Elevated mean neutrophil volume represents altered neutrophil composition and reflects damage after myocardial
G P J van Hout1, W W van Solinge2, C M Gijsberts3,4
1Laboratory of Experimental Cardiology (room G02.523), University Medical Centre Utrecht, Heidelberglaan 100, PO Box 85500, 3508 GA, Utrecht, The Netherlands. g.p.j.vanhout@umcutrecht.nl.
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.
Insights
Myocardial infarction (MI) elevates mean neutrophil volume (MNV), reflecting cardiac damage and increased neutrophils. This finding offers new insights into the immune response following ischemia-reperfusion injury.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Myocardial infarction (MI) triggers an inflammatory response with neutrophils playing a key role.
- Mean neutrophil volume (MNV) is an indicator of circulating neutrophil population size.
- Understanding MNV changes post-MI can elucidate underlying pathological mechanisms.
Purpose of the Study:
- To determine the effect of MI on MNV.
- To investigate the mechanisms responsible for MNV elevation after MI.
- To assess the correlation of MNV with cardiac damage markers and function.
Main Methods:
- Comparison of MNV in MI patients versus stable angina patients.
- Correlation of MNV with creatine kinase (CK) levels in MI patients.
- In vivo study in pigs undergoing coronary balloon occlusion to measure MNV, infarct size, and ejection fraction.
- Analysis of neutrophil composition (banded vs. mature) and MNV in coronary sinus and arterial blood post-MI.
Main Results:
- MNV was significantly higher in MI patients compared to stable angina patients and correlated with CK levels.
- In pigs, post-MI MNV elevation correlated with infarct size and inversely with left ventricular ejection fraction.
- Increased presence of higher-MNV banded neutrophils was observed post-MI.
- MNV was higher in coronary sinus blood than in arterial blood post-MI, suggesting localized neutrophil activation.
Conclusions:
- Elevated MNV is a consequence of myocardial infarction and reflects cardiac damage.
- MNV increase is attributed to altered neutrophil composition and systemic neutrophil activation.
- MNV may serve as a valuable prognostic marker for MI and offers insights into ischemia-reperfusion-induced innate immune responses.
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