Table 1.

Effects of inflammation on thrombosis–haemostasis

1	Inflammatory cytokines modulate the haemostatic properties of the endothelium
2	Local effects of inflammatory cells on digestion of the fibrous cap lead to plaque disruption and thrombus formation
3	Inflammation can affect systemic haemostatic activity by IL-6 mediated stimulation of hepatocytes to produce acute phase reactants (coagulation factors, PAI-1)
4	Enhanced CD40L-CD40 interaction promotes thrombotic activity by enhancing tissue factor expression in macrophages and through the direct regulation of endothelial procoagulant activity
5	Activated platelets may mediate the homing of leucocytes by interaction with the subendothelial matrix under shear stresses
6	Oxidised 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
7	Acute 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)

IL, interleukin; LDL, low density lipoprotein; PAI, plasminogen activator inhibitor.