title: Erythrocyte-rich thrombus aspirated from patients with ST-elevation myocardial infarction: association with oxidative stress and its impact on myocardial reperfusion.
abstract: OBJECTIVE
  Recent studies have demonstrated that erythrocytes are a potential component in atheromatous lesions and thrombus formation in patients with ST-elevation myocardial infarction (STEMI). The purpose of this study was to determine the associations of red blood cell (RBC) component of coronary thrombi with oxidative stress and myocardial reperfusion.
  
  
  RESULTS
  Aspirated thrombi from 178 STEMI patients within 12 h of symptom onset were investigated immunohistochemically using antibodies against platelets, RBCs, fibrin, macrophages, and neutrophils [myeloperoxidase (MPO)]. The thrombi were divided into tertiles according to the percentage of glycophorin-A-positive area: low (glycophorin-A-positive area <33%; n = 60), intermediate (<54 to 33%; n = 59), and high group (≥54%; n = 59). We also measured plasma MPO levels on admission. In the thrombi, the number of MPO-positive cells in the high-RBC group was significantly greater than that in the low-RBC group (high, 927 ± 385; intermediate, 765 ± 406; low, 279 ± 220 cells/mm(2); P< 0.0001). Plasma MPO levels were significantly higher in the high-RBC group than that in the low-RBC group [low 43.1 (25.0-71.6); intermediate 71.0 (32.9-111.2); high 74.3 (31.1-126.4)ng/mL; P< 0.005]. Distal embolization occurred more frequently in the high-RBC group (P= 0.0009). Moreover, the signs of impaired myocardial reperfusion, as indicated by incomplete ST-segment resolution (STR) and lower myocardial blush grades (MBG), and progression of left ventricular remodelling at 6 months were frequently observed in the high-RBC group (high vs. low: STR, P= 0.056; MBG, P< 0.01; remodelling, P< 0.01).
  
  
  CONCLUSIONS
  The present study demonstrated that erythrocyte-rich thrombi contain more inflammatory cells and reflect high thrombus burden, leading to impaired myocardial reperfusion in STEMI patients.
authors.affiliation: Department of Cardiology, Osaka City General Hospital, Osaka, Japan.
authors.forename: Kei
authors.initials: K
authors.lastname: Yunoki
authors.forename: Takahiko
authors.initials: T
authors.lastname: Naruko
authors.forename: Kenichi
authors.initials: K
authors.lastname: Sugioka
authors.forename: Mayumi
authors.initials: M
authors.lastname: Inaba
authors.forename: Yoko
authors.initials: Y
authors.lastname: Iwasa
authors.forename: Ryushi
authors.initials: R
authors.lastname: Komatsu
authors.forename: Akira
authors.initials: A
authors.lastname: Itoh
authors.forename: Kazuo
authors.initials: K
authors.lastname: Haze
authors.forename: Takeshi
authors.initials: T
authors.lastname: Inoue
authors.forename: Minoru
authors.initials: M
authors.lastname: Yoshiyama
authors.forename: Anton E
authors.initials: AE
authors.lastname: Becker
authors.forename: Makiko
authors.initials: M
authors.lastname: Ueda
mesh_terms: D015906:Angioplasty, Balloon, Coronary / Q000379:methods; D017023:Coronary Angiography / Q000379:methods; D003328:Coronary Thrombosis / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D004912:Erythrocytes / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000379:methods; D018384:Oxidative Stress / Q000502:physiology*; D017131:Thrombectomy / Q000379:methods; D016896:Treatment Outcome; D020257:Ventricular Remodeling / Q000502:physiology