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Blood markers of cardiovascular disease.

The use of blood markers to indicate the coagulation status of the cardiovascular system has been advocated by a number of authors. Measuring such coagulation fragments has been proposed as a method of assessing the thrombotic state of an individual since during systemic or even local coagulation and lysis a number of fragments are generated. The value of such measurements depends on the various fragments being detected accurately in peripheral blood samples, taking into account other factors such as age or changes in renal function that could lead to misinterpretation of results. During normal haemostatic mechanisms thrombin initiates fibrin formation and at the same time promotes destruction of the same fibrin. Thus, tissue plasminogen activator, the main activator of the fibrinolytic system, is bound in with fibrin as are inhibitors of the fibrinolytic system such as plasminogen activator inhibitor-1. The combination of bound tissue plasminogen activator and plasminogen to fibrin generates plasmin. The balance between fibrin generation and the influence of bound lytic factors will determine whether or not the fibrin will contribute to thrombus formation, and any clinical sequelae, or whether it is degraded to fibrin degradation products. An activated fibrinolytic system protects against further thrombin generation through the activity of components such as fibrin degradation products and formed activated protein C. There are various markers of thrombin generation. The effect of factor Xa on prothrombin and the conversion of prothrombin to thrombin generates prothrombin fragments (F1+2). Plasma levels of F1+2 reflect the enzymatic activity of Factor Xa on prothrombin, and thus thrombin generation. The formation of thrombin with its natural inhibitor antithrombin III (TAT complex) can also be used as a measure of thrombin generation. In the process of converting fibrinogen into fibrin monomers,