title: Inflammatory and vasoactive factors in the aspirate from the culprit coronary artery of patients with acute myocardial infarction.
abstract: BACKGROUND
  Besides distal embolization of thrombus and plaque debris, locally increased inflammatory markers at the site of ruptured plaque in acute myocardial infarction (AMI) are thought to have an adverse impact on myocardial reperfusion during primary percutaneous coronary intervention (PCI). However, there is lack of data on such factors. Therefore, we investigated the presence of locally increased inflammatory and vasoactive factors in culprit coronary artery.
  
  
  METHODS
  We performed primary PCI with PercuSurge GuideWire system in 18 AMI patients. We collected blood samples from the femoral artery before PCI and from culprit coronary artery after first predilation while inflating the distal protection balloon and after completing PCI. We determined concentrations of C-reactive protein, soluble CD40 ligand, Interleukin (IL-6), serotonin, tissue factor, and factor VIIa.
  
  
  RESULTS
  While the concentrations of soluble CD40 ligand (2.84+/-3.74 vs 0.98+/-0.63 ng/mL, p=0.004), IL-6 (33.67+/-32.63 vs 17.08+/-21.41 pg/mL, p<0.001), serotonin (2.05+/-0.76 vs 0.92+/-0.60 ng/mL, p<0.001), tissue factor (257.17+/-84.34 vs 154.60+/-87.99 pg/mL, p<0.001) and factor VIIa (34.30+/-27.30 vs 24.19+/-28.00 ng/mL, p=0.016) were significantly higher in the culprit coronary artery than in the femoral artery, CRP levels did not differ. The locally elevated concentrations of various factors were successfully reduced after multiple aspirations of blood using the PercuSurge GuideWire system.
  
  
  CONCLUSIONS
  We found increased levels of soluble CD40 ligand, IL-6, serotonin, tissue factor and factor VII in the culprit coronary artery compared to those in peripheral blood. The clinical impact of such locally increased soluble factors in the culprit coronary artery needs to be investigated in further studies.
authors.affiliation: Cardiology Division, Yonsei Cardiovascular Center and Cardiovascular Research Institute, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul, 120-752 Republic of Korea. ygko@yumc.yonsei.ac.kr
authors.forename: Young-Guk
authors.initials: YG
authors.lastname: Ko
authors.forename: Jae-Hun
authors.initials: JH
authors.lastname: Jung
authors.forename: Sungha
authors.initials: S
authors.lastname: Park
authors.forename: Euiyoung
authors.initials: E
authors.lastname: Choi
authors.forename: Boyoung
authors.initials: B
authors.lastname: Joung
authors.forename: Ki-Chul
authors.initials: KC
authors.lastname: Hwang
authors.forename: Jong-Won
authors.initials: JW
authors.lastname: Ha
authors.forename: Donghoon
authors.initials: D
authors.lastname: Choi
authors.forename: Yangsoo
authors.initials: Y
authors.lastname: Jang
authors.forename: Namsik
authors.initials: N
authors.lastname: Chung
authors.forename: Won-Heum
authors.initials: WH
authors.lastname: Shim
authors.forename: Seung-Yun
authors.initials: SY
authors.lastname: Cho
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D023201:CD40 Ligand / Q000097:blood; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000378:metabolism*; D015942:Factor VIIa / Q000378:metabolism; D005260:Female; D005263:Femoral Artery / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000628:therapy*; D012701:Serotonin / Q000097:blood; D013925:Thromboplastin / Q000378:metabolism
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D023201:CD40 Ligand; D012701:Serotonin; D002097:C-Reactive Protein; D013925:Thromboplastin; D015942:Factor VIIa