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Novel Insights into Genetics of Arterial Thrombosis

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Clinical Cardiogenetics

Abstract

The vast majority of arterial thrombotic complications develop either on the top of an atherosclerotic lesion, or as thromboemboli originating in the heart, mostly related to atrial fibrillation. The origin of these two entities is quite distinct. While atherothrombosis is largely dependent on vessel wall characteristics (plaque lesion size and composition), emboli from the heart are more dependent on flow and blood composition characteristics. In all the cases, the three components that were indicated by Rudolph Virchow, abnormalities in the blood flow, hypercoagulability of the blood, and injury to the vessel wall, are operational and there is no black-and-white distinction between the different mechanisms of thromboembolic disease.

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Abbreviations

ACS:

Acute coronary syndrome

ADP:

Adenosine diphosphate

(A)MI:

(Acute) myocardial infarction

Bp:

Base pair

CAD:

Coronary artery disease

CHD:

Coronary heart disease

EPCR:

Endothelial protein C receptor

F:

Coagulation factor

GP:

Glycoprotein

HMWK:

High molecular weight kininogen

HVR:

Hypervariable region

PAI-1:

Plasminogen activator inhibitor-1

PAR:

Protease-activated receptor

PCI:

Percutaneous coronary intervention

PlA:

Platelet antigen

(s)TM:

(Soluble) Thrombomodulin

STE-ACS:

ST-segment elevation ACS

TAFI:

Thrombin activatable fibrinolysis inhibitor

TF:

Tissue factor

tPA:

Tissue type plasminogen activator

uPA:

Urokinase plasminogen activator

VNTR:

Variable number of tandem repeats

vWF:

von Willebrand factor

vWD:

von Willebrand disease

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Konings, J., Govers-Riemslag, J.W.P., ten Cate, H. (2011). Novel Insights into Genetics of Arterial Thrombosis. In: Baars, H., Doevendans, P., van der Smagt, J. (eds) Clinical Cardiogenetics. Springer, London. https://doi.org/10.1007/978-1-84996-471-5_21

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