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Arterial thrombosis—insidious, unpredictable and deadly

Abstract

The formation of blood clots—thrombosis—at sites of atherosclerotic plaque rupture is a major clinical problem despite ongoing improvements in antithrombotic therapy. Progress in identifying the pathogenic mechanisms regulating arterial thrombosis has led to the development of newer therapeutics, and there is general anticipation that these treatments will have greater efficacy and improved safety. However, major advances in this field require the identification of specific risk factors for arterial thrombosis in affected individuals and a rethink of the 'one size fits all' approach to antithrombotic therapy.

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Figure 1: Adhesion and activation mechanisms supporting the hemostatic and prothrombotic function of platelets.
Figure 2: Differential composition and localization of arterial thrombi relative to hemostatic plugs.
Figure 3: The antiadhesive phenotype of endothelial cells is maintained through four intrinsic pathways: ecto-ADPase, prostaglandin I2 (PGI2), nitric oxide (NO) and the thrombomodulin (TM)-activated protein C (APC) pathways.
Figure 4: Arterial thrombosis and the rapid progression of atherosclerotic lesions.
Figure 5: Platelet procoagulant activity necessary for α-thrombin generation, fibrin formation and thrombus stability.

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Peter Libby, Julie E. Buring, … Eldrin F. Lewis

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Acknowledgements

I would like to thank S. Schoenwaelder for preparation of the figures, constructive advice and for assistance with the manuscript. I also acknowledge H. Salem, M. Cooper and Z. Kaplan for their constructive advice and assistance with the manuscript. This work was supported by the National Health and Medical Research Council of Australia (NHMRC). I am an NHMRC Australia Fellow.

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Jackson, S. Arterial thrombosis—insidious, unpredictable and deadly. Nat Med 17, 1423–1436 (2011). https://doi.org/10.1038/nm.2515

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