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Platelet Monocyte Aggregates and Monocyte Chemoattractant Protein-1 are not Inhibited by Aspirin in Critical Limb Ischaemia

Lookup NU author(s): Dr Jonathan Smout, Professor Gerard Stansby


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Objectives: Platelet monocyte aggregates (PMA) and monocyte chemoattractant protein-1 (MCP-1) play a significant role in atherosclerotic disease but the effect of aspirin and their role in peripheral arterial disease (PAD) requires further investigation. We have compared p-selectin, PMA and MCP-1 in patients with PAD treated with aspirin (75mgs daily), with age matched controls not treated with aspirin. Materials and methods: Using flow cytometry and ELISA, P-selectin, PMA and MCP-1 were compared in 3 populations; healthy controls (n = 12), intermittent claudication (n = 19) and critical limb ischaemia (CLI), (n = 10). Results: P-selectin was significantly higher in CLI patients (3.48% positive) compared to the claudicants (1. 36% positive) and the controls (1.76% positive). PMA levels were significantly higher for CLI population (44.5% positive) compared to the claudicants (20.48% positive) and the controls (28.33% positive). MCP-1 levels expression was significantly higher for the CLI patients (175.4 pg/mL) compared to the claudicants (76.1 pg/mL) and the controls (117.0 pg/mL). Conclusion: Despite aspirin treatment CLI patients have higher platelet activation and MCP-1 expression than controls and claudicants. With increasing severity of disease aspirin is unable to suppress markers of platelet activation and pro-atherosclerotic chemokine expression which may represent another form of aspirin resistance. © 2007 Elsevier Ltd. All rights reserved.

Publication metadata

Author(s): Cleanthis M, Bhattacharya V, Smout J, Ashour H, Stansby G

Publication type: Article

Publication status: Published

Journal: European Journal of Vascular and Endovascular Surgery

Year: 2007

Volume: 33

Issue: 6

Pages: 725-730

ISSN (print): 1078-5884

ISSN (electronic): 1532-2165

Publisher: Elsevier Ltd


DOI: 10.1016/j.ejvs.2006.12.025

PubMed id: 17296320


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