| Pathophysiological role of blood-borne tissue factor: should the old paradigm be revisited? | |
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MedLine Citation:
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PMID: 20607451 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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The term "vulnerable plaque" identifies atherosclerotic lesions prone to rupture. Plaque disruption facilitates the interaction of the inner components of the lesion, tissue factor (TF) among them, with the flowing blood. This results in activation of the coagulation cascade, ultimately leading to thrombus formation, and abrupt vascular occlusion. Despite the central role of vulnerable plaques in the onset of acute coronary syndromes (ACS), there are certain conditions (e.g., eroded plaques) where a hyperactive, "vulnerable" blood, may play a predominant pathophysiological role. Recently, two distinct pools of circulating TF have been identified. One, associated with cell-derived microparticles probably originating from apoptotic cells, such as macrophages, smooth muscle cells, and endothelium. The most recent, blood-borne TF, circulates in an "inactive" form (encryption) and has to be activated (decryption) to exert its thrombogenic activity. Certain pathological conditions associated with an increased rate of thrombotic complications have been associated with high levels of circulating TF. It is thought that the blood-borne TF perpetuates the initial thrombogenic stimulus, leading to the formation of larger or more stable thrombus, and thus, more severe ACS. Thus, the concept of vulnerable blood could represent a new link between the vulnerable lesion and the high-risk patient. Therefore, the assessment of selected biomarkers associated with "vulnerable or hyperreactive blood", e.g., blood-borne tissue factor, may represent a useful tool to identify patients with a high-risk profile of developing major cardiovascular events. |
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Authors:
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Giovanni Cimmino; Paolo Golino; Juan Jose Badimon |
Publication Detail:
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Type: Journal Article Date: 2010-07-07 |
Journal Detail:
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Title: Internal and emergency medicine Volume: 6 ISSN: 1970-9366 ISO Abbreviation: Intern Emerg Med Publication Date: 2011 Feb |
Date Detail:
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Created Date: 2011-02-02 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101263418 Medline TA: Intern Emerg Med Country: Italy |
Other Details:
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Languages: eng Pagination: 29-34 Citation Subset: IM |
Affiliation:
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Atherothrombosis Research Unit, Mount Sinai Hospital, New York, NY, USA. |
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Descriptor/Qualifier:
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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