(Circulation. 2008;118:6-8.)
© 2008 American Heart Association, Inc.
Editorial |
From the Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass.
Reprint requests to C. Michael Gibson, MS, MD, 350 Longwood Ave, First Floor, Boston, MA 02115. E-mail mgibson@perfuse.org
Key Words: Editorials angioplasty microcirculation myocardial infarction
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Article p 49
There have been efforts to identify mechanical and pharmacological strategies to improve myocardial perfusion after primary PCI. Compared with the systemic administration of intravenous pharmacotherapies, highly localized administration of intracoronary pharmacotherapy may be associated with a several-hundred-fold increase in the local concentration of an agent in the epicardial artery and microcirculation. A number of pharmacotherapies, including adenosine,5,6 calcium channel blockers,7
-blockers,8 β2-receptor activators,9 other vasodilators, antithrombotics,10,11 and antiplatelet agents,12–14 have been used to treat microvascular dysfunction.
There are tens of thousands of glycoprotein IIb/IIIa (GPIIb/IIIa) receptors on the platelet surface.15 Platelet receptor occupancy studies have demonstrated that if there are fewer GPIIb/IIIa receptors free and available for cross-linking with fibrinogen, then myocardial perfusion is improved.16 To estimate the number of GPIIb/IIIa receptors available for cross-linking, the absolute platelet count has been multiplied by the percent of receptors available to cross link to calculate an index of the absolute number of GPIIb/IIIa receptors available. The absolute number of GPIIb/IIIa receptors available for cross-linking is reduced
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