The analysis stressed the importance of adhering to the NINDS protocol. The results of an analysis of the NINDS data showed that individuals treated 0 to 90 minutes from stroke onset achieved a more favorable outcome at 3 months than patients treated later than 90 minutes ( 57). Although the rate of symptomatic intracerebral hemorrhage was significantly higher in patients treated with tPA (6.4% tPA, 0.6% placebo), the mortality rates were similar between the 2 groups.Īdditional evidence suggested earlier treatment within the 3-hour window is more effective than delayed therapy. The benefit of tPA was shown across all ischemic stroke subtypes and was not affected by age, sex, or ethnicity. The study was a randomized, multicenter, placebo-controlled trial. #PRE ACTIVATION PRETTY GOOD SOLITAIRE 19.2 TRIAL#Data obtained from the National Institute of Neurological Disorders and Stroke (NINDS) trial demonstrated that tPA given within 3 hours of stroke onset improved the functional outcome at 3 months ( 79). #PRE ACTIVATION PRETTY GOOD SOLITAIRE 19.2 ACTIVATOR#At present, tissue plasminogen activator is the only drug approved for use in the treatment of acute ischemic stroke by the United States Food and Drug Administration. The recanalization rate is dependent on a variety of factors, including the age, composition, and size of the thrombus, as well as the site of occlusion. The dissolution of the thrombus is largely mediated by fibrinolysis localized within the thrombus and degradation of fibrin by plasmin. The size and duration of the penumbra are unknown for any individual patient. Prompt restoration of adequate blood flow to this area may prevent further injury and diminish the degree of subsequent neurologic dysfunction. This region has been referred to as the ischemic penumbra ( 09). With the disruption in blood flow, an ischemic core is produced surrounded by a region of potentially viable tissue. There is a brief period of time when the injury is completely reversible if adequate blood flow is restored after prolonged ischemia, though, the injury becomes permanent, and no intervention will produce recovery. Permanent focal damage begins within several minutes after a significant reduction in cerebral blood flow and is complete within approximately 6 hours. There is a finite amount of time available before ischemia produces an irreversible injury. #PRE ACTIVATION PRETTY GOOD SOLITAIRE 19.2 FREE#Other factors may play a role in the severity of the injury produced, including the inflammatory response, the breakdown of the blood-brain barrier, and release of free radicals. The disturbance in blood flow reduces the availability of nutrients leading to the production of acidic end products and, ultimately, the reduction in intracellular pH. #PRE ACTIVATION PRETTY GOOD SOLITAIRE 19.2 SERIES#The infarction of brain tissue is the result of a series of pathophysiologic events. Such results set the stage for further investigation into the efficacy of thrombolysis in acute ischemic stroke. Data from another study demonstrated the successful recanalization of occluded middle cerebral arteries in primates using intra-arterial urokinase ( 22). One study demonstrated significant improvement in the neurologic function of rabbits treated with intravenous tPA after small blood clots were injected into the carotid circulation ( 84). The enthusiasm over the use of thrombolytic agents in acute stroke was renewed with the publication of certain animal stroke experiments. In the early clinical trials, treatment with agents such as streptokinase and urokinase resulted in a high rate of intracerebral hemorrhage without any significant clinical benefit. The early attempts were unsuccessful for a variety of reasons, including lack of CT imaging that invariably led to the treatment of patients with intracerebral hemorrhage. The first use of thrombolytic agents for acute stroke occurred in the late 1950s. The basic mechanism of action entails converting plasminogen into plasmin, resulting in the degradation of fibrin and subsequent recanalization of the vessel. The goal of thrombolytic treatment is to promote the dissolution of thrombus and restore blood flow. By identifying patients at high risk and initiating appropriate therapy, up to 80% of strokes can be prevented.īecause most acute ischemic strokes are caused by a thromboembolic occlusion of an intracranial artery ( 29), the use of thrombolytic agents was a natural choice for acute therapy. In addition to acute therapeutic interventions, a number of medical and surgical strategies have been devised to prevent the occurrence of stroke. Acute ischemic stroke is now categorized as an emergency and requires rapid assessment and intervention in order to reduce the degree of brain injury and subsequent functional impairment. Since the United States Food and Drug Administration approval of intravenous tissue plasminogen activator (tPA) for use in acute ischemic stroke in June 1996, the approach to stroke treatment has changed dramatically.
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