New findings on venous thrombogenesis

James R. Byrnes; Alisa S. Wolberg

doi:10.5482/HAMO-16-09-0034

Hämostaseologie, Table of Contents

Hamostaseologie 2017; 37(01): 25-35
DOI: 10.5482/HAMO-16-09-0034

Plenary lecture

Schattauer GmbH

New findings on venous thrombogenesis

Neue Erkenntnisse zur Venenthrombose

James R. Byrnes

¹Department of Pathology and Laboratory Medicine and McAllister Heart Institute, University of North Carolina, Chapel Hill, United States

,

Alisa S. Wolberg

¹Department of Pathology and Laboratory Medicine and McAllister Heart Institute, University of North Carolina, Chapel Hill, United States

› Author Affiliations

Abstract

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.

Keywords

Tissue factor - factor XII - antithrombotic - thrombosis models

Schlüsselwörter

Gewebefaktor - Faktor XII - antithrombotisch - Thrombose-Modell

Full Text

References

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