Evidence regarding venous thromboembolism (VTE) risk in palliative care populations remains scarce, and current thromboprophylaxis recommendations are largely extrapolated from non-palliative oncology cohorts. This study aimed to determine the 90-day incidence of VTE and associated clinical risk factors in hospitalized patients with advanced cancer receiving palliative care. This multicenter retrospective cohort study included adults with advanced cancer enrolled in a palliative care program who were hospitalized between 2018 and 2024 at two tertiary care centers in Bogotá, Colombia. VTE incidence was calculated, and clinical risk factors were identified using multivariable Cox proportional hazards models. A total of 782 patients were included (mean age 61 years; 58.7
Atrial fibrillation (AF) is the most common arrhythmia in adults and significantly increases the risk of stroke. Due to common threats like systemic inflammation and treatment-related cardiotoxicity, individuals with cancer have a noticeably increased chance of developing AF. Managing AF in this population presents dual challenges: reducing thromboembolic risk while minimizing bleeding complications. Traditionally, warfarin, a vitamin K antagonist, has been the most widely used anticoagulant. However, the emergence of direct oral anticoagulants (DOACs), which offer equal or superior efficacy compared to warfarin with fewer dietary and drug interactions, has shifted clinical practice. This narrative review explores the complex clinical relationship between AF, anticoagulation, and bleeding as a potential early indicator of occult cancer. An expanding body of evidence from extensive cohort studies and meta-analyses supports this association, showing a significantly increased risk of gastrointestinal, genitourinary, respiratory, and, to a lesser extent, intracranial bleeding in anticoagulated patients that may precede cancer diagnosis. Although bleeding is a recognized difficulty of oral anticoagulation, it may expose occult malignancy, resulting in timely detection of cancer and more favorable outcomes. Perhaps it is time to regard occult gastrointestinal bleeding for what it may be: an early warning sign of malignancy. The increased risk of both thromboembolism and bleeding in cancer patients poses a challenge in clinical practice. Though bleeding has increasingly been recognized as a potential harbinger of occult cancer, uniform guidelines for malignant lesion screening after a hemorrhagic episode remain to be established. It is essential to establish a solid, evidence-based therapeutic protocol to achieve the best possible treatment and results for patients.
Catheter-related thrombosis (CRT) is a clinically relevant complication in patients with malignancy receiving central venous access devices, but early individualized risk assessment remains limited. This study developed and internally validated a prediction model incorporating D-dimer, platelet count, and albumin for estimating 30-day CRT risk after catheter placement. This single-center retrospective cohort study included hospitalized adult patients with malignancy who underwent peripherally inserted central catheter (PICC), central venous catheter (CVC), or implantable venous access port (PORT) placement between January 2018 and December 2025. The primary outcome was imaging-confirmed CRT within 30 days after catheter insertion, including both symptomatic events and incidentally detected asymptomatic thrombosis. Core laboratory predictors included log-transformed D-dimer, platelet count, and albumin. Non-core clinical, tumor-related, and catheter-related predictors were selected using least absolute shrinkage and selection operator regression. A multivariable logistic regression model was developed, internally validated using 1,000 bootstrap resamples, and evaluated by discrimination, calibration, decision curve analysis, risk stratification, and sensitivity analyses. Among 1,876 eligible patients, 145 developed 30-day CRT, corresponding to an incidence of 7.73
In patients with acute pulmonary embolism (PE), hypoxia may increase pulmonary vascular resistance and worsen right ventricular dysfunction (RVD), which is a key prognostic factor. However, associations between hypoxia, RVD and clinical outcomes have not been well described. To describe associations between hypoxia, RVD and clinical outcomes in patients with PE. We performed a retrospective, single-center cohort study of patients treated by the Massachusetts General Hospital Pulmonary Embolism Response Team (PERT) from 10/2012 to 08/2021. Inclusion criteria included confirmed PE, recorded oxygen saturation prior to PERT activation, and echocardiogram within three days of PERT activation. Patients were categorized into four subgroups based on (1) hypoxia status (SaO₂ below vs. above 95
Deep vein thrombosis (DVT), a prevalent vascular disease, frequently manifests in conjunction with post-thrombotic syndrome (PTS), a condition that can markedly compromise prognoses. The objective of this study is to investigate the internal mechanisms and pathways associated with DVT recanalization, with a view to establishing a foundation for the development of relevant drug targets. The SD rat inferior vena cava (IVC) ligation model was constructed, and thrombus (n = 3) and normal IVC tissues (n = 3) were obtained for standard single-cell RNA sequencing (scRNA-seq) analysis. The aim was to characterise the DVT-associated single-cell transcriptional profiles and localise key cellular subpopulations. In combination with lentiviral knockdown/overexpression (KD/OE) assays, the present study explored the functional regulatory role of caveolin-1 (CAV-1) on target cells and the corresponding key signalling pathways, and illustrated its biological effects on DVT at the animal model level. Based on the analysis of the scRNA-seq standard process, the heterogeneity of each cell population related to the DVT microenvironment was demonstrated after cell dimensionality reduction, population size and annotation, and neutrophils and fibroblasts were the most obvious. In addition, it was speculated that the presence of endothelial progenitor cells (EPCs) in DVT plays a regulatory role through subpopulation annotation, cell communication analysis and pseudotime analysis. Through multi-angle experiments of cell counting kit-8 (CCK-8), flow cytometry, immunofluorescence (IF) and transwell assay proved that up-regulation of CAV-1 can promote EPC proliferation and migration ability. Subsequently, the utilisation of animal models was employed to demonstrate that up-regulation of CAV-1 promotes angiogenesis and enhances EPC survival. Furthermore, the PI3K-AKT signalling pathway was discovered and validated as a key pathway in the aforementioned process. Furthermore, the spatial transcriptome provided further evidence for alterations in CAV-1 levels and key inflammatory pathways. The combination of scRNA-seq and functional experiments has led to the proposal that CAV-1 is a regulator of EPC function associated with PI3K/AKT signalling and DVT recanalization.
