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Decreased small arterial compliance with increased serum vascular endothelial growth factor-A and circulating endothelial progenitor cell in dilated cardiomyopathy

摘要Background Evidence showed that both myocardium and blood vessels were damaged in dilated cardiomyopathy (DCM).However,the changes in arterial compliance,serum cytokines and circulating endothelial progenitor ceIls(EPC),and their correlations remain unknown.Methods Sixty-five DCM patients and 49 healthy volunteers were studied.Both large artery compliance(C1)and small artery compliance(C2)were measured with the CVProfilor DO-2020.Quantitative enzyme-linked immunosorbent assays (ELISAs)were used to measure the levels of vascular endothelial growth factor-A(VEGF-A)and VEGF receptor 2(VEGF-R2).Circulating EPC was assessed by EPC colony-forming assays and flow cytometry(CD133+/CD34+cells).Phagocytized Dil-acLDL and binded FITC-UEA-I were used to analyze endothelial lineage marker expression by immunofluorescence.Results Although C2 was markedly lower in DCM patients than in control group((3.8±1.8)ml/mmHg×100 vs(5.0±2.2)ml/mmHg×100,P<0.0001),there was no statistically significant difference in C1 between the two groups(P>0.05).Levels of VEGF-A,the numbers of colony-forming units(CFU)and the fractions of EPC were obviously highein DCM patients than in control group((127.61±39.5)pg/ml vs(58.8±42.9)pg/ml,P<0.0001;(2.5±1.5)%vs(0.5±0.3)%,P<0.05;23.5±12.8 vs 10.8±7.4,P<0.01,respectively)and however,there was no significant difference in VEGF-R2 between two groups(P>0.05).LgVEGF-A was positively correlated with the number of EPC-CFU(r=0.435;P<0.05)and inversely correlated with C2(r=0.543;P<0.001)in DCM patients.Conclusions The reduction of C2,a sensitive marker reflecting endothelial dysfunction,was observed in DCM patients and closely related to the increase in serum VEGF-A.

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作者单位 Department of Cardiology,First Affiliated Hospital of Nanjing Medical University,Nanjing,Jiangsu 210029,China [1]
分类号 R3
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发布时间 2008-04-02
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中华医学杂志(英文版)

中华医学杂志(英文版)

2008年121卷4期

316-320页

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