Key result
Currently available platelet function inhibitors focus almost exclusively on the biochemical events from platelet stimulation to ligand binding to the platelet fibrinogen receptor GPIIb-IIIa.
A review of the mechanism of action and clinical utility of platelet function inhibitors available in the year 2000.
May constrain antiplatelet strategies to one pathway; leaves open discovery of complementary platelet targets.
Summary Platelet thrombi are responsible for much of the morbidity and mortality of arterial vascular disease (1). Because platelet inhibitors such as aspirin have proven to be of benefit to patients with these disorders, there has been a directed search for more potent anti-platelet agents. The following discussion addresses the mechanism of action and clinical utility of the currently available platelet function inhibitors. Although in theory these agents could impair platelet adhesion, aggregation, secretion, or platelet procoagulant activity, in practice they are focused almost exclusively on the biochemical events that proceed from platelet stimulation to ligand binding to the platelet fibrinogen receptor GPIIb-IIIa.
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A 2001 study conducted a review in Arterial vascular disease. Platelet function inhibitors was evaluated. Currently available platelet function inhibitors focus almost exclusively on the biochemical events from platelet stimulation to ligand binding to the platelet fibrinogen receptor GPIIb-IIIa.
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