Early Clinical Considerations Basic Science Rationale

The vast majority of acute strokes are ischemic in nature. Either an embolus or an in situ thrombosis causes a cessation of blood flow, which triggers multiple pathways that cause ischemia and eventual cell death—events of a cascade that occurs in a time-dependent fashion. At the time of clinical significance, a core of tissue is already infarcted. However, surrounding tissue, called the ischemic penumbra, is at risk for future infarction. If blood flow is not restored to this vascular territory, the area of the ischemic penumbra will also become infarcted. Research thus far has mainly focused on investigating methods of reperfusing this "at-risk tissue" as quickly as possible, while decreasing the risk of hemorrhage transformation. Thus, significant emphasis has been placed on understanding the coagulation pathway and intervening in it as a strategy for improving early poststroke reperfusion. In short, vascular injury initiates the extrinsic pathway, which, along with the intrinsic pathway, activates factor X, eventually leading to thrombin activation, which, in turn, stimulates fibrin-clot formation and platelet aggregation (Fig. 1).

Physiologic dissolution of a fibrin clot is mediated by the activation of the circulating and fibrin-bound zymogen plasminogen to the active serine protease plasmin. The manipulation of this natural, fibrinolytic pathway is at the core of current acute stroke care. The traditional thrombolytics that have been used in acute stroke research (rtPA, streptokinase, and urokinase) work by potentiating conversion of plasminogen to plasmin.

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