Blood coagulation and the risk of atherothrombosis: a complex relationship.
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Discussion
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Implication
Mechanistic review reveals how inflammation overwhelms natural anticoagulant defenses in advancing atherosclerosis, highlighting hypercoagulability as a critical driver of arterial thrombosis.
Key Points
- To delineate the dynamic role of blood coagulation across the successive stages of atherosclerosis and its direct contribution to atherothrombotic risk.
- Reviewed pathophysiological mechanisms linking Virchow's triad, vascular wall damage, and blood composition changes to atherothrombosis.
- Synthesized molecular and clinical evidence contrasting early plaque development with advanced, inflammation-driven atherothrombotic disease.
- In early atherosclerosis, coagulation maintains a predominantly anticoagulant role as thrombin activates protein C via endothelial thrombomodulin.
- In advanced atherosclerosis, interleukin-6 and elevated C-reactive protein downregulate thrombomodulin and endothelial protein C receptors while upregulating tissue factor.
- Persistent inflammatory stimulation maintains continuous thrombin and fibrin formation, establishing systemic hypercoagulability marked by elevated D-dimer fragments.
Cite This Study
Spronk et al. (2004) studied this question.