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Antiplatelet treatment for coronary heart disease
  1. N Clappers,
  2. M A Brouwer,
  3. F W A Verheugt
  1. Radboud University Nijmegen Medical Center, Heartcenter, Nijmegen, The Netherlands
  1. Correspondence to:
    Professor Freek W A Verheugt
    Radboud University Nijmegen Medical Center, Heartcenter, 670 Cardiology, PO Box 9101, Nijmegen, The Netherlands 6500 HB; f.verheugt{at}cardio.umcn.nl

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Platelets play an essential role in the pathogenesis of acute coronary syndromes (ACS).1 Therefore an important part of the treatment of ACS, and of primary and secondary preventive measures in coronary heart disease, consists of antiplatelet treatment. Over the years antiplatelet treatment has evolved, and currently several types of antiplatelet drugs are available, each with their specific pharmacological target and with their specific clinical indications. Although antiplatelet treatment is beneficial for vascular patients as a group, some individual patients appear to derive less benefit. In this context the term antiplatelet-drug resistance has been introduced. To date, however, no definite cause, definition, or treatment has been determined for this phenomenon. These issues will be discussed in this article.

PLATELET ACTIVATION

In the case of vascular endothelial damage, the first haemostatic reaction is vasoconstriction. Thereafter, the platelets come into action and the coagulation system is activated. Through disruption of the endothelial layer of the vessel wall, tissue factor is exposed, initiating the coagulation cascade, resulting in thrombin formation. Also subendothelial collagen and Von Willebrand factor are exposed to the flowing blood. Following this event, platelets start to adhere to collagen and Von Willebrand factor through their respective receptors, forming a platelet monolayer covering the damaged part of the vessel wall. This monolayer serves as a base for thrombin generation and platelet aggregation. Adhered platelets undergo shape change, form podocytes, and start to secrete thromboxane A2 (TXA-2) and their granule contents, such as adenosine diphosphate (ADP). Through their specific receptors on the platelet surface, thrombin, TXA-2, ADP and other substances help recruit and further activate platelets at the site of endothelial damage. Activated platelets express the glycoprotein IIb/IIIa receptor, which is the receptor for fibrinogen. This receptor is essential for irreversible aggregation for which fibrinogen serves as the glue between the platelets (fig 1). …

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