Platelet Pathophysiology and its Role in Thrombosis

Paul A. Gurbel; Udaya S. Tantry

doi:10.1002/9781118493984.ch1

Platelet Pathophysiology and its Role in Thrombosis

Paul A. Gurbel, Udaya S. Tantry

Research output: Chapter in Book/Report/Conference proceeding › Chapter

Abstract

Multiple lines of evidence support the important role of platelets in thrombosis and subsequent clinical manifestations. Following platelet activation, the two agonists such as thromboxane A2 (TxA2) and adenosine diphosphate (ADP) generated at the site of vascular injury play a critical role in the amplification of platelet activation in response to other stimuli and in the final activation of glycoprotein (GP) IIb/IIIa receptors. Currently, the antiplatelet agents such as aspirin (inhibits platelet cyclooxygenase-1 enzyme and subsequent TxA2 generation), P2Y12 receptor blockers, and GPIIb/IIIa blockers constitute a major part of the pharmacological strategy to prevent thrombosis, an important cause of myocardial infarction and death.

Original language	English (US)
Title of host publication	Antiplatelet Therapy in Cardiovascular Disease
Publisher	Wiley-Blackwell
Pages	1-7
Number of pages	7
ISBN (Electronic)	9781118493984
ISBN (Print)	9781118275757
DOIs	https://doi.org/10.1002/9781118493984.ch1
State	Published - Jun 3 2014
Externally published	Yes

Keywords

Coagulation
Coronary artery disease
Cyclooxygenase-1 enzyme
GPIIb/IIIa receptor
Hemostasis
Myocardial infarction
P2Y12 receptor
Platelets
Stent thrombosis
Thrombosis

ASJC Scopus subject areas

General Medicine

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10.1002/9781118493984.ch1

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title = "Platelet Pathophysiology and its Role in Thrombosis",

abstract = "Multiple lines of evidence support the important role of platelets in thrombosis and subsequent clinical manifestations. Following platelet activation, the two agonists such as thromboxane A2 (TxA2) and adenosine diphosphate (ADP) generated at the site of vascular injury play a critical role in the amplification of platelet activation in response to other stimuli and in the final activation of glycoprotein (GP) IIb/IIIa receptors. Currently, the antiplatelet agents such as aspirin (inhibits platelet cyclooxygenase-1 enzyme and subsequent TxA2 generation), P2Y12 receptor blockers, and GPIIb/IIIa blockers constitute a major part of the pharmacological strategy to prevent thrombosis, an important cause of myocardial infarction and death.",

keywords = "Coagulation, Coronary artery disease, Cyclooxygenase-1 enzyme, GPIIb/IIIa receptor, Hemostasis, Myocardial infarction, P2Y12 receptor, Platelets, Stent thrombosis, Thrombosis",

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AU - Tantry, Udaya S.

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N2 - Multiple lines of evidence support the important role of platelets in thrombosis and subsequent clinical manifestations. Following platelet activation, the two agonists such as thromboxane A2 (TxA2) and adenosine diphosphate (ADP) generated at the site of vascular injury play a critical role in the amplification of platelet activation in response to other stimuli and in the final activation of glycoprotein (GP) IIb/IIIa receptors. Currently, the antiplatelet agents such as aspirin (inhibits platelet cyclooxygenase-1 enzyme and subsequent TxA2 generation), P2Y12 receptor blockers, and GPIIb/IIIa blockers constitute a major part of the pharmacological strategy to prevent thrombosis, an important cause of myocardial infarction and death.

AB - Multiple lines of evidence support the important role of platelets in thrombosis and subsequent clinical manifestations. Following platelet activation, the two agonists such as thromboxane A2 (TxA2) and adenosine diphosphate (ADP) generated at the site of vascular injury play a critical role in the amplification of platelet activation in response to other stimuli and in the final activation of glycoprotein (GP) IIb/IIIa receptors. Currently, the antiplatelet agents such as aspirin (inhibits platelet cyclooxygenase-1 enzyme and subsequent TxA2 generation), P2Y12 receptor blockers, and GPIIb/IIIa blockers constitute a major part of the pharmacological strategy to prevent thrombosis, an important cause of myocardial infarction and death.

KW - Coagulation

KW - Coronary artery disease

KW - Cyclooxygenase-1 enzyme

KW - GPIIb/IIIa receptor

KW - Hemostasis

KW - Myocardial infarction

KW - P2Y12 receptor

KW - Platelets

KW - Stent thrombosis

KW - Thrombosis

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BT - Antiplatelet Therapy in Cardiovascular Disease

PB - Wiley-Blackwell

ER -

Platelet Pathophysiology and its Role in Thrombosis

Abstract

Keywords

ASJC Scopus subject areas

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