There are many approaches to assessing platelet reactivity and many uses for such measurements. Initially, measurements were based on the ability of platelets separated from other blood cells to aggregate together following activation with an appropriate 'aggregating agent'. Later, measurements of platelet aggregation in blood itself were performed, and this led to a point-of-care approach to platelet function testing. Measurement of secretory activity through the appearance of the activation marker Pselectin on platelets now provides an alternative approach, which enables remote testing. Measurement of vasodilator-stimulated phosphoprotein phosphorylation is also moving toward application in situations remote from the testing laboratory. Here we provide an overview of the various approaches that are now available, assess their advantages and disadvantages, and describe some of the clinical situations in which they are being used.
Keywordsaspirin, flow cytometry, light transmission aggregometry (LTA), multiplate electrode aggregometry (MEA), P-selectin, P2Y12 antagonists, platelet aggregation, platelet reactivity, VASP phosphorylation, VerifyNow Platelet reactivity is a broad term indicating the degree of the response of blood platelets to an external stimulus, usually an 'aggregating agent'. Platelet reactivity can be measured in many different ways and the purpose of this review is to summarize the approaches, with an emphasis on the newer approaches that are becoming available.Platelets play an important role in the hemostatic process [1,2]. They contribute to the formation of a hemostatic plug that serves to prevent blood loss from injured blood vessels. The hemostatic plug contains thousands of platelets that have aggregated together within a network of fibrin. However, platelets also contribute to the generation of a thrombotic mass in a coronary or cerebral artery or in an artificial stent leading to blockage and resulting in conditions such as heart attack, stroke and stent thrombosis [3,4]. A thrombus is also composed of platelet aggregates within a fibrin network. So thrombus formation can thus be considered to be hemostasis in the wrong place.