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Effect of atorvastatin on peripheral endothelial function and systemic inflammatory markers in patients with stable

Hannes Franz Alber1, Matthias Frick, Alois Süssenbacher

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

Wiener Medizinische Wochenschrift (1946)
|March 7, 2007
PubMed

Insights

Atorvastatin therapy improved endothelial function and reduced inflammatory markers in patients with stable coronary artery disease (CAD). These findings suggest potential pleiotropic effects of statins beyond lipid-lowering.

Area of Science:

  • Cardiology
  • Pharmacology
  • Vascular Biology

Background:

  • Endothelial dysfunction, indicated by impaired flow-mediated vasodilation (FMD), is linked to elevated proinflammatory markers.
  • Statins improve FMD and reduce inflammatory markers, but atorvastatin's effect on both in stable coronary artery disease (CAD) patients is unstudied.

Purpose of the Study:

  • To investigate the impact of atorvastatin on endothelial function (FMD) and inflammatory markers in patients with stable CAD.
  • To determine if atorvastatin therapy influences soluble intercellular adhesion molecule-1 (sICAM-1), high-sensitivity C-reactive protein (hsCRP), and soluble E-selectin.

Main Methods:

  • Thirty hypercholesterolemic patients with stable CAD were randomized to 3 months of placebo or atorvastatin (20 mg/d).
  • Flow-mediated vasodilation (FMD) was assessed via high-resolution ultrasound.
  • hsCRP, sE-selectin, and sICAM-1 levels were measured using specific assays (Latex agglutination, ELISA).

Main Results:

  • Atorvastatin significantly improved FMD (6.7% to 8.5%, p<0.01), while placebo showed no change (8.2% to 8.9%, p=NS).
  • Atorvastatin reduced sICAM-1 (274.2 to 197.9 ng/ml, p<0.01) and hsCRP (0.57 to 0.18 mg/dl, p<0.01); placebo had no effect.
  • sE-selectin levels were not significantly altered by either treatment. No correlations were found between FMD changes and inflammatory markers or lipids.

Conclusions:

  • Atorvastatin treatment enhances endothelial function and decreases inflammatory markers in stable CAD patients.
  • The lack of correlation between FMD and inflammatory marker changes suggests potential pleiotropic effects of atorvastatin beyond lipid reduction.
Abstract

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