The role of thrombin and antithrombin-therapy in interventional cardiology

Thrombin and thrombus. The plasma coagulation system is activated in response to vascular injury and, within several minutes, thrombin is generated by a series of linked proteolytic reactions that take place on cell surfaces. These reactions are balanced by naturally occurring inhibitory and procoagulant molecules. Thrombin has three major actions which are it's powerfull stimulus for platelet aggregation and activation; fibrinogen conversion to insoluble fibrin strands in the final common pathway for strengthening of the platelet plug; and it can activate factor XIII which leads to crosslinking and stabilisation of the fibrin clot. In addition, thrombin regulates many postthrombotic cellular events like chemoattraction of inflammatory cells and growth regulation of endothelial and vascular cells. Thus, thrombin is involved in both acute coronary occlusion and late restenosis following coronary angioplasty. Although the haemostatic system has evolved to minimise blood loss from injured vessels, there is little actual difference between the physiological process of normal haemostasis and the pathological events leading to coronary thrombosis and related events. Because of this similarity, thrombosis has been described as haemostasis occurring in the wrong place at the wrong time. The triggering event is the interaction of normal blood components with the abnormal vessel wall surface as in a diseased and atherosclerotic vessel or after successful coronary angioplasty. Antithrombotic therapy Antithrombotic therapy has changed little during the past few decades. Despite their limitations aspirin, heparin and warfarin have been the mainstays in the treatment of the majority of cardiovascular and cerebrovascular thrombotic diseases.

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