Article Text
Abstract
Background Clinical evidence suggests that intracoronary thrombus formation is associated with a high incidence of late restenosis after successful coronary intervention in patients with myocardial infarction (MI). However, little is known about the mechanism by which intracoronary thrombi play pathological roles.
Methods and Results We analysed the cellular constituents of 108 thrombi aspirated from coronary lesions with a thrombectomy device in 62 patients who underwent emergent coronary intervention for the treatment of acute (<24 h) or recent (24–72 h) ST-segment elevation MI (44 men, 18 women, aged 68.0±19.3 years). Immunohistological analysis of aspirated thrombotic materials revealed that the content of platelets, as determined by immunostaining for CD42a, had a negative correlation with the time after the onset of chest pain (correlation coefficient −0.683, p<0.01). Immunofluorescent staining for CD34 and breast cancer-resistant protein-1 (bcrp-1) detected primitive cells in intracoronary thrombi. Furthermore, the ratio of CD34-positive cells in intracoronary thrombi had a significant positive correlation with restenosis at follow-up coronary angiography (correlation coefficient 0.76, p=0.01).
Conclusions The findings of this study indicate that the early accumulation of primitive cells in platelet aggregates may play a role in neointimal growth after successful coronary intervention in patients with acute coronary syndrome.
- Primitive stem cell
- restenosis
- ST-elevation myocardial infarction
- thrombus
Statistics from Altmetric.com
Footnotes
Funding This study was supported in part by the Program for the Promotion of Basic and Applied Researches for Innovations in Bio-oriented Industry and by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan (Knowledge Cluster and New Research Area) and the Ministry of Health, Labor and Welfare of Japan.
Competing interests None.
Ethics approval This study was conducted with the approval of the ethics committee of the University of Tokyo.
Provenance and peer review Not commissioned; externally peer reviewed