures like ejection fraction. Cardiac MRI plays a critical role, offering high diagnostic accuracy. Endomyocardial biopsy confirms ICIrM and provides both diagnostic and prognostic information based on the presence or absence of myocyte necrosis. For confirmed ICIrM, corticosteroids remain the cornerstone of therapy, with high-dose regimens shown to reduce major adverse cardiovascular events. In steroid-refractory or severe cases, adjunctive immunomodulators such as mycophenolate mofetil, janus kinase inhibitors, and notably abatacept are utilized, although evidence is largely case-based. Abatacept, a CTLA-4 fusion protein, is the only drug under investigation in a randomized trial as a targeted therapy for ICIrM. In conclusion, ICIrM represents a diagnostic and therapeutic challenge due to its rarity, heterogeneous presentation, and the limitations of current tools. By describing the management of three illustrative real-life cases, this article aims to provide a framework for individualized management of ICIrM in adults, integrating current guidelines, literature, and clinical experience. Continued research and prospective trials are critical to refine diagnostic algorithms and improve patient outcomes.

Background: Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy, offering significant survival benefits across diverse malignancies. However, growing evidence suggest an increased occurrence of cardiovascular adverse events (CVAEs) following ICI, which remain poorly characterized in large, real-world populations.

Objectives: To quantify the incidence and spectrum of CVAEs following ICI initiation and identify demographic, clinical, and treatment-related risk factors for CVAE development.

Methods: We conducted a retrospective cohort study using electronic health record data from the OneFlorida + Clinical Research Network. Adult cancer patients (≥ 18 years) with cancer who started FDA-approved ICIs between January 1, 2018, and December 31, 2023, were included. Eligible patients had either ≥ 1 inpatient or ≥ 2 outpatient encounters after. The primary outcome was new-onset CVAE within one year. Kaplan-Meier survival analyses and multivariable Cox regression evaluated associations with risk factors.

Results: Among 9,541 patients initiating ICIs, 2,320 (24.3%) developed a CVAE within one year, with arrhythmia (15.7%), heart failure (5.2%), and stroke (4.1%) being the most common. Cardiometabolic comorbidities (hypertension, hyperlipidemia, diabetes, and obesity) were independently associated with increased CVAE risk. CVAE incidence varied significantly by cancer type, with highest risk observed in breast, liver, and lung cancers compared to melanoma. Triple checkpoint blockade (CTLA-4 + PD-(L)1 + LAG-3) conferred a modest but significant increase in CVAE risk.

Conclusion: CVAEs occurred frequently after ICI initiation, with substantial variation by cancer type, comorbidities, and treatment regimen. These findings highlight the importance of cardiovascular risk assessment and monitoring to optimize outcomes in immuno-oncology.

Background: Recent studies have shown that heart failure (HF) and left ventricular (LV) dysfunction are associated with enhanced tumor growth. However, whether treating LV dysfunction mitigates its impact on cancer progression remains unknown. We hypothesized that HF treatments would attenuate tumor growth in a rodent model of post-myocardial infarction (MI)-induced LV dysfunction, and that different pharmacological agents (carvedilol, enalapril, and empagliflozin) might exert distinct effects on tumor progression.

Methods: MI was induced in female BALB/c mice, leading to LV dysfunction. Mice with LV ejection fraction < 40% two weeks after MI received daily vehicle or one of three HF treatments by gavage. Two weeks later, 2 × 10⁵ 4T1 metastatic breast cancer cells were injected, with a three-week follow-up. The effects of HF treatments on cancer progression were assessed by analyzing: (i) tumor size in vivo over 22 days, (ii) lung metastasis development and (iii) gene expression levels in tumor tissue by RNA sequencing.

Results: Enalapril reversed several MI-induced transcriptomic changes in tumor tissue. Empagliflozin reduced primary tumor growth, while carvedilol reduced metastatic clusters. These effects were absent in control mice without MI, and neither drug directly affected cultured 4T1 cells. Transcriptomic analysis revealed treatment-specific inflammatory pathway regulation. Notably, carvedilol and empagliflozin restored MI-suppressed IFN-γ expression in tumors, accompanied by increased STAT1 expression in 4T1 cells.

Conclusion: Specific HF treatments can mitigate cancer growth in a mouse model of MI-induced LV dysfunction, with outcomes varying by treatment. These benefits occurred only with LV dysfunction, suggesting they result from changes in HF pathophysiology rather than direct drug effects on tumor cells. Restoration of immune signaling may contribute to these effects.