(Circulation. 2003;107:1556.)
© 2003 American Heart Association, Inc.
Special Review |
From the Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to A. Michael Lincoff, MD, Associate Professor of Medicine, Department of Cardiovascular Medicine, Desk F25, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail LincofA@ccf.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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The processes leading to adverse prognosis after revascularization in diabetics are likely multifactorial and relate to widespread atheroma, small vessel vasculopathy, impaired collateral formation, exuberant neointimal hyperplasia, and adverse remodeling.10,11 There is also evidence that hypercoagulability contributes to accelerated atherosclerosis and exaggerated injury response after revascularization in diabetics.1113 Diabetes is associated with increased levels of circulating fibrinogen, thrombin, and factor VII, and with diminished plasma fibrinolytic and antithrombin III activity. Moreover, platelets in diabetic patients are increased in size, are more frequently activated, and exhibit greater adhesiveness, thromboxane synthesis, glycoprotein (GP) IIb/IIIa expression, and mitogenic activity.
| Glycoprotein IIb/IIIa Inhibitors and Diabetes |
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