EDITORIALS
Ensuring appropriate use of antiplatelet agents in the treatment of acute coronary syndromes—have cardiovascular physicians been given enough grace in getting it right?
Correspondence to:
Anthony H Gershlick, Department of Cardiology, University Hospitals of Leicester Glenfield Hospital, Leicester LE3 9QP, UK; agershlick@aol.com
| The first 150 words of the full text of this article appear below. |
Understanding the pathology of acute coronary syndromes has led to significant improvements in patient outcome. Platelet adhesion to the arterial wall, especially under high shear forces, such as are present in stenotic arteries, is facilitated through multiple high-affinity interactions between platelet membrane receptors and ligands within the exposed subendothelium, most notably collagen and von Willebrand factor. Platelet activation, initiated by the collagen exposed by plaque disruption and locally-generated soluble platelet agonists (primarily thrombin, ADP, and thromboxane A2), results in release of growth factors and adhesion molecules and most importantly the activation of the coagulation pathway. Activation of adjacent platelets occurs, with conformational changes in the platelet GP IIb IIIa receptor. Platelet aggregation, mediated primarily by interaction between the activated platelet GP IIb IIIa receptor and its ligands, fibrinogen and vWF, results in the formation of the platelet-rich thrombus. It is the formation of this platelet-rich clot and its extent at
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Heart 2008 94: 159-165.[Abstract] [Full Text] [PDF]
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