Abstract
Platelets are a central cellular interface of the thrombotic and inflammatory processes of coronary atherosclerosis and modulate this interface by binding to leukocytes and altering their function. In addition, platelet activation; formation of leukocyte- platelet aggregates (monocyte-platelet aggregates and neutrophil-platelet aggregates); and platelet secretion of inflammatory modulators that affect leukocyte function, such as CD40 ligand, are associated with progression of disease across the entire spectrum of atherothrombosis. Monocyte-platelet aggregates are elevated in stable coronary artery disease and further elevate with plaque rupture, characteristic of percutaneous coronary intervention, acute coronary syndromes, and myocardial infarction. Through this interaction, activated platelets may contribute to the pathogensis of ischemic heart disease by localizing and activating monocytes to the site of the atherosclerotic lesion. These heterotypic aggregates have potential for a number of clinical applications, including measurement as an early marker for plaque rupture, evaluation of the efficacy of antiplatelet therapy, and as a potential target for therapeutic intervention. Additional investigations evaluating these applications as well as the relationship between monocyte-platelet aggregates and outcome are needed.
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Linden, M.D., Furman, M.I. (2006). Monocyte-Platelet Aggregates in Patients With Ischemic Heart Disease. In: Morrow, D.A. (eds) Cardiovascular Biomarkers. Contemporary Cardiology. Humana Press. https://doi.org/10.1007/978-1-59745-051-5_28
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DOI: https://doi.org/10.1007/978-1-59745-051-5_28
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