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(Stroke. 2004;35:2604.)
© 2004 American Heart Association, Inc.

Emerging Therapies

Thoughts Evoked by MATCH and Other Trials

From the Beth Israel Deaconess Medical Center, Boston, Mass.

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

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

Are Two "Antiplatelet" Drugs Better Than One?

Many different processes are involved in platelet activation. Most drugs affect one of these chemical reactions. Theoretically, platelet functions (secretion, aggregation, and adhesion) can be reduced most effectively by using >1 agent or by inhibiting the final step in the attachment of the platelet to fibrin at the level of the glycoprotein IIb/IIIa (GpIIb/IIIa) receptor. Preliminary experience with oral and intravenous GpIIb/IIIa inhibitors has shown that bleeding is an important problem. In MATCH, 2 platelet function inhibitors, clopidogrel and aspirin, did prevent slightly more strokes (but not with statistical significance) but at the price of significantly more excess bleeding. Killing platelets causes bleeding.

What About the Endothelium Platelet Attachment to the Endothelium?

Platelets seem to swim happily in the blood until they reach an area of irregular or damaged endothelium, for example, on the surface of an ulcerated atherosclerotic plaque in a large artery. They then stick to that irregular surface and to each other in an attempt to heal the vascular irregularity. The white platelet–fibrin thrombus can break loose and embolize. The platelet plug also activates the coagulation cascade, promoting the formation of a red erythrocyte–fibrin-rich clot. Perhaps rather than killing the platelet, it might be better to inhibit platelet attachment to the endothelium. Antiplatelet drugs might do this but have not been tested thoroughly for their effect on endothelial–platelet interaction.

Does the Underlying Cardiac-Cervico-Cranial Arterial-Hematological Cause of Brain Ischemia Matter in Trials of Antiplatelet Agents?

Theoretically, antiplatelet agents should work by inhibiting formation of white clots. These tend to form on irregular endothelial surfaces of the cardiac and valvular endocardium and on the endothelial surfaces of the aorta and large neck and . . . [Full Text of this Article]

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