title: Systemic inflammatory responses in acute coronary syndrome: increased activity observed in polymorphonuclear leukocytes but not T lymphocytes.
abstract: BACKGROUND
  Local inflammation within the coronary arteries is involved in the pathogenesis of acute coronary syndrome. However, the contribution of a systemic inflammatory response to the pathogenesis of this syndrome has not been well characterized. Accordingly, we investigated systemic inflammatory responses in patients with acute coronary syndrome.
  
  
  METHODS
  A total of 83 patients with ischemic heart disease (15 with stable exertional angina and 68 with acute coronary syndrome) were studied. The luminol-dependent chemiluminescence (CL) response of polymorphonuclear leukocytes (PMNs), which reflects their ability to generate oxygen species, was used as a marker for PMN activation. Soluble interleukin-2 receptor (sIL-2R) levels were measured to assess T-lymphocyte activation.
  
  
  RESULTS
  CL counts of whole blood from patients with acute coronary syndrome were twice those of patients with stable angina (2.38 +/- 0.22 vs 1.10 +/- 0.17 x 10(6) counts, P < 0.05). A comparison of CL counts between patients with unstable angina and those with acute myocardial infarction revealed no significant differences. T-lymphocyte activity, measured by serum sIL-2R, was significantly lower in patients with acute coronary syndrome than those with stable angina (214.3 +/- 11.5 vs. 358.3 +/- 115.7 U/ml, P < 0.05).
  
  
  CONCLUSIONS
  This investigation shows that there is a systemic increase in PMN activity and a decrease in T-lymphocyte activity in patients with acute coronary syndrome. This contrasts with the pattern of cellular activation seen at sites of local inflammation within atherosclerotic plaques, suggesting that two independent inflammatory processes (local and systemic) may be involved in the pathogenesis of this syndrome.
authors.affiliation: Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan. satoshi-t@in.aix.or.jp
authors.forename: S
authors.initials: S
authors.lastname: Takeshita
authors.forename: T
authors.initials: T
authors.lastname: Isshiki
authors.forename: M
authors.initials: M
authors.lastname: Ochiai
authors.forename: T
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Nishiyama
authors.forename: T
authors.initials: T
authors.lastname: Fusano
authors.forename: H
authors.initials: H
authors.lastname: Toyoizumi
authors.forename: K
authors.initials: K
authors.lastname: Kondo
authors.forename: Y
authors.initials: Y
authors.lastname: Ono
authors.forename: T
authors.initials: T
authors.lastname: Sato
mesh_terms: D000208:Acute Disease; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000276:immunology / Q000473:pathology; D003327:Coronary Disease / Q000097:blood / Q000276:immunology / Q000473:pathology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000276:immunology / Q000473:pathology; D008163:Luminescent Measurements; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000276:immunology / Q000473:pathology; D017202:Myocardial Ischemia / Q000097:blood / Q000276:immunology / Q000473:pathology; D009504:Neutrophils / Q000473:pathology*; D015375:Receptors, Interleukin-2 / Q000097:blood; D013577:Syndrome; D013601:T-Lymphocytes / Q000473:pathology*
chemical_list: D015375:Receptors, Interleukin-2