Cardio-oncology最新文献

Background: Anthracyclines can cause dose-dependent cardiotoxicity that may be irreversible. To minimize cardiotoxic effects, substituting doxorubicin for liposomal doxorubicin (LD) has been explored as a cardioprotective strategy.

Objectives: To describe randomized clinical trials (RCTs) comparing the efficacy and safety of LD with other anthracycline-based regimens.

Methods: We conducted a systematic review and meta-analysis of RCTs comparing LD with other anthracycline-based regimens, using data from Medline, Embase, Emcare, the Cochrane Central Register, and LILACS.

Results: Twelve studies including 3027 patients with breast cancer (6), multiple myeloma (2), lymphoma (2), sarcoma (1), and acute lymphocytic leukemia (1) were included. Most participants (86%) were women with breast cancer. Nine studies compared LD with conventional doxorubicin and three with epirubicin. Overall, the risk of bias was classified as "some concerns". Follow-up ranged from 24-72 months - the median follow-up time among the studies was 37 months. There was a reduction in heart failure (HF) incidence in the LD group compared to the control (RR 0.32, 95%CI 0.18-0.55). A significant decrease in left ventricular ejection fraction (LVEF), as defined by each study´s criteria, was less frequent in the LD group compared to other anthracycline-based therapies (RR 0.39, 95%CI 0.30-0.51). All-cause mortality (RR 0.98, 95%CI 0.90-1.07) and tumor response (RR 0.99, 95%CI 0.93-1.05) did not differ between the groups.

Conclusions: LD use was associated with a decrease in the occurrence of HF compared to other anthracycline-based therapies, with no worse cancer outcomes. A significant decrease in LVEF was also less frequent in the LD group; however, no difference was found in cardiovascular mortality.

Background: Treatment of breast cancer by chemotherapy or radiotherapy exposes the patient to the risk of cardiotoxicity, which can be assessed pre-therapeutically using scores such as the Heart Failure Association and International Cardio-Oncology Society (HFA-ICOS) score. We aimed to evaluate the risk of cardiotoxicity using the HFA-ICOS score in a group of Cameroonian women before treatment of breast cancer by chemotherapy and/or radiotherapy.

Methods: We conducted a cross-sectional analytic study using retrospective data collected from the Cardiology and Oncology departments at Yaounde Central Hospital and the Internal Medicine department at Yaounde General Hospital over an eight-year period, from 2017 to 2024, with a focus on the nine months from November 2023 to June 2024. Inclusion criteria consisted of patients with histologically confirmed breast cancer treated with chemotherapy and/or radiotherapy. We performed a multivariate analysis to determine the factors associated with moderate and high risk of cardiotoxicity, with a significance threshold of p ≤ 0.05.

Results: Of the 130 patients recruited, the median age was 46.5 years (interquartile range, IQR, 36.75-58.00), with extremes of 21 and 76 years. Comorbidities mainly were overweight/obesity in 92 (70.7%) cases and arterial hypertension in 32 (24.6%) cases. Invasive ductal carcinoma was the main histological type, accounting for 126 (96.9%) cases, and triple-negative carcinoma was the most frequent molecular subtype, comprising 55 (42.3%) cases. Treatment consisted of exclusive chemotherapy in 96 (73.8%) cases and radiotherapy associated with chemotherapy in 27 (20.8%) cases. Based on the HFA-ICOS score, the cardiotoxicity risk was low in 93 (71.5%) patients. The independent factors associated with the risk of moderate to severe cardiotoxicity were age ≥ 60 years (adjusted OR: 5.97; 95% CI 1.73-20.60; adjusted p = 0.005), obesity (adjusted OR: 5.81; 95% CI 1.78-18.91; p = 0.003) and hypertension (adjusted OR: 27.10; 95% CI 7.51-97.76; p < 0.001). Exclusive chemotherapy was a protective factor (adjusted OR: 0.24; 95% CI 0.07-0.81; adjusted p = 0.021).

Conclusion: Women with breast cancer in Cameroon tend to be relatively young and present a low risk of cardiotoxicity before starting anti-cancer treatment.

Background: Anthracycline-induced cardiomyopathy is a leading cause of morbidity and mortality in survivors of childhood cancer. The mitochondrion is a key mediator of the cytotoxic effects of anthracycline treatment and mitochondrial dysfunction is a hallmark of cardiomyopathy and heart failure. We sought to evaluate whether mitochondrial processes differ between anthracycline-exposed childhood cancer survivors who developed cardiomyopathy versus those who did not.

Methods: Peripheral blood was collected from 40 childhood cancer survivors who developed cardiomyopathy (cases) and 64 matched survivors who did not (controls). From these samples, gene expression was determined by RNA-Sequencing. Following bioinformatic processing, differential gene expression at the mRNA-level between cases and controls was determined. Human MitoCarta3.0, was utilized to determine if genes involved in mitochondrial processes were enriched for differential expression, and to identify differentially regulated mitochondrial pathways at the mRNA-level.

Results: 900 genes were identified as differentially expressed at the mRNA-level. The odds of a gene being differentially expressed were 2.43 times greater if it encodes for a protein that localizes to the mitochondria. Mitochondrial processes that were enriched for differentially expressed genes at the mRNA-level included electron transport chain complexes; reactive oxygen species metabolism; apoptosis, mitophagy, and autophagy; mitochondrial ribosome; mitochondrial transport and chaperones; and heme synthesis and processing. Additionally, we observed that a measure of pro-apoptotic balance (BAX to BCL-2 gene expression at the mRNA-level) was highest in severe cardiomyopathy, intermediate in mild cardiomyopathy, and lowest in survivors without cardiomyopathy.

Conclusions: We observed substantial evidence that the expression of genes involved in mitochondrial processes differs in childhood cancer survivors who develop cardiomyopathy versus those who do not.

Background: Early identification of cardiac involvement in oncology patients is critical but challenging. To date, no validated protocol integrates dedicated cardiac magnetic resonance imaging (CMR) within routine whole-body (WB) ¹⁸F-FDG PET/MRI examinations.

Objectives: This proof-of-concept study evaluated the feasibility and effectiveness of a novel hybrid imaging protocol combining CMR and WB ¹⁸F-FDG PET/MRI for oncology patients.

Methods: Fifteen patients with suspected or confirmed multiple myeloma (MM) were enrolled. All participants scheduled for oncologic ¹⁸F-FDG PET/MRI underwent an integrated protocol incorporating dedicated CMR sequences prior to WB PET/MRI. The CMR sequences included cine imaging, native T1 and T2 mapping, and feature-tracking to assess cardiac structure, function, and tissue characteristics. Feasibility, safety, and the prevalence of clinically relevant cardiac abnormalities were evaluated.

Results: The protocol was successfully completed in all participants without adverse events, enabling comprehensive cardiac and oncologic assessment within an average procedure time of 115 min (cumulative scanning time 65.5 ± 9.8 min). Clinically relevant cardiac abnormalities were identified in 4 patients (27%), including reduced left ventricular ejection fraction, concentric hypertrophy, and increased myocardial ¹⁸F-FDG uptake.

Conclusions: This study demonstrates the feasibility of a novel, time-efficient, integrated ¹⁸F-FDG PET/MRI protocol combining oncologic staging with comprehensive cardiac assessment in a single examination. This approach serves as an ideal strategy for cardio-oncology, bridging the gap between cancer treatment and cardiac care.

Introduction: Cardiovascular disease (CVD) and cancer are the two leading causes of death in the US. Preclinical models support a direct effect of cardiovascular disease (CVD) on accelerated cancer growth and spread. Our objective is to test the hypothesis that individuals with prevalent CVD are at an increased risk of presenting with more advanced prostate cancer at diagnosis.

Methods: We conducted a case-control study in the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked databases from 2010-2019. The analysis was undertaken from October 2024 to February 2025. We included male individuals aged ≥ 67 years diagnosed with invasive prostate cancer with at least two healthcare interactions and evidence of PSA screening in the 3 to 24 months prior to cancer diagnosis. Our exposure of interest was CVD in the 3 to 24 months prior to cancer diagnosis. Our a priori hypothesis tested the odds of prevalent CVD in patients with localized (T1-2 and N0 and M0) versus advanced (T3-4 or N + or M +) prostate cancer at diagnosis.

Results: Our analysis included 12,120 matched individuals, with median age 75 years (interquartile range 71-80), of which 88% were white, 8% were black, and 59% had prevalent CVD. Multivariable adjusted models demonstrated that individuals with advanced prostate cancer at diagnosis had a statistically significant 10% increased odds of prevalent CVD (OR, 1.10; 95% CI, 1.00-1.22; p = 0.047). This finding was strongest when examining individuals with regional or distant spread at diagnosis (N + or M + ; OR, 1.19; 95% CI, 1.05-1.34; p = 0.006). Further, individuals with Gleason score ≥ 8 disease at diagnosis, had an increased odds of prevalent CVD (OR, 1.07; 95% CI, 1.01-1.13; p = 0.020).

Conclusion: We demonstrate an association between prevalent CVD and advanced prostate cancer at diagnosis. Our results may help guide patients regarding personalized screening decisions, given current guidelines recommending shared decision-making, and can be used to facilitate targeted screening approaches.

Background: Immune checkpoint inhibitors (ICIs) have become the standard for treating various cancers. Nevertheless, their use may lead to significant cardiovascular immune-related adverse events (CV irAEs).

Objectives: We aimed to assess whether pre-treatment coronary artery calcium (CAC) deposition predicts CV irAEs in patients treated with ICIs.

Methods: A retrospective single-center cohort of patients treated with ICIs who performed pre-treatment chest computed tomography. A visual CAC assessment was categorized into Positive or Negative calcium deposits. Patients with pre-existing ischemic heart disease were excluded. The primary endpoint was the composite CV irAEs, including myocarditis, acute coronary syndrome, heart failure, and arrhythmias, and the secondary endpoint was all-cause mortality.

Results: The cohort included 240 patients with a median age of 67 (IQR 59-73) years and 47% female. The most prevalent type of cancer was lung cancer (36%), and the prominent ICIs was pembrolizumab (54%). Patients with Positive CAC (38%) were predominantly male, with higher rates of cardiovascular comorbidities. The primary outcome occurred in 36 cases (15%) at a median of 94 (IQR 48-338) days from the first ICIs dose. The Positive CAC group observed a non-significant trend toward a higher hazard for CV irAEs (HR 1.66, 95% CI 0.86-3.21, p = 0.13), with no significant difference in all-cause mortality (HR 1.15, 95% CI 0.88-1.51, p = 0.30).

Conclusion: Pre-treatment CAC deposition did not demonstrate an independent predictive role in assessing the risk of CV irAEs and all-cause mortality in patients treated with ICIs.

Background: Cancer therapy-related cardiac dysfunction (CTRCD) is recognized complication of antineoplastic therapies, and is particularly associated with anthracyclines. Treatment revolves around heart failure management, with limited evidence for other medications. Specifically, the aim of this study is to evaluate the role of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in patients with CTRCD.

Methods: All adult cancer patients with a diagnosis of anthracycline induced CTRCD between 2012 and 2022 were retrieved from the TriNetX Research Network. Baseline characteristics, oncology data, and laboratory parameters were also abstracted. Patients were grouped based on administration of GLP-1RAs, with the development of a propensity matched non-GLP-1RA treatment cohort. Clinical outcomes were compared between the cohorts including all-cause mortality, all cause hospitalizations, acute heart failure events, acute renal failure, new atrial fibrillation, and cardiac arrest.

Results: Overall, 2282 cancer patients with CTRCD were identified. Following propensity matching, a control cohort of 201 patients who did not receive GLP-1RAs were compared to 201 patients receiving GLP-1RAs. Over a mean follow-up of 295.4 ± 109.6 days, patients receiving GLP-1RAs treatment had significantly lower risk of all-cause hospitalization (HR 0.617, 95% CI 0.474-0.803, p < 0.001), acute heart failure events (HR 0.612, 95% CI 0.428-0.875, p = 0.007), and acute renal failure (HR 0.577, 95% CI 0.408-0.815, p = 0.002). There were no significant differences in the risk of all-cause mortality, atrial fibrillation, or cardiac arrest.

Conclusion: In cancer patients with anthracycline induced CTRCD, those treated with GLP-1RAs had significantly lower risk of adverse clinical outcomes.

Background: Fruquintinib is a highly selective tyrosine kinase inhibitor that targets vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, which play a critical role in angiogenesis and tumor growth. As a novel anti-angiogenic agent, Fruquintinib has demonstrated promising efficacy in the treatment of various advanced malignancies, including metastatic colorectal cancer. However, concerns about its cardiovascular safety have emerged, given that VEGFR inhibition is often associated with cardiovascular adverse events.

Methodology: We conducted a systematic search through PubMed, Scopus, Embase, and Web of Science to identify randomized controlled trials and cohort studies that assessed the safety of Fruquintinib compared with placebo in patients with metastatic colorectal and other cancers. The evaluated outcomes included hypertension, coronary artery disease, cerebrovascular accidents, peripheral artery disease, heart failure, thromboembolism, arrhythmias, aortic dissection, and superior vena cava syndrome. Two independent reviewers screened the titles/abstracts based on predefined inclusion and exclusion criteria, followed by a full-text review of potentially relevant studies. Any disagreements between the reviewers were resolved through consultation with a third reviewer to ensure the accuracy and consistency of the study selection.

Results: Fifteen reports were included in our study. Out of 3832 patients taking Fruquintinib monotherapy, a total of 997 developed hypertension with a pooled estimate incidence of 0.329 (95% CI: 0.248, 0.410; P < 0.001). In comparison to placebo, Fruquintinib was associated with significantly higher odds of developing hypertension (OR: 6.856; 95% CI: 5.071, 9.268; P < 0.001). Compared to Regorafenib, Fruquintinib demonstrated an OR of 1.549 (95% CI: 0.804, 2.983; P = 0.191) for the development of hypertension. Additionally, patients taking Fruquintinib had a pooled estimate incidence of 0.041 (95% CI: 0.021, 0.060, P < 0.001) for thromboembolism development with an OR of 2.092 (95% CI: 0.813, 5.385; P = 0.126) compared to placebo. Other reported cardiovascular side effects included sinus tachycardia, superior vena cava syndrome, peripheral edema, heart failure, myocardial enzymes elevation, and vascular access complications.

Conclusion: Our study found that Fruquintinib is associated with significant cardiovascular risks, with hypertension being the most common adverse event, while thromboembolism did not reach statistical significance. Therefore, close monitoring for treatment-related cardiovascular events should be considered in these patients.