Aspirin, but not clopidogrel, reduces collateral conductance in a rabbit model of femoral artery occlusion

J Am Coll Cardiol. 2005 Sep 20;46(6):994-1001. doi: 10.1016/j.jacc.2005.02.094.

Abstract

Objectives: The objective of this study was to test the potential of aspirin and clopidogrel to influence collateral artery growth (arteriogenesis).

Background: Aspirin and clopidogrel are antiplatelet agents commonly used in the treatment of ischemic cardiovascular disease. Both inhibit platelet aggregation; however, they differ mechanistically because aspirin acts via cyclooxygenase (COX) inhibition, while clopidogrel noncompetitively antagonizes the P2Y12 adenosine diphosphate receptor. We hypothesized that aspirin, due to its anti-inflammatory effects through inhibition of COX activity could inhibit arteriogenesis. Given that clopidogrel does not affect COX activity, it would be less likely to interfere with collateral artery growth.

Methods: Fifty-four New Zealand White rabbits received either saline, aspirin (10 mg/kg), or clopidogrel (10 mg/kg) for seven days after femoral artery ligation. Maximal collateral conductance was assessed with fluorescent microspheres under maximal vasodilation; cellular migration and proliferation (Ki-67) was evaluated by quantitative immunohistology.

Results: Collateral conductance was significantly reduced by aspirin treatment, whereas clopidogrel had a neutral effect (saline: 0.94 +/- 0.04; clopidogrel: 0.94 +/- 0.05; aspirin: 0.64 +/- 0.03 ml x min(-1) x 100 mm Hg(-1) x g(-1); p < 0.001). Ki-67 proliferation indexes were consistent with these results (saline: 23.1 +/- 2.9%; clopidogrel: 23.5 +/- 1.1%; aspirin: 19.2 +/- 1.1% Ki-67-positive cells). Immunohistochemistry showed COX expression in collateral arteries and a significantly decreased monocyte/macrophage accumulation in the perivascular tissue after aspirin treatment. Cell adhesion molecule expression on monocytes after activation was significantly reduced by aspirin, which might explain the reduced migratory ability.

Conclusions: In summary, clopidogrel had a neutral effect on natural arteriogenesis. Aspirin significantly inhibited collateral artery growth, probably due to its anti-inflammatory effect. Additional studies are needed to substantiate these results before translation into clinical practice.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arterial Occlusive Diseases / drug therapy*
  • Arterial Occlusive Diseases / physiopathology*
  • Aspirin / therapeutic use*
  • Clopidogrel
  • Disease Models, Animal*
  • Electrophysiology
  • Femoral Artery / drug effects*
  • Femoral Artery / physiopathology*
  • Rabbits
  • Ticlopidine / analogs & derivatives*
  • Ticlopidine / therapeutic use

Substances

  • Clopidogrel
  • Ticlopidine
  • Aspirin