Cardio-oncology最新文献

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.

Radiation-induced cardiotoxicity remains a significant concern in breast cancer (BC) patients treated with radiotherapy (RT), with both cardiac radiation exposure and systemic inflammation emerging as key contributors to early cardiovascular complications. This study investigated whether cardiac radiation dose triggers independently or synergistically with systemic inflammation, characterized by C-reactive protein (CRP) elevation to predict coronary artery calcification (CAC) progression in BC survivors. We analyzed 101 chemotherapy-naïve BC women who underwent cardiac CT before and 24 months after RT, with dosimetric analysis of left ventricle (LV) radiation exposure. Sustained CRP elevation was defined as increased CRP at both end of RT and 6 months post-RT. CAC progression was observed in 28 patients (27.7%). Both sustained CRP elevation (OR = 3.42; 95% CI: 1.12-10.5) and mean LV dose (OR = 1.20 per Gy; 95% CI: 1.03-1.40) were independently associated with CAC progression. Although no statistically significant interaction was observed, stratified analyses showed a stronger association between mean LV dose and CAC progression among patients with sustained inflammation (OR = 1.39, 95%CI: 1.07-1.81), whereas this association was weaker and non-significant in patients without systemic inflammation (OR = 1.12, non-significant). The combined model incorporating both predictors showed improved discriminative performance (AUC = 0.733). These findings suggest that systemic inflammation may amplify the effect of cardiac irradiation and that combining inflammatory and dosimetric data improves early prediction of CAC risk. This may help identify high-risk subgroups who could benefit from enhanced cardiovascular monitoring or preventive strategies after BC RT.

Background: Adult survivors of childhood cancers are thought to be at high risk for late-onset cardiovascular complications of prior anti-cancer treatments. While cancer therapy-related cardiac dysfunction (CTRCD) has previously been observed in this population, data are limited regarding the utility of longitudinal echocardiographic monitoring.

Methods: 124 adult survivors of childhood cancer who were previously treated with anthracyclines and/or radiation therapy as children were included in this longitudinal cohort study. Participants were enrolled in Northwestern Medicine's survivorship clinic: Survivors Taking Action and Responsibility (STAR) Program and followed for up to10 years between 2009 and 2022. Serial echocardiography was performed at baseline then at 1, 3, 5, and 7-10 years post-enrollment. Clinical data was collected by chart review. Major adverse cardiovascular events (MACE) and CTRCD were adjudicated according to ACC/AHA MACE criteria and the ESC Cardio-Oncology guidelines respectively.

Results: Over 10 years of follow-up in the STAR Program, 17.7% (22/124) of participants developed MACE, with the highest incidence observed in patients treated with radiation alone. 10.5% (13/124) of patients developed CTRCD by left ventricular ejection fraction (LVEF) criteria while 36.3% (45/124) developed CTRCD by global longitudinal strain (GLS) criteria. New incidence of MACE and CTRCD occurred as late as 7-10 years post-enrollment. Participants who developed CTRCD showed subsequent improvement in both LVEF and GLS by the end of 10 years of follow-up and treatment in the STAR Program.

Conclusions: Survivors of childhood cancer are at high risk for both MACE and CTRCD even many years after initial diagnosis. Patients who received treatment for pediatric cancer, then subsequently enrolled in the STAR Program as adults and received appropriate cardiovascular monitoring and treatment showed improvement in both LVEF and GLS by the end of follow-up, underscoring the importance of a dedicated survivorship clinic for adult survivors of pediatric cancer.

Background: Evidence-based and/or consensus guidance regarding exercise and return-to-play for the adolescent and young adult (AYA) athlete with cardio-oncology concerns is lacking. Many of the recommendations utilized for the diagnosis, surveillance, and management of cancer therapeutic-related cardiotoxicity in children have been extrapolated from adult literature and myocarditis guidelines, the latter of which are primarily concerned with potential for arrhythmias secondary to inflammation and myocardial scarring. In addition, the athlete's heart itself brings about several diagnostic challenges including physiologic changes due to endurance or isometric training. Exercise-induced cardiac remodeling, with enlarged cavity size, lower resting ejection fraction and increased left ventricular wall thickness, depending on the type of exercise, can mimic disease states including both underlying pathologies and the response to cancer therapeutics.

Case presentation: A high school cancer survivor had borderline ejection fraction and abnormal strain indices. He was able to return to competitive sports without complication after clinical evaluation and through a shared decision-making process.

Conclusions: The difficulty in differentiating physiologic from potentially pathologic echocardiographic changes can result in unnecessary disqualification, depriving athletes from social, psychological, and possibly financial benefits. Stress echocardiography indices, such as contractile reserve and mitral E/e' ratio, may inform assessment of systolic and diastolic function, respectively, and may be helpful in risk stratifying and understanding potential performance limitations in AYA athletes with cardio-oncology concerns for exercise and return-to-play. Most recent consensus statements regarding sports participation in the athlete with heart disease focus on a shared decision-making process amongst all stakeholders involved to formulate an informed, safe, and cohesive prescription to enable the athlete to safely re-engage in sports after recovering from a cardiac illness or surgery. Multidisciplinary recommendations emphasize the importance of exercise before, during, and after chemotherapy in an individualized approach to reduce risk factors in oncology patients and improve cardiovascular outcomes. Further research is needed to delineate protocols for the adolescent and young adult cardio-oncology athlete regarding exercise prescriptions and their return-to-play following oncology treatment.