Institute of Health Research-INCLIVA, Valencia, Spain.
Cardiology Department, Hospital Clinico Universitario, Valencia, Spain.
PLoS One. 2018 Oct 26;13(10):e0206344. doi: 10.1371/journal.pone.0206344. eCollection 2018.
We characterized the dynamics of eosinophils in blood and in the infarcted myocardium in patients and in a swine model of reperfused myocardial infarction (MI). The association of eosinophil dynamics with various outcomes was assessed.
Serial eosinophil count and pre-discharge cardiac magnetic resonance were carried out in a prospective series of 620 patients with a first ST-elevation MI. In a swine model of reperfused MI, the dynamics of circulating eosinophils and their presence in the infarcted myocardium were determined. In autopsies from chronic MI patients, eosinophils were quantified.
Patient eosinophil count sharply decreased 12h post-reperfusion compared to arrival. A lower minimum eosinophil count was associated with more extensive edema, microvascular obstruction, and infarct size as measured by cardiac magnetic resonance, and also with a higher rate of cardiac events (death, re-infarction, or heart failure) during follow-up. In the experimental model, eosinophil count boosted during ischemia and dropped back immediately post-reperfusion. Myocardial samples revealed progressive eosinophil migration into the infarcted myocardium, especially areas with microvascular obstruction. Markers of eosinophil maturation and survival (interleukin-5), degranulation (eosinophil cationic protein) and migration (eotoxin-1) were detected in the blood of patients, and in porcine myocardium. Eosinophil infiltration was detected in autopsies from chronic MI patients.
Eosinopenia post-MI was associated with an impaired cardiac structure and adverse events. The decay in circulating eosinophils soon after reperfusion mirrors their migration into the infarcted myocardium, as reflected by their presence in heart samples from swine and patients. Further studies are needed to understanding this unexplored pathway and its therapeutic implications.
我们对患者和再灌注心肌梗死（MI）猪模型中的血液和梗死心肌中的嗜酸性粒细胞动态进行了特征描述。评估了嗜酸性粒细胞动力学与各种结局的关联。
对 620 例首次 ST 段抬高型 MI 患者进行了前瞻性系列研究，进行了嗜酸性粒细胞连续计数和出院前心脏磁共振检查。在再灌注 MI 猪模型中，确定了循环嗜酸性粒细胞的动态及其在梗死心肌中的存在。在慢性 MI 患者的尸检中，对嗜酸性粒细胞进行了量化。
与到达时相比，患者的嗜酸性粒细胞计数在再灌注后 12 小时急剧下降。最低嗜酸性粒细胞计数较低与心脏磁共振测量的更广泛的水肿、微血管阻塞和梗死面积较大以及随访期间更高的心脏事件（死亡、再梗死或心力衰竭）发生率相关。在实验模型中，嗜酸性粒细胞计数在缺血期间增加，并在再灌注后立即下降。心肌样本显示嗜酸性粒细胞逐渐向梗死心肌迁移，特别是在微血管阻塞区域。患者血液和猪心肌中检测到嗜酸性粒细胞成熟和存活的标志物（白细胞介素 5）、脱颗粒（嗜酸性粒细胞阳离子蛋白）和迁移（嗜菌素-1）。在慢性 MI 患者的尸检中检测到嗜酸性粒细胞浸润。
MI 后嗜酸性粒细胞减少与心脏结构受损和不良事件有关。再灌注后循环嗜酸性粒细胞的减少反映了它们向梗死心肌的迁移，这反映在猪和患者的心脏样本中存在嗜酸性粒细胞。需要进一步研究以了解这条未被探索的途径及其治疗意义。
