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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Circulating intermediate CD14++CD16+monocytes are increased in patients with atrial fibrillation and reflect the
Atsushi Suzuki1, Koji Fukuzawa2,3, Tomoya Yamashita1
1Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Insights
Intermediate CD14++CD16+ monocytes are significantly elevated in atrial fibrillation (AF) patients, suggesting a role in AF pathogenesis. This monocyte subset may reflect left atrial remodeling in individuals with AF.
Area of Science:
- Immunology
- Cardiology
- Biomedical Science
Background:
- Intermediate CD14++CD16+ monocytes are linked to cardiovascular events.
- The specific role of this monocyte subset in atrial fibrillation (AF) pathogenesis is unclear.
Purpose of the Study:
- To compare circulating monocyte subsets in AF patients and healthy controls.
- To investigate the potential role of intermediate CD14++CD16+ monocytes in AF pathophysiology.
Main Methods:
- A case-control study involving 44 AF patients and 40 healthy controls.
- Exclusion of patients with systemic diseases and inflammation.
- Analysis of monocyte subsets (classical, intermediate, non-classical) using flow cytometry.
Main Results:
- AF patients exhibited a higher proportion of intermediate CD14++CD16+ monocytes (17.0% vs. 7.5%, P < 0.001).
- The proportion of intermediate CD14++CD16+ monocytes was independently associated with AF presence (OR: 1.316, P = 0.003).
- These monocytes correlated negatively with left atrial appendage flow and positively with brain natriuretic peptide levels.
Conclusions:
- Intermediate CD14++CD16+ monocytes may be closely associated with AF pathogenesis.
- This monocyte subset could serve as a biomarker reflecting left atrial functional remodeling in AF.
Aims:
A recent large clinical study demonstrated the association between intermediate CD14++CD16+monocytes and cardiovascular events. However, whether that monocyte subset contributes to the pathogenesis of atrial fibrillation (AF) has not been clarified. We compared the circulating monocyte subsets in AF patients and healthy people, and investigated the possible role of intermediate CD14++CD16+monocytes in the pathophysiology of AF.
Methods And Results:
This case-control study included 44 consecutive AF patients without systemic diseases referred for catheter ablation at our hospital, and 40 healthy controls. Patients with systemic diseases, including structural heart disease, hepatic or renal dysfunction, collagen disease, malignancy, and inflammation were excluded. Monocyte subset analyses were performed (three distinct human monocyte subsets: classical CD14++CD16-, intermediate CD14++CD16+, and non-classical CD14+CD16++monocytes). We compared the monocyte subsets and evaluated the correlation with other clinical findings. A total of 60 participants (30 AF patients and 30 controls as an age-matched group) were included after excluding 14 AF patients due to inflammation. Atrial fibrillation patients had a higher proportion of circulating intermediate CD14++CD16+monocytes than the controls (17.0 ± 9.6 vs. 7.5 ± 4.1%, P < 0.001). A multivariable logistic regression analysis demonstrated that only the proportion of intermediate CD14++CD16+monocytes (odds ratio: 1.316; 95% confidence interval: 1.095-1.582, P = 0.003) was independently associated with the presence of AF. Intermediate CD14++CD16+monocytes were negatively correlated with the left atrial appendage flow during sinus rhythm (r= -0.679, P = 0.003) and positively with the brain natriuretic peptide (r = 0.439, P = 0.015).
Conclusion:
Intermediate CD14++CD16+monocytes might be closely related to the pathogenesis of AF and reflect functional remodelling of the left atrium.
