THERE ARE only 2 proved indications for intravenous heparin in acute stroke: prevention of recurrent cardiac embolism and treatment of anxiety in the administering physician. Despite the lack of firm evidence for or against its use in other circumstances, heparin is still widely administered for plausible but unproved indications, such as progression of a neurologic deficit in acute stroke.
Much of the practice stems from the belief that neurologic deterioration results from clot growth and further arterial occlusion. Although about a third of stroke patients worsen after admission to hospital, most do so from the evolution of the initial cerebral lesion. Sandercock, a leader of the International Stroke Trial, interprets its results to mean that "there really is no evidence to support the use of [intravenous] heparin in any clinical indication in acute ischemic stroke." Grau and Hacke argue that the results of the International Stroke Trial with high-dose subcutaneous heparin, without monitoring of activated partial thromboplastin time or mandatory prior computed tomographic scan, cannot be used to rule out a therapeutic effect of heparin. Although Grau and Hacke make a case for the use of short-term heparin in proved or highly probable cardiac embolism, symptomatic intracranial stenoses, deficiency of protein S, protein C, or antithrombolin III, and high-grade symptomatic internal carotid artery stenoses until surgery, they reluctantly conclude that a further randomized trial is needed. Moreover, they make the intriguing suggestion that clinicians may be able to select patients with lower risk for cerebral hemorrhage, a hypothesis that could be tested in such a clinical trial.
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