title: Soluble CD40 ligand and interleukin-6 in the coronary circulation after acute myocardial infarction.
abstract: BACKGROUND
  Inflammation, operated by blood, vascular and immune cells interaction, is implicated in plaque disruption and CD40 ligand (CD40L) was identified on activated T cells and platelets. We sought to investigate the roles of local inflammation in acute myocardial infarction (AMI).
  
  
  METHODS
  Coronary sinus (CS) and arterial (A) levels of interleukin (IL)-6 and soluble CD40L (sCD40L) and matrix metalloproteinase (MMP)-9 activity in serial blood samples obtained until 48 h after percutaneous coronary intervention (PCI) were determined. In tissue specimens obtained by aspirating thrombectomy and directional coronary atherectomy, CD40L was immunohistochemically stained.
  
  
  RESULTS
  Trans-cardiac gradient (CS-A) of IL-6, indicating cardiac release into the coronary circulation, significantly increased at 24 h after PCI in patients with AMI (group MI, n=17) in contrast with angina pectoris (n=10). Soluble CD40L levels in CS showed earlier peak, yielding trans-cardiac gradient, at 9 h in both groups. The maximum (max) release of IL-6 in MI, but not sCD40L, positively correlated with end-diastolic volume index (R=0.84) and negatively with ejection fraction (R=-0.66) by contrast ventriculography at 6-month follow up. Immunohistological study revealed the expression of CD40L in intra-coronary occlusive and mural thrombi. Aspirating thrombectomy significantly reduced the increase in both sCD40L levels and MMP-9 activity, but not max IL-6 release in MI.
  
  
  CONCLUSIONS
  In contrast with myocardial injury represented by IL-6 release, acute rise in sCD40L levels with the MMP-9 activation in the coronary circulation may possibly reflect local inflammation with platelet activation and be a novel marker of plaque damage by PCI.
authors.affiliation: Department of Cardiology, Miki City Hospital, 58-1 Kasa, Miki City 673-0402, Japan. ohashiyo@nifty.com
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Ohashi
authors.forename: Seinosuke
authors.initials: S
authors.lastname: Kawashima
authors.forename: Takao
authors.initials: T
authors.lastname: Mori
authors.forename: Mitsuyasu
authors.initials: M
authors.lastname: Terashima
authors.forename: Shinobu
authors.initials: S
authors.lastname: Ichikawa
authors.forename: Junya
authors.initials: J
authors.lastname: Ejiri
authors.forename: Kojiro
authors.initials: K
authors.lastname: Awano
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000503:physiopathology; D015906:Angioplasty, Balloon, Coronary; D017225:Atherectomy, Coronary; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D023201:CD40 Ligand / Q000378:metabolism*; D003326:Coronary Circulation; D003328:Coronary Thrombosis / Q000097:blood / Q000503:physiopathology; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000378:metabolism*; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology* / Q000628:therapy; D009205:Myocarditis / Q000097:blood / Q000503:physiopathology; D013318:Stroke Volume; D017131:Thrombectomy; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D023201:CD40 Ligand; D002097:C-Reactive Protein; D052279:Creatine Kinase, MB Form; D020780:Matrix Metalloproteinase 9