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

Circulation
|November 9, 2000
PubMed

Insights

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.
Abstract