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Updated: Jun 12, 2025

Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
Eosinopenia in patients with acute myocardial infarction- longitudinal imaging insights from the CAPRI study
Bilal Bawamia1, Ashish Gupta1, Muntaser Omari1
1Department of Cardiothoracic Services, Freeman Hospital, Freeman Road, Newcastle-upon-Tyne, NE7 7DN, UK.
Insights
Low eosinophil counts in ST-segment elevation myocardial infarction (MI) patients are linked to worse heart function. Eosinopenia independently predicted lower left ventricular ejection fraction (LVEF) at 12 weeks post-MI.
Area of Science:
- Cardiology
- Immunology
- Biomarkers
Background:
- Eosinophils are involved in the inflammatory response following myocardial infarction (MI).
- Eosinopenia, a low eosinophil count, has been associated with adverse outcomes in various conditions.
- The impact of eosinopenia on cardiac imaging biomarkers after ST-segment elevation MI (STEMI) requires further investigation.
Purpose of the Study:
- To assess the association between eosinopenia and cardiac imaging biomarkers in STEMI patients.
- To determine if low eosinophil count predicts adverse cardiac remodeling and functional decline post-MI.
Main Methods:
- Post-hoc analysis of the CAPRI trial involving 52 STEMI patients.
- Cardiac MRI performed at 1 week and 12 weeks post-primary percutaneous coronary intervention.
- Eosinopenia defined as <40 cells/mL; analysis adjusted for ischemia time.
Main Results:
- 38% of patients presented with eosinopenia.
- Patients with eosinopenia had significantly longer ischemia times.
- At 12 weeks, eosinopenia was associated with larger infarct size, increased LV end-systolic volume, and reduced LVEF.
- Eosinopenia independently predicted worse LVEF at 12 weeks (P=0.038).
Conclusions:
- Eosinopenia in STEMI patients is associated with more extensive myocardial damage and adverse left ventricular remodeling.
- Low eosinophil count is an independent predictor of impaired left ventricular ejection fraction 12 weeks after STEMI.
- These findings suggest eosinophils may play a protective role in the acute phase of MI.
Abstract:
Eosinophils are recruited to the heart during acute myocardial infarction (MI) and are considered part of the inflammatory response associated with adverse clinical outcomes. We assessed the impact of eosinopenia on cardiac imaging biomarkers in patients presenting with ST-segment elevation MI. This is a post-hoc analysis of the Evaluating the effectiveness of intravenous Ciclosporin on reducing reperfusion injury in pAtients undergoing PRImary percutaneous coronary intervention (CAPRI) trial. Patients underwent cardiac MRI within 1 week and 12 weeks and low eosinophil was defined as less than 40 cells/ml. The study included 52 patients and 38% had low eosinophil. Ciclosporin administration was comparable between patients with low versus normal eosinophils. The ischaemia time was significantly longer in low eosinophil patients [262 (205-325) vs. 138 (102-195) minutes, P < 0.001]. At 12 weeks, patients with eosinopenia had larger infarct size [9.8% (5.7-18.4) vs. 7.4% (1.9-10.2), P = 0.045], larger left ventricle (LV) end systolic volume (89 ± 28 vs. 68 ± 23, P = 0.02), and lower LV ejection fraction (EF) (49 ± 9 vs. 58 ± 7, P < 0.001). After adjustments for significant predictors, including ischaemia time, low eosinophil count was an independent predictor of worse LVEF at 12 weeks [-5.78, 95% CI (-11.22 to -0.34), P = 0.038] but not infarct size [1.83, 95% CI (-2.77 to 6.43), P = 0.43]. Patients with low eosinophil count had larger infarct size and LV volumes and worse adverse remodeling compared to those with normal eosinophil count. At 12 weeks, eosinopenia was an independent predictor of worse LVEF but not infarct size.
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