Thrombotic Mechanisms in Heart Failure
Summary
Heart failure is increasingly recognised as a prothrombotic condition in which vascular stasis, endothelial dysfunction and hypercoagulability converge to promote clot formation. Neurohormonal activation in heart failure triggers endothelial injury and up-regulation of adhesion molecules, while platelet hyperreactivity and augmented coagulation factor expression further tip the balance towards thrombosis. At the microvascular level, emerging evidence points to neutrophil extracellular traps and platelet–leucocyte aggregates as key drivers of intramyocardial and pulmonary microthrombi, which impair tissue perfusion and contribute to decompensation. Clinically, patients with reduced ejection fraction or preserved function face heightened risk of venous thromboembolism, stroke and device-related thrombosis. Current therapeutic approaches employ anticoagulants to interrupt the coagulation cascade, yet bleeding risk remains a concern. Novel strategies targeting specific elements of the thromboinflammatory response seek to mitigate clot formation without compromising haemostasis.
Research from Nature Portfolio
Recent studies have illuminated the role of neutrophil extracellular traps in heart failure, demonstrating that these DNA-protein webs accumulate in the microvasculature and foster platelet adhesion, thereby exacerbating myocardial ischaemia. In parallel, inhibition of factor XIa in preclinical heart failure models has shown a marked reduction in thrombus formation with minimal impact on primary haemostasis, suggesting a therapeutic window for anticoagulation with lower bleeding risk. Advanced in vivo imaging of cardiac microcirculation has further revealed that transient microthrombi predict episodes of dyspnoea and fluid retention in patients with preserved ejection fraction, highlighting the prognostic value of microvascular thrombosis and guiding timing for targeted interventions.
Thrombotic Mechanisms in Heart Failure publication trend
The graph below shows the total number of articles in thrombotic mechanisms in heart failure across all publications each year (not limited to Nature Index journals).
Technical terms
Endothelial dysfunction: Impairment of the inner vascular lining that promotes procoagulant and proinflammatory changes.
Neutrophil extracellular traps (NETs): Web-like DNA and protein structures released by activated neutrophils that trap pathogens but also activate platelets and coagulation.
Virchow’s triad: The trio of stasis, endothelial injury and hypercoagulability that underpins thrombus formation.
Factor XIa: Activated form of coagulation factor XI, involved in amplification of thrombin generation.
Microvascular thrombosis: Formation of clots in small vessels, impairing local tissue perfusion.
Venous thromboembolism (VTE): Clots that originate in the venous circulation, including deep vein thrombosis and pulmonary embolism.
Fibrinolysis: The enzymatic breakdown of fibrin clots, primarily mediated by plasmin.
References
- Associations between blood coagulation markers, NT-proBNP and risk of incident heart failure in older men: The British Regional Heart Study. International Journal of Cardiology (2016).
- Reduced cardiac function and risk of venous thromboembolism in Asian countries. Thrombosis Journal (2017).
- The coagulation system changes in patients with chronic heart failure. Medicina (2010).
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