P laque rupture with activation of inflammatory cells and thrombus formation is the most frequent mechanism causing acute coronary syndromes (ACS). Among inflammatory cells, in the last decades, the scientific community has focused its attention mostly on the role of neutrophils and lymphocytes in the pathogenesis of coronary instability.
1,2However, some studies have suggested that, at least in a subset of patients, eosinophils and basophils also may play a pathogenetic role.3,4 These cells, indeed, are rich in small granules, which contain many chemical mediators, released by a process called degranulation following activation of the cell. So, this process can favor thrombus formation and enhance vasoconstriction at coronary level. 5,6 Importantly, eosinophils have been recently involved in thrombus growth and coronary vasospasm. 7,8 Of note, we reported that higher eosinophil cationic protein (ECP) levels were associated to the atherosclerotic burden and to a worse prognosis in patients undergoing stent implantation. 9,10 Moreover, in a postmortem study, eosinophil infiltration was found at the site of late drug-eluting stent thrombosis.
11However, to date, the role of eosinophils in coronary instability has not been addressed in detail. Furthermore, the Background-The role of allergic inflammation in acute coronary syndromes (ACS) has not been clearly defined to date.Aim of this study was to assess eosinophil and basophil activation in ACS and the prognostic role of eosinophil cationic protein in ST-segment-elevation myocardial infarction. Methods and Results-In a cross-sectional study, we prospectively enrolled 51 patients undergoing percutaneous coronary intervention (60.8% patients with ACS and 39.2% with stable angina). Flow cytometry analysis assessed CD66b, CD69, and CD203c median fluorescence intensity expression. In a follow-up study, 181 patients presenting with ST-segmentelevation myocardial infarction, undergoing primary percutaneous coronary intervention, were prospectively enrolled with a follow-up of 24 months. Eosinophil activation (CD66b)