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-segment–elevation myocardial infarction, undergoing primary percutaneous coronary intervention, were prospectively enrolled with a follow-up of 24 months. Eosinophil activation (CD66b) was similar in patients with ACS and stable angina (6.61 [4.91–7.72] versus 6.62 [5.27–8.73], P=0.63), whereas eosinophil degranulation (CD69) and basophil activation (CD203c) were higher in ACS patients compared with stable angina patients (1.38 [1.16–1.52] versus 1.17 [1–1.31], P=0.01); 0.97 [0.89–1.11] versus 0.92 [0.87–0.95], P=0.03, respectively). Eosinophil cationic protein serum levels were significantly higher in ST-segment–elevation myocardial infarction patients with major adverse cardiac events as compared with those without (21.1 [10.37–25.65] versus 7.83 [3.37–12.8] μg/L, P=0.01) and in patients with thrombus score >3 compared with those with thrombus score ≤3 (15.0 [9.8–24.7] versus 5.2 [3.5–22.9] μg/L, P=0.006). Eosinophil cationic protein serum levels predicted major adverse cardiac events during follow-up (odds ratio =1.041, 95% confidence interval 1.012–1.071, P=0.005). C-reactive protein serum levels showed a borderline statistical significance (odds ratio =0.904, 95% confidence interval 0.806–1.014, P=0.085). CONCLUSIONS—These findings are the first demonstration of in vivo eosinophil degranulation and basophil activation during ACS and of the prognostic role of eosinophil cationic protein in ST-segment–elevation myocardial infarction.
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