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Updated: Jul 14, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Soluble CD40 ligand and atrial fibrillation: relationship to platelet activation, and endothelial damage/dysfunction
Insights
Soluble CD40L (sCD40L) levels are marginally increased in atrial fibrillation (AF) patients. The exact source of elevated sCD40L in AF remains unclear, as it did not correlate with platelet or endothelial markers.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biochemistry
Background:
- Elevated plasma soluble CD40L (sCD40L) is linked to cardiovascular diseases and poor prognosis.
- The source of sCD40L in cardiovascular conditions, particularly atrial fibrillation (AF), is not fully understood.
- This study investigates sCD40L levels in non-rheumatic AF and explores its potential origin.
Discussion:
- Plasma sCD40L levels were marginally higher in AF patients compared to controls.
- While von Willebrand factor (vWf) and soluble P-selectin were elevated in AF, soluble E-selectin was not.
- No significant correlations were found between sCD40L and the measured platelet or endothelial markers.
Key Insights:
- Soluble CD40L (sCD40L) shows a marginal increase in atrial fibrillation (AF).
- The study did not find a significant correlation between sCD40L and platelet-derived soluble P-selectin or endothelial markers (vWf, soluble E-selectin).
- These findings suggest that neither platelets nor the endothelium alone are the primary source of elevated sCD40L in AF.
Outlook:
- Further research is needed to elucidate the precise stimulus and source of increased sCD40L in AF.
- Investigating other potential cellular sources or inflammatory pathways involved in sCD40L production in AF is warranted.
- Understanding the origin of sCD40L may reveal novel therapeutic targets for managing AF and its cardiovascular complications.
Abstract:
Increased plasma soluble CD40L (sCD40L) is present in many cardiovascular diseases and predicts poor outcome, but levels in atrial fibrillation (AF) are unknown. Although the platelet is frequently cited as the source of sCD40L, this view is not universal. We hypothesised (a) raised sCD40L in non-rheumatic AF, and (b) that sCD40L correlates with platelet, but not endothelial, markers, thus suggesting a platelet origin. Plasma sCD40L, platelet marker soluble P-selectin and endothelial markers von Willebrand factor (vWf) and soluble E-selectin were measured by ELISA in 54 AF patients free of diabetes or major cardiovascular disease, and in 28 age/sex matched controls. Median (inter-quartile range) sCD40L in AF was 0.82 (0-4.8) ng/mL compared to 0.21 (0-5.5 ng/mL) in controls (p=0.0397). vWf and soluble P-selectin (p<0.005), but not soluble E-selectin, were raised in AF, but none of the indices inter-correlated significantly. We find that sCD40L is marginally raised in AF but the stimulus for this is unclear. The lack of clear correlation with relevant plasma markers suggests that the source is unlikely to be the endothelium or platelet alone.
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