Venous thromboembolism (VTE) and arterial thrombosis (AT) are distinct yet closely related pathological processes. While traditionally considered separate entities, accumulating evidence suggests that they share common risk factors, such as inflammation and endothelial dysfunction (ED). This review explores the parallels and differences between venous and arterial thrombosis, with particular attention to the role of unprovoked VTE and its potential links to atherosclerosis and systemic inflammation.
View Article and Find Full Text PDFThe study of endothelial dysfunction (ED) is crucial to identify the pathogenetic mechanism(s) and provide indications for patient management in cardiovascular diseases. It is currently hindered by the limited availability of patient-specific primary endothelial cells (ECs). Endothelial colony-forming cells (ECFCs) represent an optimal non-invasive tool to overcome this issue.
View Article and Find Full Text PDFCancer is one the most prevalent risk factors in patients diagnosed with deep vein thrombosis or pulmonary embolism. Patients with cancer and venous thromboembolism have a higher risk of mortality when compared to patients with cancer without venous thromboembolism and a higher risk of recurrent thrombosis when compared with patients with venous thromboembolism without cancer. This increased risk of recurrence is not only observed after anticoagulant treatment is stopped, but also during anticoagulant treatment.
View Article and Find Full Text PDFFor the detection of unwanted outcomes of new interventions, physicians rely on adverse event reporting. We attempt to quantify the reported incidence of venous thromboembolism (VTE) and arterial thrombosis (AT) in randomized clinical trials (RCTs), and evaluate the extent of under-reporting. We selected all therapeutic RCTs published in the four highest-impact general medicine journals between January 2011 and July 2011.
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