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Circulation. 2003;107:1556-1559
doi: 10.1161/01.CIR.0000055653.52489.E9
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(Circulation. 2003;107:1556.)
© 2003 American Heart Association, Inc.


Special Review

Important Triad in Cardiovascular Medicine

Diabetes, Coronary Intervention, and Platelet Glycoprotein IIb/IIIa Receptor Blockade

A. Michael Lincoff, MD

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
 
Diabetes mellitus is a potent risk factor for greater prevalence, complexity, and complications of cardiovascular disease, and diabetics thus constitute a sizable proportion of patients for whom coronary revascularization is required. However, both percutaneous and surgical revascularization techniques are associated with particular challenges in this population. Diabetics typically have an increased likelihood of restenosis and repeat revascularization procedures after stenting compared with their non-diabetic counterparts.1 Trends toward higher death rates in diabetics have also been observed over 1 year or longer after stenting,1–4 and patients with diabetes thus remain one of the few groups for whom percutaneous coronary intervention (PCI) does not yet provide survival benefit commensurate with that of coronary artery bypass surgery.5–7 Diabetes mellitus is also a predictor of elevated mortality risk and accelerated disease progression after surgical revascularization.5,8,9

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.11–13 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
 
Adjunctive antiplatelet therapy with GP IIb/IIIa blockade reduces the incidence of acute ischemic events by as much as 35% to 50% among the . . . [Full Text of this Article]




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