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

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 abso- lute 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.