ABSTRACT
The mechanisms of thrombosis in the arterial system center on two phases: formation of a platelet-rich thrombus (platelet-dependent thrombosis), followed by thrombin activation leading to development of a fibrin deposition (fibrin-rich thrombus). Balancing forces include endogenous anticoagulant and fibrinolytic systems. Arterial hemostasis and thrombosis are initiated and principally mediated by platelet adhesion, activation, and aggregation. A secondary phase of thrombin and fibrin generation produces fibrin deposition into the thrombus, facilitated by the activated platelet phospholipid surface. Control of the propagation and extension of thrombosis is mediated to some extent by endogenous anticoagulants and by the fibrinolytic system. Many aspects of procoagulant, anticoagulant, and fibrinolytic mechanisms are altered in peripheral vascular disease. These derangements include heightened shear stresses due to stenotic vessels, leading to enhanced platelet adhesion and activation; increased tissue factor elaboration along damaged vessels, resulting in increased thrombin generation; and imbalances in the fibrinolytic system that limit the capacity to control thrombosis.
