(Circulation. 2005;111:2019-2021.)
© 2005 American Heart Association, Inc.
Editorial |
From the Division of Cardiology, Brown University, Providence, RI.
Correspondence to David O. Williams, MD, APC 814, Rhode Island Hospital, 593 Eddy St, Providence, RI 02903. E-mail dowilliams@lifespan.org
Key Words: Editorials clopidogrel angioplasty trials platelets
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In trying to explain how balloon angioplasty relieved coronary narrowing, Andreas Gruentzig often displayed a photograph of footprints in fresh snow. He proposed that balloon expansion resulted in gentle, uniform plaque compression. Subsequent histological examination in the porcine coronary model and of postmortem and ultrasound findings in humans indicated more traumatic effects of angioplasty, including deep medial fissuring and adventitial stretching. Such injury causes the release of potent substances from the arterial wall that have profound vasoactive and thrombotic effects. One early response is platelet activation and deposition over the injured arterial surface, creating the substrate for thrombosis. Stent implantation appears to be associated with even greater platelet activation than balloon angioplasty alone. Importantly, the magnitude of platelet activation is associated with an increased risk for adverse clinical events after coronary intervention.1
See p 2099
Aspirin, administered as an agent to inhibit platelet activity, has been a standard component of the angioplasty protocol since the inception of the procedure. More recently, substantial evidence indicates that supplementing aspirin and unfractionated heparin with agents that antagonize the platelet glycoprotein (GP) IIb/IIIa receptor further reduces the incidence of abrupt coronary closure and the magnitude of periprocedural cardiac enzyme elevations and, in certain patient subsets, may enhance survival.26 To decrease the risk of stent thrombosis, practice guidelines call for augmented antiplatelet therapy (aspirin and a thienopyridine) for weeks to months after hospital discharge.
In this issue of Circulation, Patti et al7 extend our knowledge about antiplatelet therapy and percutaneous coronary intervention (PCI), particularly
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