Table 1

Effects of inflammation on thrombosis–haemostasis

IL, interleukin; LDL, low density lipoprotein; PAI, plasminogen activator inhibitor.
1Inflammatory cytokines modulate the haemostatic properties of the endothelium
2Local effects of inflammatory cells on digestion of the fibrous cap lead to plaque disruption and thrombus formation
3Inflammation can affect systemic haemostatic activity by IL-6 mediated stimulation of hepatocytes to produce acute phase reactants (coagulation factors, PAI-1)
4Enhanced CD40L-CD40 interaction promotes thrombotic activity by enhancing tissue factor expression in macrophages and through the direct regulation of endothelial procoagulant activity
5Activated platelets may mediate the homing of leucocytes by interaction with the subendothelial matrix under shear stresses
6Oxidised LDL induces tissue factor expression in macrophages and decreases the anticoagulant activity of endothelium by interfering with thrombomodulin expression and inactivating tissue factor pathway inhibitor
7Acute phase reactants are associated with an increased risk of future cardiovascular events which are mediated by acute thrombosis (for example, C reactive protein, fibrinogen, factor VIII)