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Endothelial activation in patients with cardiac syndrome X
G Desideri1, A Gaspardone, M Gentile
1Department of Internal Medicine and Public Health, University of L'Aquila, L'Aquila, Italy. gbdesi@freemail.it
Patients with cardiac syndrome X show normal baseline endothelin-1 levels. However, glucose loading reveals increased endothelin-1 release, suggesting heightened susceptibility in these patients.
Area of Science:
- Cardiology
- Vascular Biology
- Endocrinology
Background:
- Cardiac syndrome X is characterized by angina and ischemia despite normal coronary angiograms.
- Endothelial dysfunction and elevated endothelin-1 levels in these patients remain debated.
- Assessing endothelial function markers is crucial for understanding cardiac syndrome X pathophysiology.
Purpose of the Study:
- To evaluate endothelial dysfunction in patients with cardiac syndrome X.
- To investigate endothelin-1 plasma concentrations under baseline and post-glucose load conditions.
- To assess nitric oxide production and adhesion molecule levels as markers of endothelial health.
Main Methods:
- Radioimmunoassay and HPLC were used to measure endothelin-1 levels.
- Plasma nitrite-plus-nitrate and soluble vascular cell adhesion molecule-1 were quantified.
- 24 patients with cardiac syndrome X and 14 healthy controls were studied under baseline and post-glucose load conditions.
Main Results:
- No significant differences in baseline endothelin-1, nitrite-plus-nitrate, or soluble vascular cell adhesion molecule-1 between patients and controls.
- Significantly higher endothelin-1 concentrations were observed in patients post-glucose ingestion compared to controls.
- This suggests an altered endothelin-1 response to metabolic stress in cardiac syndrome X.
Conclusions:
- Patients with cardiac syndrome X do not exhibit basal endothelial damage.
- Increased endothelin-1 responsiveness to glucose loading indicates a heightened susceptibility to its release under stress.
- These findings highlight a potential role for endothelin-1 dysregulation in the pathophysiology of cardiac syndrome X.
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