Haemostasis and thrombosis: an overview

@article{Rasche2001HaemostasisAT,
  title={Haemostasis and thrombosis: an overview},
  author={H. Rasche},
  journal={European Heart Journal Supplements},
  year={2001},
  volume={3}
}
  • H. Rasche
  • Published 1 December 2001
  • Medicine
  • European Heart Journal Supplements
Physiology of haemostasis
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Control of the blood-polymer interface by plasma treatment.
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The extrinsic pathway of blood coagulation is initiated when blood is exposed to non-vascular-cell–bound tissue factor in the subendothelial space and activates factors IX and X of the intrinsic and common coagulated pathways, respectively.
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Understanding of how red blood cells can be damaged by the turbulent flow fields associated with current prosthetic mechanical heart valve designs improves, but continued advances in understanding the hemolytic complications associated with different valve designs will depend on the development of more sophisticated in vitro quantitative engineering techniques.
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The overall theme of this review, apart from an insight into various aspects of the haemostatic balance, is that blood has a strong tendency to clot when tissue is damaged, and the intact vasculature requires major anticoagulant systems to prevent clots adhering to and stabilising in the vasculatures.
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TLDR
Endothelium produces and secretes von Willebrand factor, which mediates platelet adhesion and shear-stress-induced aggregation, and releases prostacyclin and nitric oxide, potent inhibitors of platelet and monocyte activation and vasodilators.
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Conditions involving a genetic predisposition to venous thrombosis, one of the leading causes of mortality and morbidity, increases from 1 per 100,000 during childhood to 1 every 100 in old age, is discussed.
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Investigation of the frequency of hypercoagulable states in patients with MHV who had recurrent thrombosis at least twice after valve implantation found that these states are highly prevalent, and surgical replacement of the MHV with a bioprosthesis should be considered.
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