title: CRP, interleukin-6, secretory phospholipase A2 group IIA, and intercellular adhesion molecule-1 during the early phase of acute coronary syndromes and long-term follow-up.
abstract: OBJECTIVE
  The objectives of this study were to examine the time course of the inflammatory response in acute coronary syndromes (ACS) and to assess the markers of inflammation and their relation to disease severity.
  
  
  METHODS
  We prospectively studied 134 patients with ACS who survived for at least 30 months. The patients were divided into four groups: acute myocardial infarction (MI) with (n=54) or without (n=46) ST-segment elevation and unstable angina with (n=14) or without (n=20) increased risk. Plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), secretory phospholipase A2 group IIA (sPLA2-IIA), and intercellular adhesion molecule-1 (ICAM-1) were measured on days 1 and 4 and after 3 and 30 months.
  
  
  RESULTS
  The highest levels of CRP and sPLA2-IIA were seen on day 4 but for IL-6 on day 1. These three markers, but not ICAM-1, were significantly related to disease severity, CKMB, and ejection fraction. Patients in Killip class II-IV had higher levels than those in Killip class I. The individual acute-phase responses correlated with marker levels at 3 and 30 months. ICAM-1 correlated with the development of congestive heart failure.
  
  
  CONCLUSIONS
  In ACS there seems to be an individual predisposition to inflammatory response. Plasma IL-6 is the first marker to rise, while sPLA2-IIA and CRP peak later. All three markers, especially CRP, may discriminate between MI and non-MI. ICAM-1 seems to reflect other aspects of the inflammatory processes than the other markers. The results emphasize the complexity of the inflammatory response in ACS and stress the need for further studies involving multiple markers.
authors.affiliation: Department of Cardiology, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. amhgbg@home.se
authors.forename: Marianne
authors.initials: M
authors.lastname: Hartford
authors.forename: Olof
authors.initials: O
authors.lastname: Wiklund
authors.forename: Lillemor
authors.initials: L
authors.lastname: Mattsson Hultén
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Perers
authors.forename: Anita
authors.initials: A
authors.lastname: Person
authors.forename: Johan
authors.initials: J
authors.lastname: Herlitz
authors.forename: Eva
authors.initials: E
authors.lastname: Hurt-Camejo
authors.forename: Thomas
authors.initials: T
authors.lastname: Karlsson
authors.forename: Kenneth
authors.initials: K
authors.lastname: Caidahl
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D003325:Coronary Care Units; D005260:Female; D005500:Follow-Up Studies; D054501:Group II Phospholipases A2; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D010741:Phospholipases A / Q000097:blood*; D054467:Phospholipases A2; D011446:Prospective Studies; D018570:Risk Assessment
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein; D010741:Phospholipases A; D054501:Group II Phospholipases A2; D054467:Phospholipases A2