title: Inflammatory markers at the site of ruptured plaque in acute myocardial infarction: locally increased interleukin-6 and serum amyloid A but decreased C-reactive protein.
abstract: BACKGROUND
  Acute myocardial infarction (AMI) is associated with inflammation. However, it remains unclear whether it originates from the ruptured plaque or represents a systemic process.
  
  
  RESULTS
  In 42 patients with AMI, a balloon-based embolization protection device and aspiration catheter (PercuSurge) were used during acute coronary interventions. Samples from the site of the ruptured plaque were taken under distal balloon occlusion. Systemic samples were taken from the aorta. Sera, plaques, and thrombi were analyzed for inflammatory markers and lipoproteins. Systemic levels of C-reactive protein (CRP), interleukin-6 (IL-6), and serum amyloid A (SAA) in the aorta amounted to 3.0 mg/L, 5.0 ng/L, and 22.1 mg/L, respectively (interquartile ranges [IQRs], 1.1 to 7.4 mg/L, 5.0 to 6.5 ng/L, and 13.9 to 27.0 mg/L, respectively). In blood surrounding ruptured plaques, local levels of IL-6 (8.9 ng/L; IQR, 5.0 to 16.9 ng/L) and SAA (24.3 mg/L; IQR, 16.3 to 44.0 mg/L) were significantly higher, whereas CRP levels (2.5 mg/L; IQR, 0.9 to 7.7 mg/L) were decreased compared with the aorta (all P<0.0001). The coronary levels of IL-6 determined in vivo showed biological activity in vitro. Harvested thrombus contained CD68-positive monocytes expressing IL-6 and showed extracellularly and intracellularly positive staining for SAA, whereas CRP was found exclusively in the cytoplasm of phagocyting white blood cells.
  
  
  CONCLUSIONS
  Coronary levels of IL-6 and SAA at the site of plaque rupture were increased relative to the systemic circulation, indicating local production of biologically active inflammatory mediators. In contrast, CRP was locally decreased, at least in part by uptake by the phagocyting cells, suggesting a systemic origin of the protein.
authors.affiliation: Division of Cardiology, University Hospital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland. karmaiew@usz.unizh.ch
authors.forename: Willibald
authors.initials: W
authors.lastname: Maier
authors.forename: Lukas A
authors.initials: LA
authors.lastname: Altwegg
authors.forename: Roberto
authors.initials: R
authors.lastname: Corti
authors.forename: Steffen
authors.initials: S
authors.lastname: Gay
authors.forename: Martin
authors.initials: M
authors.lastname: Hersberger
authors.forename: Friedrich E
authors.initials: FE
authors.lastname: Maly
authors.forename: Gabor
authors.initials: G
authors.lastname: Sütsch
authors.forename: Marco
authors.initials: M
authors.lastname: Roffi
authors.forename: Michel
authors.initials: M
authors.lastname: Neidhart
authors.forename: Franz R
authors.initials: FR
authors.lastname: Eberli
authors.forename: Felix C
authors.initials: FC
authors.lastname: Tanner
authors.forename: Sharon
authors.initials: S
authors.lastname: Gobbi
authors.forename: Arnold
authors.initials: A
authors.lastname: von Eckardstein
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Lüscher
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001011:Aorta / Q000737:chemistry; D001161:Arteriosclerosis / Q000378:metabolism*; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis*; D003328:Coronary Thrombosis / Q000378:metabolism; D003331:Coronary Vessels / Q000737:chemistry; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis* / Q000097:blood; D008074:Lipoproteins / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism* / Q000628:therapy; D009928:Organ Specificity; D012422:Rupture, Spontaneous; D000685:Serum Amyloid A Protein / Q000032:analysis*
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D008074:Lipoproteins; D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein