Figure 4.

Intrinsic and extrinsic coagulation pathways, platelet activation, adhesion and aggregation, in both healthy and diseased states

Activation of both the intrinsic and extrinsic coagulation pathways drives prothrombin activation, in turn up-regulating thrombin-dependent conversion of fibrinogen into fibrin, promoting platelet activation. This platelet activation causes platelet plug formation and a localised inflammatory response under normal pathological conditions, which cause collagen deposition and wound repair. In a diseased state like that seen in COPD, this process becomes dysregulated, driving platelet hyperactivation, exaggerated inflammatory responses, collagen deposition and immune cell activation, all of which are contributing factors of atherosclerotic lesion formation, vascular dysfunction and plaque instability that can ultimately lead to myocardial infarction, cerebral artery occlusion (stroke) and death.