Thromb Haemost 2008; 99(03): 602-608
DOI: 10.1160/TH07-08-0493
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

Increased thrombin generation in persons with echogenic carotid plaques

Ann-Trude With Notø
1   Center for Atherothrombotic Research in Tromsø (CART)
,
Ellisiv Bøgeberg Mathiesen
2   Department of Neurology, Institute of Clinical Medicine
,
Bjarne Østerud
3   Institute of Community Medicine, and Institute of Medical Biology, University of Tromsø, Tromsø, Norway
,
Jean Amiral
4   HYPHEN BioMed, Neuville sur Oise, France
,
Anne Marie Vissac
4   HYPHEN BioMed, Neuville sur Oise, France
,
John-Bjarne Hansen
1   Center for Atherothrombotic Research in Tromsø (CART)
› Author Affiliations

Financial support: CART is supported by an independent grant from Pfizer Norway AS. The study has received a grant from Center for Research in Elderly. Ann-Trude With Notø was financed by a grant from Norwegian Health Association. Ellisiv B. Mathiesen was financed by a grant from the Norwegian Research Council.
Further Information

Publication History

Received: 05 August 2007

Accepted after major revision: 21 January 2008

Publication Date:
07 December 2017 (online)

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Summary

Echolucent carotid plaques are associated with higher risk for future ischemic cerebrovascular events (CVE) than echogenic plaques independent of the degree of stenosis.Elevated markers of thrombin generation are associated with atherosclerotic plaques and are increased in the acute and chronic phases of CVE. The present study was conducted to investigate the influence of plaque morphology on thrombin generation in persons with carotid stenosis. One hundred twenty-eight persons with carotid stenosis (≥35% lumen diameter reduction) and 136 matched controls without stenosis were recruited from the health survey of the Tromsø Study. Blood samples were collected and plaque morphology determined by ultrasonography. Thrombin generation was assessed by thrombin-antithrombin complexes (TAT) and by prothrombin fragment 1+2 (F1+2).Persons with echogenic plaques (n=63) had significantly higher levels of TAT (5.24 μg/l, 4.33–6.14) (mean, 95%CI) than persons with echolucent plaques (n=65) (3.44 μg/l, 2.91–3.96, p<0.001) and controls (n=136) (3.33 μg/l, 3.06–3.60, p<0.001).They also had significantly higher levels of F1+2 (2.14 nM, 1.83–2.45) than persons with echolucent plaques (1.54 nM, 1.38–1.71, p<0.001) and controls (1.49 nM, 1.40–1.58, p<0.001). TAT and F1+2 increased linearly with plaque echogenicity (p=0.002 and p=0.001, respectively) independent of the degree of stenosis. Increased thrombin generation was associated with a significant increase in plasma factorV levels among persons with echogenic plaques compared to echolucent plaques (p=0.049) and controls (p=0.025). The present findings indicate that increasing plaque echogenicity, rather than plaque echolucency and the degree of stenosis, is associated with thrombin generation in persons with carotid stenosis.