Individuals vary in their thrombotic response to vascular injury. The reasons for this are numerous, involving heterogeneity in multiple platelet responses. Platelet research has tended to focus on functioning at the molecular level, and many experiments reflect results obtained in isolated, in vitro systems. However, platelets function in a complex and dynamic in vivo environment with the potential for a wide range of biological influences. This article reviews the evidence for diversity in platelet responses and the implications for individual variability in propensity to arterial thrombosis. Three overarching phenomena are considered. First, platelets can vary quantitatively and qualitatively in their responses to agonists. Second, platelets appear to have different intrinsic levels of procoagulant activity. Third, responses to various procoagulant, regulatory, and mediating factors likewise differ within and among individuals and can be influenced by blood-borne factors. These phenomena may help to explain differences in experimental arterial thrombosis observed in individuals.
|Number of pages||7|
|State||Published - 2008|
Bibliographical noteFunding Information:
This work was supported by grants from Accumetrics, Inc., San Diego, California; Eli Lilly and Company, Indianapolis, Indiana; AstraZeneca, Wilmington, Delaware; The Medicines Company, Parsippany, New Jersey; Sanofi-Aventis, Bridgewater, New Jersey; and Bristol-Myers Squibb, Overland Park, Kansas. Drs. Smyth, Monroe, Wysokinski, McBane, and Whiteheart have no conflicts of interest to report. Dr. Becker has received research support from Bristol-Myers Squibb and The Medicines Company. Dr. Steinhubl has consulted for Sanofi-Aventis, The Medicines Company, AstraZeneca, and Eli Lilly and Company. The authors thank Pat French of Left Lane Communications for writing and editorial assistance in the development of this manuscript.
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