title: Endothelial dysfunction and systemic inflammation in persons with echolucent carotid plaques.
abstract: Echolucent carotid plaques are associated with high risk for future ischemic cerebrovascular events independent of the degree of stenosis. Elevated levels of markers of systemic inflammation and endothelial dysfunction are predictors for future myocardial infarction and stroke. The present study was undertaken to investigate the relations between plaque morphology, endothelial dysfunction assessed by tissue-plasminogen activator antigen (t-PA ag) and vonWillebrand factor (vWF), and systemic inflammation in persons with carotid stenosis. We conducted a crosssectional study including 133 persons with carotid stenosis and 138 controls without stenosis recruited from the populationbased Tromsø Study. High-resolution B-mode and colour Doppler/pulsed-wave Doppler ultrasonography of both carotid arteries was performed, and plaque morphology in terms of echogenicity was assessed. Persons with carotid stenosis had significantly higher plasma t-PA and vWF concentrations than controls. There was a significant inverse relationship between t-PA ag and plaque echogenicity (p = 0.034). The increased plasma t-PA ag in persons with carotid stenosis was not associated with increased plasminogen activator inhibitor-I (PAI-1). Persons with echolucent carotid plaques had higher degree of systemic inflammation, and plasma t-PA and vWF concentration increased significantly across quartiles of WBC, fibrinogen, and hs-CRP. Our findings may suggest that plasma t-PA may be superior to vWF as a marker for endothelial dysfunction due to its ability to discriminate between various plaque echogenicity, and that the predictive role of t-PA ag in cardiovascular disease is independent of inhibited fibrinolysis.
authors.affiliation: Center for Atherothrombotic Research in Tromsø (CART), Institute of Clinical Medicine, University of Tromsø, 9037 Tromsø, Norway. anntrude@fagmed.uit.no
authors.forename: Ann-Trude
authors.initials: AT
authors.lastname: With Notø
authors.forename: Ellisiv
authors.initials: E
authors.lastname: Bøgeberg Mathiesen
authors.forename: Jean
authors.initials: J
authors.lastname: Amiral
authors.forename: Anne Marie
authors.initials: AM
authors.lastname: Vissac
authors.forename: John-Bjarne
authors.initials: JB
authors.lastname: Hansen
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000032:analysis; D016893:Carotid Stenosis / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000473:pathology*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000175:diagnosis*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D010959:Tissue Plasminogen Activator / Q000032:analysis; D018608:Ultrasonography, Doppler / Q000379:methods; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator