Admission eosinophil count is associated with favorable cardiac remodeling after ST-segment elevation myocardial infarction.

Experimental studies suggest that eosinophils promote myocardial repair after myocardial infarction; however, their clinical significance in post-infarction cardiac remodeling remains unclear. We investigated the association between admission peripheral eosinophil counts and left ventricular (LV) and left atrial (LA) remodeling after ST-segment elevation myocardial infarction (STEMI). This retrospective single-center study included 452 consecutive patients with first-time STEMI who underwent successful primary percutaneous coronary intervention between 2016 and 2024. Patients were divided into high and low eosinophil groups according to the median admission eosinophil count (70 cells/µL). Echocardiography was performed during the acute phase and at 6-12 months. Changes in LV end-diastolic diameter (ΔLVDd) and left atrial volume index (ΔLAVI) were evaluated. Multivariable linear regression analysis was performed to identify independent predictors of remodeling. Patients with higher eosinophil counts showed significantly smaller increases in LVDd (ΔLVDd: - 0.4 ± 6.3 vs. + 1.0 ± 4.8 mm, p = 0.03) and greater reductions in LAVI (ΔLAVI: - 2.2 ± 9.6 vs. + 1.1 ± 11.4 mL/m2, p = 0.01) than those with lower eosinophil counts. Admission eosinophil count was independently associated with ΔLVDd (standardized β = - 0.154, p = 0.046), whereas no independent association was observed with ΔLAVI. In subgroup analysis, the favorable association between eosinophils and LA remodeling was observed primarily in patients with LAD infarction. No significant differences were observed in one-year mortality or heart failure readmission. Higher admission eosinophil counts were associated with favorable LV and LA remodeling after STEMI. Admission eosinophil count was independently associated with attenuation of LV remodeling, suggesting that it may serve as a practical biomarker for identifying patients at lower risk of adverse cardiac remodeling after STEMI.