title: Impact of primitive cells in intracoronary thrombi on lesion prognosis: temporal analysis of cellular constituents of thrombotic material obtained from patients with acute coronary syndrome.
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.
  
  
  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.
authors.affiliation: Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. hiroiwata-circ@umin.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iwata
authors.forename: Masataka
authors.initials: M
authors.lastname: Sata
authors.forename: Jiro
authors.initials: J
authors.lastname: Ando
authors.forename: Hideo
authors.initials: H
authors.lastname: Fujita
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Morita
authors.forename: Daigo
authors.initials: D
authors.lastname: Sawaki
authors.forename: Masao
authors.initials: M
authors.lastname: Takahashi
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Hirata
authors.forename: Shuichiro
authors.initials: S
authors.lastname: Takanashi
authors.forename: Minoru
authors.initials: M
authors.lastname: Tabata
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Hirata
authors.forename: Ryozo
authors.initials: R
authors.lastname: Nagai
mesh_terms: D000070997:ATP Binding Cassette Transporter, Subfamily G, Member 2; D018528:ATP-Binding Cassette Transporters / Q000378:metabolism; D054058:Acute Coronary Syndrome / Q000378:metabolism / Q000473:pathology* / Q000628:therapy; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D018952:Antigens, CD34 / Q000378:metabolism; D023903:Coronary Restenosis / Q000473:pathology; D003328:Coronary Thrombosis / Q000378:metabolism / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D009363:Neoplasm Proteins / Q000378:metabolism; D010974:Platelet Aggregation; D011379:Prognosis; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*; D017131:Thrombectomy
chemical_list: C116614:ABCG2 protein, human; D000070997:ATP Binding Cassette Transporter, Subfamily G, Member 2; D018528:ATP-Binding Cassette Transporters; D018952:Antigens, CD34; D009363:Neoplasm Proteins