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Endogenous Fibrinolysis: An Important Mediator of Thrombus Formation and Cardiovascular Risk

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Endogenous Fibrinolysis : An Important Mediator of Thrombus Formation and Cardiovascular Risk. / Okafor, Osita N; Gorog, Diana A.

In: Journal of the American College of Cardiology, Vol. 65, No. 16, 28.04.2015, p. 1683-1699.

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@article{b0bdaab12a6f4ba4ade68ee136bbb055,
title = "Endogenous Fibrinolysis: An Important Mediator of Thrombus Formation and Cardiovascular Risk",
abstract = "Most acute cardiovascular events are attributable to arterial thrombosis. Plaque rupture or erosion stimulates platelet activation, aggregation, and thrombosis, whilst simultaneously activating enzymatic processes that mediate endogenous fibrinolysis to physiologically maintain vessel patency. Interplay between these pathways determines clinical outcome. If proaggregatory factors predominate, the thrombus may propagate, leading to vessel occlusion. However, if balanced by a healthy fibrinolytic system, thrombosis may not occur or cause lasting occlusion. Despite abundant evidence for the fibrinolytic system regulating thrombosis, it has been overlooked compared with platelet reactivity, partly due to a lack of techniques to measure it. We evaluate evidence for endogenous fibrinolysis in arterial thrombosis and review techniques to assess it, including biomarkers and global assays, such as thromboelastography and the Global Thrombosis Test. Global assays, simultaneously assessing proaggregatory and fibrinolytic pathways, could play a role in risk stratification and in identifying impaired fibrinolysis as a potential target for pharmacological modulation.",
keywords = "Acute Coronary Syndrome, Biomarkers, Cardiovascular Diseases, Fibrinolysis, Humans, Thrombelastography, Thrombosis, Journal Article, Review",
author = "Okafor, {Osita N} and Gorog, {Diana A}",
note = " {\textcopyright} 2015 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION. PUBLISHED BY ELSEVIER INC. ",
year = "2015",
month = apr,
day = "28",
doi = "10.1016/j.jacc.2015.02.040",
language = "English",
volume = "65",
pages = "1683--1699",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "16",

}

RIS

TY - JOUR

T1 - Endogenous Fibrinolysis

T2 - An Important Mediator of Thrombus Formation and Cardiovascular Risk

AU - Okafor, Osita N

AU - Gorog, Diana A

N1 - © 2015 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION. PUBLISHED BY ELSEVIER INC.

PY - 2015/4/28

Y1 - 2015/4/28

N2 - Most acute cardiovascular events are attributable to arterial thrombosis. Plaque rupture or erosion stimulates platelet activation, aggregation, and thrombosis, whilst simultaneously activating enzymatic processes that mediate endogenous fibrinolysis to physiologically maintain vessel patency. Interplay between these pathways determines clinical outcome. If proaggregatory factors predominate, the thrombus may propagate, leading to vessel occlusion. However, if balanced by a healthy fibrinolytic system, thrombosis may not occur or cause lasting occlusion. Despite abundant evidence for the fibrinolytic system regulating thrombosis, it has been overlooked compared with platelet reactivity, partly due to a lack of techniques to measure it. We evaluate evidence for endogenous fibrinolysis in arterial thrombosis and review techniques to assess it, including biomarkers and global assays, such as thromboelastography and the Global Thrombosis Test. Global assays, simultaneously assessing proaggregatory and fibrinolytic pathways, could play a role in risk stratification and in identifying impaired fibrinolysis as a potential target for pharmacological modulation.

AB - Most acute cardiovascular events are attributable to arterial thrombosis. Plaque rupture or erosion stimulates platelet activation, aggregation, and thrombosis, whilst simultaneously activating enzymatic processes that mediate endogenous fibrinolysis to physiologically maintain vessel patency. Interplay between these pathways determines clinical outcome. If proaggregatory factors predominate, the thrombus may propagate, leading to vessel occlusion. However, if balanced by a healthy fibrinolytic system, thrombosis may not occur or cause lasting occlusion. Despite abundant evidence for the fibrinolytic system regulating thrombosis, it has been overlooked compared with platelet reactivity, partly due to a lack of techniques to measure it. We evaluate evidence for endogenous fibrinolysis in arterial thrombosis and review techniques to assess it, including biomarkers and global assays, such as thromboelastography and the Global Thrombosis Test. Global assays, simultaneously assessing proaggregatory and fibrinolytic pathways, could play a role in risk stratification and in identifying impaired fibrinolysis as a potential target for pharmacological modulation.

KW - Acute Coronary Syndrome

KW - Biomarkers

KW - Cardiovascular Diseases

KW - Fibrinolysis

KW - Humans

KW - Thrombelastography

KW - Thrombosis

KW - Journal Article

KW - Review

U2 - 10.1016/j.jacc.2015.02.040

DO - 10.1016/j.jacc.2015.02.040

M3 - Review article

C2 - 25908074

VL - 65

SP - 1683

EP - 1699

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 16

ER -