title: Markers of inflammation, thrombosis and endothelial activation correlate with carotid IMT regression in stable coronary disease after atorvastatin treatment.
abstract: OBJECTIVE
  MIAMI is a prospective multicenter clinical study designed to investigate the relationship between changes in carotid intima-media thickness (C-IMT) and changes in circulating markers of inflammation, thrombosis and endothelial activation in stable coronary patients treated for 20+/-3.7 months with 20mg/day atorvastatin.
  
  
  RESULTS
  Eighty-five subjects had their C-IMT, blood lipids and soluble markers measured at baseline, at the 12th month and at the end of the study. Almost all soluble markers decreased upon treatment except for high-sensitivity C-reactive protein (hs-CRP), interleukin-18 (IL-18), tissue factor pathway inhibitor-free (TFPI-free) and soluble vascular cell adhesion molecules-1 (sVCAM-1) which did not change significantly, and interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and soluble CD40 ligand (sCD40L) which increased. sCD40L, fibrinogen, tissue factor pathway inhibitor-total (TFPI-total), soluble intercellular adhesion molecules-1 (sICAM-1), sE-selectin, interleukin-8 (IL-8) and von Willebrand factor (vWF) changed significantly even after application of the Bonferroni correction for multiple comparisons. Changes in lipids did not correlate with C-IMT regression either when considered singly or when combined in a lipid score. Changes in soluble markers correlated poorly with C-IMT regression when analyzed singly, but strongly when combined in relevant composite scores (inflammation/coagulation score, endothelial activation score, soluble markers score and total score).
  
  
  CONCLUSIONS
  In patients with stable coronary artery disease treated with moderate doses of atorvastatin, carotid IMT regression correlated with changes of inflammation, thrombosis and endothelial activation profiles.
authors.affiliation: Monzino Cardiology Center IRCCS, 20138 Milan, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Baldassarre
authors.forename: B
authors.initials: B
authors.lastname: Porta
authors.forename: M
authors.initials: M
authors.lastname: Camera
authors.forename: M
authors.initials: M
authors.lastname: Amato
authors.forename: M
authors.initials: M
authors.lastname: Arquati
authors.forename: B
authors.initials: B
authors.lastname: Brusoni
authors.forename: C
authors.initials: C
authors.lastname: Fiorentini
authors.forename: P
authors.initials: P
authors.lastname: Montorsi
authors.forename: S
authors.initials: S
authors.lastname: Romano
authors.forename: F
authors.initials: F
authors.lastname: Veglia
authors.forename: E
authors.initials: E
authors.lastname: Tremoli
authors.forename: M
authors.initials: M
authors.lastname: Cortellaro
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000000981:diagnostic imaging / Q000188:drug therapy; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000188:drug therapy*; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000188:drug therapy*; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007249:Inflammation / Q000097:blood*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy; D010949:Plasma / Q000737:chemistry; D011758:Pyrroles / Q000627:therapeutic use*; D018401:Sample Size; D013927:Thrombosis / Q000097:blood*; D014463:Ultrasonography
chemical_list: D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D000069059:Atorvastatin