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Increased platelet aggregation and activation in peripheral arterial disease

Lookup NU author(s): Professor Gerard Stansby

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Abstract

Objectives: patients with peripheral arterial disease (PAD) have a threefold increase ill cardiovascular mortality. Standard antiplatelet treatment may not confer uniform benefit in different patient groups. This study aimed to compare platelet function ill patients with lower limb PAD, carotid disease and abdominal aortic aneurysm (AAA) with age- and sex-matched healthy controls. Methods: patients with lower limb PAD (n = 20), carotid disease (n 40), AAA (n = 13) and age/sex matched healthy controls (n=20) were studied. Whole blood methods to detect spontaneous platelet aggregation (SPA), and adenosine diphosphate (ADP) and collagen-induced aggregation were used. The detection of platelet P-selectin and the PAC-1 antigen by flow cytometry were also used as markers of platelet activation and aggregation. Results: patients with lower limb PAD or AAA bad higher baseline SPA compared to normal controls (p < 0.01). There was significantly higher collagen-induced aggregation in IC patients compared to normal controls (p < 0.01). However, there was no difference in ADP-induced aggregation between lower limb PAD and control patients. There was no difference in PAC-1 binding between control patients and the patients with lower limb PAD, carotid disease or AAA. Patients with carotid disease had a higher expression of P-selectin compared to normal controls (p < 0.05). Conclusions: this study provides further evidence that platelet hyperactivity is present in patients with PAD despite the use of antiplatelet therapy. Further antiplatelet strategies may be indicated to protect these patients.


Publication metadata

Author(s): Robless PA, Okonko D, Lintott P, Mansfield AO, Mikhailidis DP, Stansby GP

Publication type: Article

Publication status: Published

Journal: European Journal of Vascular and Endovascular Surgery

Year: 2003

Volume: 25

Issue: 1

Pages: 16-22

ISSN (print): 1078-5884

ISSN (electronic): 1532-2165

Publisher: Elsevier

URL: http://dx.doi.org/10.1053/ejvs.2002.1794

DOI: 10.1053/ejvs.2002.1794


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