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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Elevated circulating soluble form of CD40 ligand in patients with cardiac syndrome X
Alberto Dominguez-Rodriguez1, Pedro Abreu-Gonzalez, Pablo Avanzas
1Hospital Universitario de Canarias, Department of Cardiology, Tenerife, Spain. adrvdg@hotmail.com
Insights
Soluble CD40 ligand (sCD40L) levels are elevated in patients with cardiac syndrome X (CSX) and correlate with ischemic burden. This finding suggests sCD40L may play a role in CSX pathogenesis.
Area of Science:
- Cardiology
- Immunology
- Pathophysiology
Background:
- Cardiac syndrome X (CSX) is characterized by angina, positive exercise tests, and normal coronary arteries.
- Its pathogenesis is linked to endothelial dysfunction and microcirculation issues, but remains unclear.
- Soluble CD40 ligand (sCD40L) may contribute to endothelial dysfunction and atherothrombosis.
Purpose of the Study:
- To investigate the association between sCD40L levels and ischemic burden in CSX patients.
- To compare sCD40L levels in CSX patients versus healthy controls.
Main Methods:
- 30 CSX patients and 28 controls underwent myocardial perfusion scintigraphy to assess ischemic burden.
- White blood cells, sCD40L, and C-reactive protein (CRP) were measured at peak exercise.
Main Results:
- CSX patients had significantly higher sCD40L, white blood cell count, and CRP levels than controls.
- sCD40L was the sole independent predictor of severe ischemic burden in CSX patients after multivariable adjustment.
Conclusions:
- This study demonstrates a novel association between sCD40L and ischemic burden in CSX.
- The inflammatory role of sCD40L in CSX pathogenesis warrants further investigation.
Background:
The presence of effort induced angina, positive exercise stress test responses and angiographically normal coronary arteries defines cardiac syndrome X (CSX). Its pathogenesis, although mostly attributed to endothelial dysfunction and coronary microcirculation abnormalities, is incompletely understood. The soluble CD40 ligand (sCD40L) has multiple autocrine, paracrine and endocrine actions that may lead to endothelial dysfunction and atherothrombosis. We sought to investigate the relationship among sCD40L levels and ischemic burden in patients with CSX and whether sCD40L levels are increased in patients with CSX compared to control subjects.
Methods:
We assessed 30 prospectively enrolled patients with CSX and 28 apparently healthy subjects matched for coronary risk factors. All CSX patients and control subjects underwent myocardial perfusion scintigraphy. The summed difference score is taken to be an index of ischemic burden. This was classified as mildly, moderately and severely abnormal. White blood cells, sCD40L and C-reactive protein (CRP) concentrations were measured at peak exercise.
Results:
At peak exercise, sCD40L levels were significantly greater in CSX patients than in the control group (P=0.008). Similarly, white blood cell count and CRP levels were higher in patients with CSX than in normal controls (P=0.02). After multivariable adjustment, sCD40L (P=0.03) was the only independent predictor of severe ischemic burden in CSX patients.
Conclusions:
The present study showed for the first time that sCD40L is associated with ischemic burden in patients with CSX. The potential role of this inflammatory molecule in the pathogenesis of CSX deserves investigation in future studies.
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