BACKGROUNDEvidence 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 cells (EPC), and their correlations remain unknown.

METHODSSixty-five DCM patients and 49 healthy volunteers were studied. Both large artery compliance (C(1)) and small artery compliance (C(2)) 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-R(2)). Circulating EPC was assessed by EPC colony-forming assays and flow cytometry (CD133(+)/CD34(+) cells). Phagocytized DiI-acLDL and binded FITC-UEA-I were used to analyze endothelial lineage marker expression by immunofluorescence.

RESULTSAlthough C(2) was markedly lower in DCM patients than in control group ((3.8+/-1.8) ml/mmHg x 100 vs (5.0+/-2.2) ml/mmHg x 100, P<0.0001), there was no statistically significant difference in C(1) 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 higher in DCM patients than in control group ((127.6+/-139.5) 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-R(2) 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 C(2) (r= -0.543; P<0.001) in DCM patients.

CONCLUSIONSThe reduction of C(2), a sensitive marker reflecting endothelial dysfunction, was observed in DCM patients and closely related to the increase in serum VEGF-A.