title: Instability mechanisms in unstable angina according to baseline serum levels of C-reactive protein: the role of thrombosis, fibrinolysis and atherosclerotic burden.
abstract: BACKGROUND
  Mechanisms of instability in patients affected by unstable angina and who exhibit low levels of C-reactive protein (CRP) on admission are unclear. We compared levels of markers of thrombin generation [thrombin-antithrombin complexes (TAT), of fibrinolysis [plasmin-antiplasmin complexes (PAP)], and angiographic severity and extent of coronary atherosclerosis in patients with severe unstable angina and high or low systemic levels of CRP.
  
  
  METHODS
  Forty consecutive patients (age 59.7+/-8.7, 76% males) admitted to our coronary care unit with severe unstable angina (Braunwald class IIIB) were included in the present study. We assayed TAT and PAP using commercially available ELISA assays and CRP with high sensitivity nephelometry. The evaluation of atherosclerotic disease severity and extent was performed. Patients were divided in two groups according to CRP levels: G1=CRP>3 mg/L and G2=CRP<3 mg/L.
  
  
  RESULTS
  Number of diseased vessels and number of stenoses plus occlusion were similar between the two groups (1.8+/-0.9 in G1 vs 2.2+/-0.9 in G2, p=NS and 2.6+/-1.9 in G1 vs 2.7+/-1.3 in G2, p=NS, respectively), as well as extent score and index (8.4+/-4.5 in G1 vs 9.2+/-3.1 in G2, p=NS and 0.6+/-0.3 in G1 vs 0.6+/-0.27 in G2, p=NS, respectively). Episodic activation of thrombin generation, as assessed by TAT was more frequent in G1 than in G2 (85% vs 47%, p=0.03). Episodic activation of the fibrinolysis was more frequent in G1 than in G2 (80% vs 40%, p=0.01).
  
  
  CONCLUSIONS
  Patients with coronary instability and systemic evidence of inflammation exhibit more frequent activation of the thrombin/fibrinolysis system than patients with a similar clinical presentation but no evidence of systemic inflammation, whereas the coronary atherosclerotic burden is similar. The mechanisms of coronary instability in the absence of systemic evidence of inflammation need to be elucidated by future studies.
authors.forename: Giampaolo
authors.initials: G
authors.lastname: Niccoli
authors.forename: Luigi M
authors.initials: LM
authors.lastname: Biasucci
authors.forename: Carmine
authors.initials: C
authors.lastname: Biscione
authors.forename: Antonio
authors.initials: A
authors.lastname: Buffon
authors.forename: Massimo
authors.initials: M
authors.lastname: Siviglia
authors.forename: Micaela
authors.initials: M
authors.lastname: Conte
authors.forename: Italo
authors.initials: I
authors.lastname: Porto
authors.forename: Francesca
authors.initials: F
authors.lastname: Graziani
authors.forename: Giovanna
authors.initials: G
authors.lastname: Liuzzo
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000175:diagnosis; D050197:Atherosclerosis / Q000097:blood* / Q000175:diagnosis; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013927:Thrombosis / Q000097:blood* / Q000175:diagnosis
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein