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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:e2.)
© 2008 American Heart Association, Inc.

Letter to the Editor

Choice of Anticoagulant Critically Affects Measurement of Circulating Platelet-Leukocyte Complexes

Stylianos Bournazos; Jillian Rennie; Simon P. Hart; Ian Dransfield

From the University of Edinburgh/Medical Research Council (MRC) Centre for Inflammation Research (S.B., J.R., S.P.H., I.D.) and the Centre for Cardiovascular Science (S.B.), Queen’s Medical Research Institute, Edinburgh, UK.

Correspondence to Ian Dransfield, The University of Edinburgh/MRC Centre for Inflammation Research, Queen’s Medical Research Institute, 47 Little France Crescent, Edinburgh, EH16 4TJ, United Kingdom. E-mail i.dransfield@ed.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In circulation, platelets adhere to leukocytes forming relatively stable complexes that have been reported to be elevated in cases of unstable angina, myocardial infarction, coronary artery disease, and postangioplasty restenosis.^1–10 For this reason, measurement of circulating platelet-leukocyte complexes has been proposed as an early and accurate marker of in vivo platelet activation and myocardial injury after infarction.^9,10 Increased levels of such complexes have also been noted in a range of chronic inflammatory diseases, including rheumatoid arthritis, end-stage renal failure, type I diabetes, and systemic lupus erythematosus.^11–13

In the majority of published studies that have examined platelet-monocyte or platelet-polymorphonuclear (PMN) leukocyte complexes in human peripheral venous blood, sodium citrate (0.32 to 0.38%), a calcium-depleting agent, has been used as the blood anticoagulant. Because platelet adhesion to leukocytes is predominantly mediated by calcium-dependent interactions between platelet P-selectin and its leukocyte counter-receptor, P-selectin glycoprotein ligand-1 (PSGL-1),¹⁴ we aimed to determine whether calcium depletion by sodium citrate could affect platelet-leukocyte complex formation.

For this reason, platelet-monocyte and -PMN leukocyte complexes in citrated blood (0.38% wt/vol final concentration) were measured using 2-color flow cytometry (described in³) and compared with those observed in blood anticoagulated by hirudin (200 U mL^–1; lepirudin), heparin (10 U mL^–1), or PPACK (D-phenylalanyl-L-propyl-L-arginine chloromethylketone; 75 µmol/L), which act independently of calcium chelation.

We observed significantly lower percentages of platelet binding to monocytes (defined as CD42a⁺/CD14⁺ events) in blood anticoagulated with sodium citrate compared with hirudin-, heparin-, or PPACK-anticoagulated blood (Figure). No . . . [Full Text of this Article]

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				S. Bournazos, J. Rennie, S. P. Hart, K. A.A. Fox, and I. Dransfield Monocyte Functional Responsiveness After PSGL-1-Mediated Platelet Adhesion Is Dependent on Platelet Activation Status Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1491 - 1498. [Abstract] [Full Text] [PDF]