Intern Emerg Med. 2026 Oct 28. doi: 10.1007/s11739-026-04574-w. Online ahead of print.
ABSTRACT
Inflammation and coagulation are tightly interconnected host-defense systems that, when dysregulated, promote pathological thrombosis. This narrative review examines mechanisms, clinical settings, and therapeutic implications of thromboinflammation (TI) across venous, arterial, and microvascular thrombosis, with particular attention to the differences in clinical translation among vascular territories. Endothelial activation, tissue factor expression, platelet-leukocyte interactions, neutrophil extracellular traps, complement activation, inflammasome signalling, and impaired fibrinolysis converge to generate a procoagulant phenotype. These mechanisms modify Virchow's triad and contribute to venous, arterial, and microvascular thrombosis, although their relative importance varies across vascular territories. Clinically, TI is relevant in inflammatory bowel disease, rheumatologic and other immune-mediated disorders, sepsis, coronavirus disease 2019, clonal haematopoiesis, complement-mediated diseases, and atherosclerotic cardiovascular disease. TI offers a unifying framework for mechanistic risk assessment and therapeutic development. In atherothrombosis, randomised trials have demonstrated that selective modulation of inflammatory pathways, particularly the NLRP3-interleukin-1β-interleukin-6 axis and colchicine-sensitive pathways, can reduce recurrent cardiovascular events. By contrast, the role of inflammation-targeted therapies for primary or secondary prevention of VTE remains uncertain. Future studies should identify disease-specific biomarkers and test targeted anti-inflammatory or immunothrombotic strategies, alone or alongside anticoagulation, to prevent thrombosis without compromising haemostasis effectively.
PMID:42955694 | DOI:10.1007/s11739-026-04574-w