Key result
Neutrophil activation markers are altered in HFrEF but fail to predict all-cause mortality.
Why the study?
Data on neutrophil activation and maturation status in heart failure with reduced ejection fraction (HFrEF) were scarce, prompting an evaluation of the role of neutrophil CD11b, CD66b, and CD64 expression.
Does peripheral neutrophil expression of activation and maturation markers (CD11b, CD66b, and CD64) correlate with disease severity and predict all-cause mortality in patients with chronic HFrEF?
Cohort (n=178)
No
Does peripheral neutrophil expression of activation and maturation markers (CD11b, CD66b, and CD64) correlate with disease severity and predict all-cause mortality in patients with chronic HFrEF?
In chronic HFrEF, elevated neutrophil CD64 reflects a low-grade proinflammatory state while lower CD11b and CD66b levels correlate with higher NT-proBNP and worse NYHA class, suggesting altered neutrophil maturation in advanced heart failure.
Answers are grounded in this paper and cite their sources.
Should not inform risk stratification in HFrEF; hypothesis-generating for neutrophil markers in severity assessment.
Background: Neutrophils are critically involved in the immune response. Inflammatory stimuli alter the expression status of their surface molecule toolset, while inflammation-stimulated granulopoiesis might also influence their maturation status. Data on neutrophil status in heart failure with reduced ejection fraction (HFrEF) are scarce. The present study aims to evaluate the role of neutrophil CD11b, CD66b and CD64 expression in HFrEF. Methods: A total of 135 HFrEF patients and 43 controls were recruited. Mean fluorescence intensity of the activation/maturation markers CD11b, CD66b and CD64 was measured on neutrophils by flow cytometry. CD10 (neprilysin) expression was simultaneously determined. Results: Neutrophil CD64 expression was higher in HFrEF compared with controls, while CD11b/CD66b levels were similar. Neutrophil CD11b and CD66b showed a significant direct correlation to neutrophil CD10 expression (rs = 0.573, p < 0.001 and rs = 0.184, p = 0.033). Neutrophil CD11b and CD66b correlated inversely with heart failure severity reflected by NT-proBNP and NYHA class (NT-proBNP: rs = −0.243, p = 0.005 and rs = −0.250, p = 0.004; NYHA class: p = 0.032 and p = 0.055), whereas no association for CD64 could be found. Outcome analysis did not reveal a significant association between the expression of CD11b, CD66b and CD64 and all-cause mortality (p = ns). Conclusions: The results underline the potential role of neutrophils in HFrEF disease pathophysiology and risk stratification and should stimulate further research, characterizing subpopulations of neutrophils and searching for key molecules involved in the downward spiral of inflammation and heart failure.
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Prausmüller et al. (2022) conducted a cohort in Chronic heart failure with reduced ejection fraction (HFrEF) (n=178). Neutrophil surface markers (CD11b, CD66b, CD64) expression measured by flow cytometry vs. Healthy controls without previously recorded comorbidities or medication (n=43) was evaluated on All-cause mortality (p=ns). Neutrophil CD64 expression was elevated in HFrEF vs controls and CD11b/CD66b correlated inversely with NT-proBNP, though none predicted all-cause mortality over 22 months.
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