Progression of non-culprit coronary artery atherosclerosis after acute myocardial infarction in comparison with stable angina pectoris

J Atheroscler Thromb. 2008 Oct;15(5):228-34. doi: 10.5551/jat.e539.

Abstract

Aim: We previously found, using a mouse model, that activation of proinflammatory cytokines after acute myocardial infarction (AMI) augments neointimal hyperplasia of a remote artery. The present study assessed the progression of luminal narrowing of non-culprit coronary arteries (NCCA) in patients following AMI.

Methods: The study group comprised 21 AMI patients successfully treated with bare-metal stents and 16 stable angina (SA) patients treated with sirolimus-eluting stents. Clinical backgrounds were similar for both groups. Quantitative coronary angiography was performed before and after stent implantation and at 6-months of follow-up.

Results: We evaluated 126 non-culprit coronary segments (73 in AMI and 53 in SA). The minimum lumen diameter (MLD) (mm) of NCCA decreased significantly from 2.61+/-0.79 to 2.44+/-0.71 in the AMI group, but changed only slightly from 2.02+/-0.56 to 2.02+/-0.50 in the SA group. The absolute change in the MLD of NCCA was significantly greater (0.17+/-0.53) in the AMI, than in the SA (0.0070+/-0.261) group.

Conclusion: luminal narrowing of non-culprit coronary segments progressed in AMI patients within 6 months of stent implantation, but progressed only slightly in SA patients.

Publication types

  • Comparative Study

MeSH terms

  • Aged
  • Angina Pectoris / pathology*
  • Angina Pectoris / therapy
  • Coronary Angiography
  • Coronary Artery Disease / pathology*
  • Coronary Artery Disease / therapy
  • Disease Progression
  • Drug-Eluting Stents
  • Female
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction*
  • Stents
  • Treatment Outcome