Bawamia Bilal, Gupta Ashish, Omari Muntaser, Farag Mohamed, Spyridopoulos Ioakim, Alkhalil Mohammad
Department of Cardiothoracic Services, Freeman Hospital, Freeman Road, Newcastle-upon-Tyne, NE7 7DN, UK.
Translational and Clinical Research Institute, Newcastle University, Newcastle-upon-Tyne, UK.
J Thromb Thrombolysis. 2025 Jan;58(1):136-144. doi: 10.1007/s11239-024-03042-6. Epub 2024 Sep 21.
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.
在急性心肌梗死(MI)期间,嗜酸性粒细胞会被募集到心脏,并且被认为是与不良临床结局相关的炎症反应的一部分。我们评估了嗜酸性粒细胞减少对ST段抬高型心肌梗死患者心脏成像生物标志物的影响。这是一项对评估静脉注射环孢素对接受直接经皮冠状动脉介入治疗(CAPRI)试验患者减少再灌注损伤有效性的事后分析。患者在1周和12周内接受心脏磁共振成像检查,低嗜酸性粒细胞定义为低于40个细胞/毫升。该研究纳入了52名患者,38%的患者嗜酸性粒细胞水平较低。嗜酸性粒细胞水平低的患者与正常患者之间环孢素的给药情况相当。嗜酸性粒细胞水平低的患者缺血时间明显更长[262(205 - 325)分钟对138(102 - 195)分钟,P < 0.001]。在12周时,嗜酸性粒细胞减少的患者梗死面积更大[9.8%(5.7 - 18.4)对7.4%(1.9 - 10.2),P = 0.045],左心室(LV)收缩末期容积更大(89 ± 28对68 ± 23,P = 0.02),左心室射血分数(EF)更低(49 ± 9对58 ± 7,P < 0.001)。在对包括缺血时间在内的显著预测因素进行调整后,低嗜酸性粒细胞计数是12周时左心室射血分数更差的独立预测因素[-5.78,95%置信区间(-11.22至-0.34),P = 0.038],但不是梗死面积的预测因素[1.83,95%置信区间(-2.77至6.43),P = 0.43]。与嗜酸性粒细胞计数正常的患者相比,嗜酸性粒细胞计数低的患者梗死面积更大、左心室容积更大且不良重塑更严重。在12周时,嗜酸性粒细胞减少是左心室射血分数更差的独立预测因素,但不是梗死面积的预测因素。