SELP and myocardial infarction: Monocyte-platelet aggregates are mainly formed via the interaction of platelet surface P-selectin with its counterreceptor P-selectin glycoprotein ligand-1 on leukocytes [6], and were shown to be an even more sensitive indicator of ongoing platelet activation than P-selectin in several pathophysiological circumstances including myocardial infarction [7].