Introduction. Inflammation plays an essential role in the initiation and progression of atherosclerosis and several inflammatory markers have been shown to be correlated with cardiovascular risk. C-IMT can be used as a marker of atherosclerosis in other vascular districts. The MIAMI study was designed to investigate the relationship between changes in C-IMT and changes of circulating markers of inflammation, thrombosis and endothelial dysfunction in a group of stable coronary patients treated for two years with moderate dosage of atorvastatin (20 mg/daily). We report here the cross-sectional relationships between the same variables measured at baseline visit. Methods. The MIAMI study is a prospective, open-label, multicenter clinical trial. Eighty-five subjects, free of statins from at least two months, were enrolled in the study. At time of enrollment, vascular cell adhesion molecules-1 (VCAM-1), intercellular adhesion molecules-1 (ICAM-1), E-selectin, interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), high-sensitivity C-reactive protein (hs-CRP), tissue factor (TF), tissue factor pathway inhibitor (TFPI), von Willebrand factor (vWF), fibrinogen, total cholesterol, high- and low-density lipoprotein, triglycerides were measured, in parallel with C-IMT assessment. Results. In cross-sectional analyses marker of endothelial perturbation (i. e. E-selectin) and TFPI were more strongly correlated with atherosclerotic burden than markers of inflammation. Conclusions. The baseline picture in this study indicates that E-selectin and TFPI are linked with atherosclerotic burden

E-selectin and TFPI are associated with carotid intima-media thickness in stable coronary patients : the baseline findings of the MIAMI Study / B. Porta, D. Baldassarre, M. Camera, M. Amato, M. Arquati, E. Tremoli, M. Cortellaro. - In: JOURNAL OF THROMBOSIS AND HAEMOSTASIS. - ISSN 1538-7933. - 5:1 suppl.(2007), pp. S450-S450. ((Intervento presentato al 21. convegno Congress of the International Society on Thrombosis and Haemostasis tenutosi a Geneva nel 2007.

E-selectin and TFPI are associated with carotid intima-media thickness in stable coronary patients : the baseline findings of the MIAMI Study

B. Porta
Primo
;
D. Baldassarre
Secondo
;
M. Camera;E. Tremoli
Penultimo
;
M. Cortellaro
Ultimo
2007

Abstract

Introduction. Inflammation plays an essential role in the initiation and progression of atherosclerosis and several inflammatory markers have been shown to be correlated with cardiovascular risk. C-IMT can be used as a marker of atherosclerosis in other vascular districts. The MIAMI study was designed to investigate the relationship between changes in C-IMT and changes of circulating markers of inflammation, thrombosis and endothelial dysfunction in a group of stable coronary patients treated for two years with moderate dosage of atorvastatin (20 mg/daily). We report here the cross-sectional relationships between the same variables measured at baseline visit. Methods. The MIAMI study is a prospective, open-label, multicenter clinical trial. Eighty-five subjects, free of statins from at least two months, were enrolled in the study. At time of enrollment, vascular cell adhesion molecules-1 (VCAM-1), intercellular adhesion molecules-1 (ICAM-1), E-selectin, interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), high-sensitivity C-reactive protein (hs-CRP), tissue factor (TF), tissue factor pathway inhibitor (TFPI), von Willebrand factor (vWF), fibrinogen, total cholesterol, high- and low-density lipoprotein, triglycerides were measured, in parallel with C-IMT assessment. Results. In cross-sectional analyses marker of endothelial perturbation (i. e. E-selectin) and TFPI were more strongly correlated with atherosclerotic burden than markers of inflammation. Conclusions. The baseline picture in this study indicates that E-selectin and TFPI are linked with atherosclerotic burden
Settore MED/09 - Medicina Interna
Settore BIO/14 - Farmacologia
2007
ISTH-International Society on Thrombosis and Haemostasis
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/44462
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