Number of endothelial progenitor cells in peripheral artery disease as a marker of severity and association with pentraxin-3, malondialdehyde-modified low-density lipoprotein and membrane type-1 matrix metalloproteinase.

Aims: Circulating endothelial progenitor cells (EPCs) were mobilized in cardiac ischemia, heart failure and vascular injuries associated with endothelial damage. Despite the occurrence of endothelial dysfunction in peripheral artery disease (PAD), few data are available on EPC mobilization in this setting.

Methods: We investigated the correlations between EPC and disease severity and also other biomarkers in PAD. EPCs assessed as CD34(+) cells co-expressing CD45(dim), CD133 and vascular endothelial growth factor receptor-2 were studied in PAD (n =48) and non-PAD (n =22) patients. Membrane type-1 matrix metalloproteinase (MT1-MMP) on peripheral blood mononuclear cells, serum malondialdehyde-modified low-density lipoprotein (MDA-LDL) and plasma pentraxin-3 were also measured.

Results: The EPC level changed in the Fontaine and Trans-Atlantic Inter-Society Consensus (TASC) II classification. EPC was increased in Fontaine class IIa as compared with class IV and non-PAD patients (p < 0.05). EPCs and pentraxin-3 were increased in TASC II type A/B as compared with type C/D and non-PAD patients (p < 0.05), whereas the expression of MT1-MMP on peripheral blood mononuclear cells was significantly decreased in TASC II type A/B (both p < 0.05 versus type C/D and non-PAD patients). The EPC level showed a positive association with pentraxin-3 (r = 0.31; p < 0.05). There was an inverse association between the EPC level and MT1-MMP (r = -0.54; p < 0.01). The cardiovascular events was associated with reduced EPC and increased MDA-LDL (p < 0.05).

Conclusion: EPC changed according to the Fontaine and TASC II classification and decreased in the advanced phases, and was associated with novel biomarkers and related to the severity of PAD.