Abstract

BackgroundRecently, it was shown that interleukin-17A (IL-17A) is involved in the pathophysiology of reperfusion injury and associated with infarct size (IS) in experimental models of myocardial infarction. Our aim was to evaluate whether the IL-17A serum level and the IL-17A active fraction was correlated with IS in humans.Methods101 patients presenting with a ST-elevated Myocardial Infarction (STEMI) referred for primary percutaneous coronary intervention (PPCI) and 10 healthy controls were included. For each participant, blood samples at admission (H0) and 4 hours after admission (H4) were collected. IL-17A serum levels were assessed using ELISA and the active fraction was assessed with a functional test. IS was determined by peak troponin and peak CK levels for every patient and by contrast-enhanced cardiac magnetic resonance (ce-CMR) for 20 patients.ResultsThe IL-17A serum level was significantly increased in STEMI patients compared to healthy controls, (0.9 pg/mL IQR [0.0–3.2] at H0 and 1.0 pg/mL IQR [0.2–2.8] at H4 versus 0.2 pg/mL IQR [0.0–0.7] for healthy controls; p<0.005). At either time points, IL-17A levels did not correlate with IS as measured by peak troponin, peak CK pr ce-CMR. Also, no correlation was found between the active fraction of IL-17A and IS.ConclusionSerum IL-17A level is significantly increased in patients at the early phase of acute MI compared to healthy controls. However, the level of IL-17A in the early hours after reperfusion does not correlate with IS.

Highlights

  • Myocardial infarction (MI) is one of the main causes of death in the world [1]

  • The IL-17A serum level was significantly increased in ST-elevated Myocardial Infarction (STEMI) patients compared to healthy controls, (0.9 pg/mL IQR [0.0–3.2] at H0 and 1.0 pg/mL IQR [0.2–2.8] at H4 versus 0.2 pg/ mL IQR [0.0–0.7] for healthy controls; p

  • IL-17A levels did not correlate with Infarct size (IS) as measured by peak troponin, peak creatine kinase (CK) pr contrast-enhanced cardiac magnetic resonance (ce-CMR)

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Summary

Introduction

Myocardial infarction (MI) is one of the main causes of death in the world [1]. Infarct size (IS) is associated with heart failure and mortality following MI [2,3]. Reperfusion is currently the most effective treatment to reduce IS resulting from MI [4,5]. Reperfusion reduces infarct size, it causes myocardial injury by itself [6]. This process is called ischemia-reperfusion (I/R) injury [7] and constitutes a target for the development of new therapies to reduce the final IS [8,9]. The different mechanisms involved in I/R injury, inflammation appears to play a significant part in the final damage to the ischemic myocardium [10]. It was shown that interleukin-17A (IL-17A) is involved in the pathophysiology of reperfusion injury and associated with infarct size (IS) in experimental models of myocardial infarction. Our aim was to evaluate whether the IL-17A serum level and the IL-17A active fraction was correlated with IS in humans

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