title: Increasing levels of interleukin (IL)-1Ra and IL-6 during the first 2 days of hospitalization in unstable angina are associated with increased risk of in-hospital coronary events.
abstract: BACKGROUND
  A growing body of evidence suggests a role for inflammation in acute coronary syndromes. The aim of this study was to assess the role of proinflammatory cytokines, their time course, and their association with prognosis in unstable angina.
  
  
  RESULTS
  We studied 43 patients aged 62+/-8 years admitted to our coronary care unit for Braunwald class IIIB unstable angina. In each patient, serum levels of interleukin-1 receptor antagonist (IL-1Ra), interleukin-6 (IL-6) (which represent sensitive markers of biologically active IL-1beta and tumor necrosis factor-alpha levels, respectively), and troponin T were measured at entry and 48 hours after admission. Troponin T-positive patients were excluded. Patients were divided a posteriori into 2 groups according to their in-hospital outcome: group 1 comprised 17 patients with an uneventful course, and group 2 comprised 26 patients with a complicated in-hospital course. In group 1, mean IL-1Ra decreased at 48 hours by 12%, and IL-6 diminished at 48 hours by 13%. In group 2, IL-1Ra and IL-6 entry levels were higher than in group 1 and increased respectively by 37% and 57% at 48 hours (P<0.01).
  
  
  CONCLUSIONS
  These findings indicate that although they receive the same medical therapy as patients who do not experience an in-hospital event, patients with unstable angina and with complicated in-hospital courses have higher cytokine levels on admission. A fall in IL-1Ra and IL-6 48 hours after admission was associated with an uneventful course and their increase with a complicated hospital course. These findings may suggest novel therapeutic approaches to patients with unstable angina.
authors.affiliation: Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy. biasucci@pelagus.it
authors.forename: L M
authors.initials: LM
authors.lastname: Biasucci
authors.forename: G
authors.initials: G
authors.lastname: Liuzzo
authors.forename: G
authors.initials: G
authors.lastname: Fantuzzi
authors.forename: G
authors.initials: G
authors.lastname: Caligiuri
authors.forename: A G
authors.initials: AG
authors.lastname: Rebuzzi
authors.forename: F
authors.initials: F
authors.lastname: Ginnetti
authors.forename: C A
authors.initials: CA
authors.lastname: Dinarello
authors.forename: A
authors.initials: A
authors.lastname: Maseri
mesh_terms: D000789:Angina, Unstable / Q000097:blood* / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D003325:Coronary Care Units; D003327:Coronary Disease / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D005260:Female; D006760:Hospitalization; D006801:Humans; D007297:Inpatients; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D012307:Risk Factors; D012680:Sensitivity and Specificity; D012795:Sialoglycoproteins / Q000097:blood*; D013997:Time Factors; D020107:Troponin T / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D015850:Interleukin-6; D017472:Receptors, Interleukin-1; D012795:Sialoglycoproteins; D020107:Troponin T; D014409:Tumor Necrosis Factor-alpha