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Stroke. 2003;34:230-231
Published online before print December 19, 2002, doi: 10.1161/01.STR.0000047036.77466.E8
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(Stroke. 2003;34:230.)
© 2003 American Heart Association, Inc.


Controversies in Stroke

Resolved: Heparin May Be Useful in Selected Patients With Brain Ischemia

Louis R. Caplan, MD

From the Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Mass.

Correspondence to Louis R. Caplan, Beth Israel Deaconess Medical Center, Dept of Neurology, Dana 779, 330 Brookline Ave, Boston, MA 02215-5400. E-mail lcaplan@caregroup.harvard.edu


Key Words: heparin • ischemia • stroke, ischemic • thrombi


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Theoretical Utility of Heparins

Heparin reduces development of erythrocyte-fibrin thrombi that form in regions of vascular stasis especially within the heart, in severely stenosed arteries sometimes engrafted on white thrombi, in acute arterial occlusions as fresh tails on existing thrombi, and within extremity and pelvic veins. Unfortunately, heparin use can be associated with severe bleeding, especially if not closely monitored.

Optimal Testing of Heparin Effectiveness and Safety

Heparin should not be indiscriminately used in all brain ischemia patients. Bleeding complications will outweigh therapeutic benefit. Unfortunately, randomized trials have not adequately studied heparins in patients with conditions likely to respond to treatment. Reported trials lumped patients with brain ischemia together without diagnostic investigations defining etiology, stroke subtypes, or vascular lesions.

Worsening and new neurologic deficits can develop when thrombi form, propagate, and embolize. Stroke worsening, even when thrombi are present, occurs in only 20% to 33% of ischemic strokes. Even when anticoagulants are stopped because of hemorrhage in prosthetic heart valve patients, recurrent embolism rarely occurred during the next 10 days.1 Most cardioembolic recurrences do not occur during the first week after an embolus.2 Worsening in patients with atherothrombotic large artery occlusive disease is due to perfusion failure often unrelated to changes in occlusive thrombi.3 Randomized trials to effectively determine heparin utility must be (1) eclectic and include only patients in whom brain and cardiac and vascular imaging show high-risk cardiac and artery-to-artery embolic brain infarcts and in patients with documented severe extracranial or intracranial large artery occlusive disease; (2) powered to account for clinical worsening and/or new brain infarcts in less . . . [Full Text of this Article]




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