Serum Galectin-3 Levels Correlate with Reduced Vascular Reactivity in Patients with Coronary Artery Disease

Po-Yu Huang1,2, Min-Han Hsieh3, Ji-Hung Wang3,4,5

  • 1Division of Nephrology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi 62247, Taiwan.

Insights

Higher serum galectin-3 levels are linked to poorer vascular reactivity and endothelial dysfunction in coronary artery disease (CAD) patients. This finding suggests galectin-3 as a potential biomarker for CAD progression and complications.

Area of Science:

  • Cardiovascular Research
  • Biomarker Discovery
  • Endothelial Function

Background:

  • Endothelial dysfunction is a key factor in coronary artery disease (CAD) development and progression.
  • Galectin-3 contributes to inflammation, fibrosis, and endothelial dysfunction.
  • Vascular reactivity index (VRI) is a measure of endothelial function.

Purpose of the Study:

  • To investigate the association between serum galectin-3 levels and VRI in patients with CAD.
  • To determine if galectin-3 is an independent predictor of endothelial dysfunction in CAD.

Main Methods:

  • 118 CAD patients were enrolled.
  • Endothelial function was assessed noninvasively using digital thermal monitoring to obtain VRIs.
  • Serum galectin-3 levels were quantified via enzyme-linked immunosorbent assay.

Main Results:

  • Patients with poor vascular reactivity were older and had higher levels of total cholesterol, LDL cholesterol, and galectin-3.
  • Galectin-3 was independently associated with lower VRIs (β = -0.488, p < 0.001).
  • Elevated galectin-3 correlated with increased odds of vascular reactivity dysfunction (OR=1.120) and poor vascular reactivity (OR=1.445).

Conclusions:

  • Serum galectin-3 is independently associated with reduced VRIs in CAD patients.
  • Elevated galectin-3 levels indicate endothelial dysfunction in individuals with coronary artery disease.
  • Galectin-3 may serve as a valuable biomarker for assessing endothelial health in CAD.

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