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DOI: 10.5482/HAMO-16-09-0034
New findings on venous thrombogenesis
Neue Erkenntnisse zur Venenthrombose Fundings The authors are supported by funding from the National Institutes of Health (R01HL126974 to A.S.W.) and the National Science Foundation (DGE-1144081 to J.R.B.).Publication History
received:
01 September 2016
accepted in revised form:
04 November 2016
Publication Date:
28 December 2017 (online)
![](https://www.thieme-connect.de/media/10.1055-s-00034925/201701/lookinside/thumbnails/10-5482-hamo-16-09-0034-1.jpg)
Summary
Venous thrombosis (VT) is the third most common cause of cardiovascular death worldwide. Complications from VT and pulmonary embolism are the leading cause of lost disability-adjusted life years. Risks include genetic (e.g., non-O blood group, activated protein C resistance, hyperprothrombinemia) and acquired (e.g., age, surgery, cancer, pregnancy, immobilisation, female hormone use) factors. Pathophysiologic mechanisms that promote VT are incompletely understood, but involve abnormalities in blood coagulability, vessel function, and flow (so-called Virchow’s Triad). Epidemiologic studies of humans, animal models, and biochemical and biophysical investigations have revealed contributions from extrinsic, intrinsic, and common pathways of coagulation, endothelial cells, leukocytes, red blood cells, platelets, cell-derived microvesicles, stasis-induced changes in vascular cells, and blood rheology. Knowledge of these mechanisms may yield new therapeutic targets. Characterisation of mechanisms that mediate VT formation and stability, particularly in aging, are needed to advance understanding of VT.
Zusammenfassung
Venenthrombosen (VT) sind die dritthäufigste Ursache kardiovaskulärer Todesfälle weltweit. Das Risiko wird durch genetische (z. B. nicht-O-Blutgruppe, aktivierte-Protein-C-Resistenz, Hyperprothrombinämie) und erworbene Faktoren (z. B. Alter, chirurgische Eingriffe, Krebs, Schwangerschaft, Immobilisation, weibliche Hormone, etc.) bestimmt. Die pathophysiologischen Mechanismen sind noch nicht vollständig geklärt. Eine große Rolle spielen dabei jedoch Veränderungen der Blutgerinnung, Gefäßfunktion und Strömungsgeschwindigkeit (sog. Virchow-Trias). Epidemiologische Studien und biochemische bzw. biophysikalische Untersuchungen haben gezeigt, dass an der Entstehung von VT das extrinsische und intrinsische Gerinnungssystem sowie Endothelzellen, Leukozyten, Erythrozyten, Thrombozyten, zelluläre Mikrovesikel, Stase-induzierte Veränderungen der Gefäßzellen und die Fließeigenschaften des Bluts beteiligt sind. Um die Entstehung der VT besser zu verstehen – insbesondere im Alter – und möglicherweise neue therapeutische Zielstrukturen zu identifizieren, ist es wichtig, die zugrundeliegenden Mechanismen der VT zu charakterisieren.
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