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Thrombin, Inflammation, and Cardiovascular Disease: Atherosclerosis, Thrombosis, and Inflammation

Thrombin, Inflammation, and Cardiovascular Disease: Atherosclerosis, Thrombosis, and InflammationThere Is a Complex Interplay Among Atherosclerosis, Thrombosis, and Inflammation
Atherosclerotic coronary heart disease commonly manifests itself clinically via a thrombotic event: so-called “atherothrombosis,” especially in younger men. As mentioned above, this has been clearly understood only since the early 1970s. As an overview, the process of blood clotting is comprised of coagulation, limited and controlled by anticoagulation; and the counterbalancing process of fibrinolysis, limited and controlled by antifibrinolysis. more
It has been known for a long time that increases or decreases in specific factor levels are associated with risk of venous clotting or bleeding. For example, the lack of factor VIII or factor IX leads to hemophilia A or B, and deficiency of the anticoagulant factor protein C leads to a propensity to form clots, such as occurs in deep vein thrombosis. Because of this knowledge, and the knowledge that blood clots are important in the risk of MI, researchers in the early 1980s pursued the importance of specific factor levels in atherothrombotic risk. Meade and colleagues pioneered this work in the Northwick Park Heart Study, and demonstrated the clear importance of fibrinogen as a CVD risk factor. This research was quickly confirmed and extended by others, and it became clear that fibrinogen, factor VIII, and several other proteins found in abundance in plasma were risk factors, at least in part, because they reflected chronic, low-level inflammation. Said another way, the specific factors that were elevated in the presence of clinical CVD, and whose levels in otherwise healthy people predicted the occurrence of future CVD, were in general known as acute-phase reactants, ie, proteins known to respond to inflammatory stimulation via the effects of proinflammatory cytokines, such as interleukin (IL)-6.