Platelet activation and its patient-specific consequences

Susan S. Smyth; Dougald M. Monroe; Waldemar E. Wysokinski; Robert D. McBane; Sidney W. Whiteheart; Richard C. Becker; Steven R. Steinhubl

doi:10.1016/j.thromres.2007.08.023

Platelet activation and its patient-specific consequences

Susan S. Smyth, Dougald M. Monroe, Waldemar E. Wysokinski, Robert D. McBane, Sidney W. Whiteheart, Richard C. Becker, Steven R. Steinhubl

Research output: Contribution to journal › Review article › peer-review

6 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	435-441
Number of pages	7
Journal	Thrombosis Research
Volume	122
Issue number	4
DOIs	https://doi.org/10.1016/j.thromres.2007.08.023
State	Published - 2008

Bibliographical note

Funding 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.

Keywords

Activation
Hemostasis
Platelets
Thrombosis

ASJC Scopus subject areas

Hematology

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10.1016/j.thromres.2007.08.023

Cite this

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title = "Platelet activation and its patient-specific consequences",

abstract = "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.",

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note = "Funding 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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AU - Wysokinski, Waldemar E.

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AU - Whiteheart, Sidney W.

AU - Becker, Richard C.

AU - Steinhubl, Steven R.

N1 - Funding 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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N2 - 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.

AB - 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.

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Platelet activation and its patient-specific consequences

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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