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Details

Autor(en) / Beteiligte
Titel
Restenosis is associated with prothrombotic plasma fibrin clot characteristics in endovascularly treated patients with critical limb ischemia
Ist Teil von
  • Journal of thrombosis and thrombolysis, 2019-05, Vol.47 (4), p.540-549
Ort / Verlag
New York: Springer US
Erscheinungsjahr
2019
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • Introduction Hypolysible fibrin clots composed of tightly packed fibers characterize patients with peripheral artery disease (PAD) especially those with critical limb ischemia (CLI). Little is known about the impact of a prothrombotic clot phenotype on restenosis following endovascular revascularization in CLI. The goal of this study was to compare fibrin clot properties and their determinants in CLI patients with restenosis after endovascular treatment (ET) and those free of this complication. Methods 85 patients with CLI and restenosis within 1 year after ET on optimal pharmacotherapy and 47 PAD control patients without restenosis were included into the study. Plasma fibrin clot permeability (Ks, a measure of the average pore size in the fibrin network) and clot lysis time (CLT) with its potential determinants were determined. During follow-up, the composite endpoint including re-intervention, amputation and death was assessed. Results Compared with the control group, patients with restenosis had reduced K s (− 9.5%, p  < 0.001), prolonged CLT (+ 12.4%, p  = 0.003), higher thrombin generation (+ 7.9%, p  < 0.001) and elevated von Willebrand factor (vWF) antigen (+ 14.2%, p  < 0.001). During a 24 months follow-up the composite endpoint occurred in 54 CLI patients with restenosis (63.5%) and nine control patients (19.1%, p  < 0.001) with no association with baseline K s and CLT. Conclusion The increased thrombin formation and unfavorable fibrin clot properties occur in patients with CLI who experienced restenosis despite optimal endovascular and pharmacological therapy.
Sprache
Englisch
Identifikatoren
ISSN: 0929-5305, 1573-742X
eISSN: 1573-742X
DOI: 10.1007/s11239-019-01826-9
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6476846

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