The role of platelets in the recruitment of monocytes and neutrophils to sites of vascular injury has long been recognized (Palabrica et al., 1992). The appearance of circulating LPAs is a dynamic process involving initial formation, vascular adhesion, potential sequestration to elements of the reticuloendothelial system, leukocyte activation, and LPA disaggregation via granulocyte proteinases (Gardiner et al., 2001). Circulating LPAs are increased in stable coronary artery disease (Furman et al., 1998), unstable angina (Ott et al., 1996), acute myocardial infarction (Furman et al., 2001; Michel-son et al., 2001), chronic venous insufficiency (Powell et al., 1999), and during cardiopulmonary bypass (Rinder et al., 1992). Circulating LPAs are also increased after coronary angioplasty, with a greater magnitude in patients experiencing late clinical events (Mickel-son et al., 1996).
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