Association between plasma thiols and immune activation marker neopterin in stable coronary heart disease

Katharina Schroecksnadel1, Roland B Walter, Guenter Weiss

  • 1Department of General Internal Medicine, Innsbruck Medical University, Innsbruck, Austria.

Insights

Elevated total cysteine levels correlate with the severity of coronary artery sclerosis, while total homocysteine does not appear to be a direct marker in stable coronary artery disease patients. These thiol markers may be interdependent with inflammation.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry
  • Immunology

Background:

  • Elevated plasma homocysteine and cysteine are linked to atherosclerosis risk.
  • The relationship between these thiols, inflammation, and sclerosis severity requires further investigation.

Purpose of the Study:

  • To investigate the association between plasma thiol levels (homocysteine, cysteine) and systemic inflammatory markers (neopterin, CRP) in patients with coronary artery disease (CAD).
  • To determine if thiol levels correlate with the extent of coronary artery sclerosis.

Main Methods:

  • Measured total homocysteine, total cysteine, neopterin, and C-reactive protein (CRP) in 242 patients undergoing coronary angiography.
  • Categorized patients into those with significant coronary artery disease (CAD) and controls without relevant stenoses.

Main Results:

  • Total cysteine concentrations were significantly higher in patients with coronary artery sclerosis and increased with sclerosis severity (p < 0.001).
  • Total homocysteine and inflammatory markers (CRP, neopterin) did not differ between groups.
  • Total homocysteine correlated with total cysteine, neopterin, and serum creatinine, indicating kidney function dependence.

Conclusions:

  • Total cysteine is a suitable marker for estimating the extent of coronary artery sclerosis.
  • In stable CAD patients, total homocysteine was not elevated compared to controls.
  • The interdependence of homocysteine, cysteine, and inflammatory markers suggests a complex interplay in CAD pathogenesis.
Abstract

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