Abstract
The pathogenesis of infective endocarditis involves complex interactions between bacteria, endothelium, extracellular matrix, platelets, and plasma. This review examines recent work on the role of these factors in mediating microbial binding to the endocardial surface, and how they may contribute to subsequent vegetation formation. In addition, new studies are detailed describing the antimicrobial properites of platelets and how they may affect the course of endovascular infection.