title: Systemic inflammation in unstable angina is the result of myocardial necrosis.
abstract: OBJECTIVE
  We investigated whether the source of the acute phase response in unstable angina (UA) lay within the culprit coronary plaque or distal myocardium.
  
  
  BACKGROUND
  An inflammatory response is an important component of the acute coronary syndromes. However, its origin and mechanism remain unclear.
  
  
  METHODS
  In 94 stable patients undergoing coronary angiography, the relationship between systemic levels of tumor necrosis factor (TNF)-alpha, interleukin-6 (IL-6) and C-reactive protein (CRP) and extent of atherosclerosis was studied. The temporal relationship between these markers and troponin T (TnT) was determined in 91 patients with UA. Cytokine levels were measured in the aortic root and coronary sinus of 36 unstable patients.
  
  
  RESULTS
  There was no relationship found between stable coronary atherosclerosis and inflammatory marker levels. Compared with this group, admission levels of IL-6 (3.6 +/- 0.3 ng/ml vs. 10.7 +/- 1.7 ng/ml, p < 0.05) and CRP (2.3 +/- 0.1 mg/l vs. 4.6 +/- 0.6 mg/l, p < 0.05) were elevated in patients with UA. In this group, IL-6 and CRP remained elevated in those who subsequently experienced major adverse cardiac events. This inflammatory response occurred in parallel to the appearance of TnT. Both TNF-alpha (19.2 +/- 3.4 ng/ml vs. 17.1 +/- 3.3 ng/ml, p < 0.001) and IL-6 (10.3 +/- 1.4 ng/ml vs. 7.7 +/- 1.1 ng/ml, p < 0.01) were elevated in the coronary sinus compared with aortic root in patients with UA. This was principally observed in those who were TnT positive. There was no cytokine gradient across the culprit plaque.
  
  
  CONCLUSIONS
  There is an intracardiac inflammatory response in UA that appears to be the result of low-grade myocardial necrosis. The ruptured plaque does not appear to contribute to the acute phase response.
authors.affiliation: Department of Cardiology, Rayne Institute, St. Thomas' Hospital, London, United Kingdom.
authors.forename: Michael R
authors.initials: MR
authors.lastname: Cusack
authors.forename: Michael S
authors.initials: MS
authors.lastname: Marber
authors.forename: Pier D
authors.initials: PD
authors.lastname: Lambiase
authors.forename: Clifford A
authors.initials: CA
authors.lastname: Bucknall
authors.forename: Simon R
authors.initials: SR
authors.lastname: Redwood
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000378:metabolism / Q000473:pathology*; D002097:C-Reactive Protein / Q000032:analysis; D017023:Coronary Angiography; D005260:Female; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D011446:Prospective Studies; D020107:Troponin T / Q000032:analysis
chemical_list: D015850:Interleukin-6; D020107:Troponin T; D002097:C-Reactive Protein