Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2005
[Concentration and significance of s-ICAM-1, s-VCAM-1, and vWF in the plasma of patients with rheumatic heart disease].
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Zhang Qing-chun, Yin Hai-hui, Yin Bang-liang
Аннотация
OBJECTIVE: To measure the concentrations of soluble intercellular adhesion molecule-1 (s-ICAM-1), soluble vascular cell adhesion molecule-1 (s-VCAM-1), and von Willebrand factor (vWF) in the plasma of patients with rheumatic heart disease (RHD), and to provide basic theory for the mechanism of valvular and myocardial damage.
METHODS: The consecutive patients with RHD (n=40) and healthy people (n=40) were chosen. All blood samples were taken from the peripheral veins. s-ICAM-1, s-VCAM-1 and vWF levels in all samples were measured by enzyme-linked immunosorbant assay.
RESULTS: s-ICAM-1, s-VCAM-1 and vWF levels were significantly elevated in patients with RHD compared with healthy people (P < 0.01. The level of sICAM-1 was elevated in patients with atrial fibrillation compared with patients without atrial fibrillation.
CONCLUSION: The concentrations of s-ICAM-1, s-VCAM-1 and vWF levels were significantly elevated in patients with static rheumatic fever, which might be one of the pathogenic mechanisms of valvular damage, endothelial dysfunction, and myocardial damage in rheumatic heart disease.
METHODS: The consecutive patients with RHD (n=40) and healthy people (n=40) were chosen. All blood samples were taken from the peripheral veins. s-ICAM-1, s-VCAM-1 and vWF levels in all samples were measured by enzyme-linked immunosorbant assay.
RESULTS: s-ICAM-1, s-VCAM-1 and vWF levels were significantly elevated in patients with RHD compared with healthy people (P < 0.01. The level of sICAM-1 was elevated in patients with atrial fibrillation compared with patients without atrial fibrillation.
CONCLUSION: The concentrations of s-ICAM-1, s-VCAM-1 and vWF levels were significantly elevated in patients with static rheumatic fever, which might be one of the pathogenic mechanisms of valvular damage, endothelial dysfunction, and myocardial damage in rheumatic heart disease.