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Reduced PAF-acetylhydrolase activity associated with Lp(a) in patients with coronary artery disease

Loukas D Tsironis1, Christos S Katsouras, Evangelia S Lourida

  • 1Laboratory of Biochemistry, Department of Chemistry, Medical School, University of Ioannina, 45110 Ioannina, Greece.

Atherosclerosis
|October 19, 2004
PubMed

Insights

Lipoprotein(a) [Lp(a)] with reduced platelet activating factor acetylhydrolase (PAF-AH) activity is linked to coronary artery disease (CAD). The apo(a) component of Lp(a) in CAD patients may impair PAF-AH function, impacting atherogenesis.

Area of Science:

  • Cardiovascular Science
  • Biochemistry
  • Lipid Metabolism

Background:

  • Lipoprotein(a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD).
  • Lp(a) carries platelet activating factor acetylhydrolase (PAF-AH), an enzyme involved in hydrolyzing atherogenic lipids.
  • The role of Lp(a)-associated PAF-AH in CAD pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the mass and catalytic properties of Lp(a)-associated PAF-AH in CAD patients.
  • To compare Lp(a)-associated PAF-AH in CAD patients with controls and hypercholesterolemic patients.
  • To explore the influence of the apo(a) moiety on PAF-AH activity in Lp(a) from CAD patients.

Main Methods:

  • Enzyme assays were performed to determine the mass, specific activity, and kinetic constants of PAF-AH associated with Lp(a) and LDL.
  • Comparisons were made between 28 CAD patients, 30 controls, and 16 hypercholesterolemic patients (Type IIA).
  • Atorvastatin therapy effects were assessed in hypercholesterolemic patients. Apo(a) removal from Lp(a) was performed via reductive cleavage.

Main Results:

  • Lp(a)-associated PAF-AH exhibited significantly lower mass, specific activity, and altered kinetic constants in CAD patients compared to controls and hypercholesterolemic patients.
  • These differences were not observed for LDL-associated PAF-AH.
  • Reductive cleavage of apo(a) from Lp(a) in CAD patients significantly increased enzyme specific activity and altered kinetic constants, suggesting apo(a) impairs PAF-AH catalytic efficiency.

Conclusions:

  • Reduced PAF-AH mass and specific activity on Lp(a) are characteristic features in CAD patients.
  • The apo(a) moiety of Lp(a) in CAD patients appears to play a crucial role in the diminished catalytic efficiency of associated PAF-AH.
  • This impaired enzyme function may reduce Lp(a)'s capability to degrade proinflammatory phospholipids, potentially contributing to atherosclerosis, though further investigation is needed.

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