E-selectin and TFPI are associated with carotid intima-media thickness in stable IHD patients: the baseline findings of the MIAMI study.
OBJECTIVE
MIAMI was a prospective multicenter clinical study designed to investigate the relationship between changes in carotid intima-media thickness (C-IMT) and those in the levels of circulating markers of inflammation, thrombosis and endothelial dysfunction. The study was performed in a group of stable coronary patients treated for two years with a moderate dosage of atorvastatin (20mg/day). In this paper the cross-sectional relationship between C-IMT and the same circulating markers of inflammation, thrombosis and endothelial dysfunction measured at baseline was investigated.


METHODS
Eighty-five subjects that had not used statins for at least two months were enrolled in the study. At time of enrollment, the levels of vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin, interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-alpha, high-sensitivity C-reactive protein (hs-CRP), tissue factor (TF), tissue factor pathway inhibitor (TFPI), von Willebrand factor (vWF), fibrinogen, total cholesterol (TC), high-density lipoprotein (HDL) and low-density lipoprotein (LDL), and triglycerides were measured, in parallel with C-IMT assessment.


RESULTS
In cross-sectional analyses, markers of endothelial perturbation (i.e. E-selectin) and TFPI were more strongly correlated with arherosclerotic burden than markers of inflammation. The baseline picture in this study indicates that E-selectin and TFPI are linked with atherosclerotic burden.
Porta
B
B
Department of Clinical Sciences, L. Sacco Hospital, Milan University, via G.B. Grassi 74, 20157 Milan, Italy.
Baldassarre
D
D
Camera
M
M
Amato
M
M
Arquati
M
M
Brusoni
B
B
Fiorentini
C
C
Montorsi
P
P
Romano
S
S
Tremoli
E
E
Cortellaro
M
M
D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000097:blood* / Q000209:etiology; D002784:Cholesterol / Q000097:blood; D019040:E-Selectin / Q000097:blood*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000503:physiopathology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use; D013925:Thromboplastin / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D017539:Tunica Intima / Q000473:pathology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
D015415:Biomarkers; D019040:E-Selectin; D006538:Heptanoic Acids; D015850:Interleukin-6; D016209:Interleukin-8; D008074:Lipoproteins; D011758:Pyrroles; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C051928:lipoprotein-associated coagulation inhibitor; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1; D005340:Fibrinogen; D002097:C-Reactive Protein; D013925:Thromboplastin; D002784:Cholesterol; D000069059:Atorvastatin