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Circulation. 1996;93:1616-1617

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(Circulation. 1996;93:1616-1617.)
© 1996 American Heart Association, Inc.


Articles

Thrombolysis in Ischemic Stroke: Double or Quits?

J. van Gijn, MD, FRCPE

From the University Department of Neurology, Utrecht, Netherlands.

Correspondence to J. van Gijn, MD, FRCPE, University Department of Neurology, PO Box 85500, 3508 GA Utrecht, The Netherlands. E-mail j.vangijn@neuro.azu.nl.


*    Introduction
 
Thrombolytic therapy to open up blocked arteries has so far appealed less to physicians caring for patients with brain infarction than to those involved in the management of myocardial infarction. The skepticism has been sustained by some important differences in pathogenesis between the two conditions. First, whereas occlusion of coronary vessels is almost invariably superimposed on local atheroma and mural thrombosis, occlusion of large intracerebral arteries is most often caused (at least in whites) by embolism from proximal sites: the internal carotid artery,1 2 the heart,3 or the aorta.4 Spontaneous recanalization is common, to judge by the difficulty in demonstrating intracranial occlusions unless angiography or transcranial ultrasound is done within 6 hours (at which time 60% to 75% of patients have impaired flow).5 6 Second, neurons are highly vulnerable to ischemia; animal experiments may have demonstrated an "ischemic penumbra" of salvageable tissue around a dense core of irreversible necrosis, but it remains uncertain whether in human disease such rescue operations are feasible or at all rewarding in terms of preserved function. Last, sudden reperfusion of necrotic brain tissue may lead to brain swelling with herniation,7 to hemorrhagic infarction, or sometimes to hemorrhage far exceeding the borders of the original infarct. Fatal hemorrhages may even complicate cerebral infarction without thrombolysis8 or thrombolysis without cerebral infarction.9 10

Of course, the proof of the pudding is in the eating—ie, clinical trials. After all, plausible treatments have proved to be ineffective or even harmful (and vice versa). Until early 1995, the collective evidence was limited to 899 . . . [Full Text of this Article]




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E. J. Topol and J. S. Yadav
Recognition of the Importance of Embolization in Atherosclerotic Vascular Disease
Circulation, February 8, 2000; 101(5): 570 - 580.
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