Abstract
Myocardial infarction (MI) induces an inflammatory response in which neutrophils fulfill a prominent role. Mean neutrophil volume (MNV) represents the average size of the circulating neutrophil population. Our goal was to determine the effect of MI on MNV and investigate the mechanisms behind MNV elevation. MNV of 84 MI patients was compared with the MNV of 209 stable angina patients and correlated to simultaneously measured CK levels. Fourteen pigs were subjected to temporary coronary balloon occlusion and blood was sampled at multiple time points to measure MNV. Echocardiography was performed followed by ex vivo infarct size assessment after 72 h. MNV was higher in MI patients compared to stable angina patients (602 SD26 AU vs. 580 SD20 AU, p < 0.0001) and correlated with simultaneously measured CK levels (R = 0.357, p < 0.0001). In pigs, MNV was elevated post-MI (451 SD11 AU vs. 469 SD12 AU), p < 0.0001). MNV correlated with infarct size (R = 0.705, p = 0.007) and inversely correlated with left ventricular ejection fraction (R = −0.718, p = 0.009). Cell sorting revealed an increased presence of banded neutrophils after MI, which have a higher MNV compared to mature neutrophils post-MI (495 SD14 AU vs. 478 SD11 AU, p = 0.012). MNV from coronary sinus blood was higher than MNV of neutrophils from simultaneously sampled arterial blood (463 SD7.6 AU vs. 461 SD8.6 AU, p = 0.013) post-MI. The current study shows MNV is elevated and reflects cardiac damage post-MI. MNV increases due to altered neutrophil composition and systemic neutrophil activation. MNV may be an interesting parameter for prognostic assessment in MI and provide new insights into pathological innate immune responses evoked by ischemia–reperfusion.
Highlights
Ischemic damage after myocardial infarction (MI) induces a detrimental inflammatory response [1, 25, 32]
Since MI induces an inflammatory response, and Mean neutrophil volume (MNV) is known to be elevated in inflammation-related diseases, in the current study we hypothesize that MNV changes after myocardial infarction in patients suffering from MI
MNV was significantly higher in ST-elevation MI (STEMI) patients (n = 84) compared to stable angina patients (n = 209) and patients without coronary artery disease (n = 80) that served as control groups (STEMI: 602 SD26 arbitrary units (AU) vs. stable AP: 580 SD20 AU, no CAD: 568 SD43 AU, p \ 0.0001) (Fig. 1a)
Summary
Ischemic damage after myocardial infarction (MI) induces a detrimental inflammatory response [1, 25, 32]. The best treatment to salvage myocardium post-MI is to restore myocardial reperfusion through percutaneous coronary intervention (PCI) [26]. Apart from myocardial salvage, reperfusion allows for immediate interaction between the damaged myocardium and circulating cells, among which neutrophils are the first responders [13, 22, 48, 53]. After myocardial reperfusion, circulating cells migrate to the infarcted tissue to clear out necrotic cells and orchestrate cardiac wound healing [18, 48]. The influx of inflammatory cells into the myocardium can result in the elimination of viable cardiomyocytes, thereby inducing infarct expansion [4, 36, 41]. Many clinical studies have shown that the severity of this inflammatory response is reflected by systemically measurable
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