Reduced number and impaired function of circulating endothelial progenitor cells in patients with abdominal aortic aneurysm

Aim

Circulating endothelial progenitor cells (EPCs) are associated with coronary artery disease (CAD) and predict its outcome. Although the pathophysiology of abdominal aortic aneurysm (AAA) is different, it shares some risk factors with CAD. Therefore, the correlation between EPCs and AAA was investigated.

Methods and results

Seventy-eight subjects (age 77.2 ± 7.8 years) with suspected AAA were prospectively enrolled. Cut-off values (men, 3.5–5.5 cm; women, 3–5 cm) were used to define normal aorta, small AAA, and large AAA on thoraco-abdominal computer tomography. Endothelial function was measured by flow-mediated vasodilation (FMD). Flow cytometry and colony-forming units (CFUs) were used to evaluate circulating EPC numbers. Circulating EPCs were defined as mononuclear cells with low CD45 staining and double-positive staining for KDR, CD34, or CD133. Late out-growth EPCs were cultured from six patients with large AAAs and six age- and sex-matched controls to evaluate proliferation, adhesion, migration, tube formation, and senescence.FMD was significantly lower with large (5.26% ± 3.11%) and small AAAs (6.31% ± 3.66%) than in controls (8.88% ± 4.83%, P = 0.008). Both CFUs (normal 38.39 ± 12.99, small AAA 21.22 ± 7.14, large AAA 6.98 ± 1.97; P = 0.026) and circulating EPCs (CD34⁺/KDR⁺ and CD133⁺/KDR⁺) were significantly fewer in AAA patients than in controls. On multivariate analysis, CFUs and circulating EPCs (CD34⁺/KDR⁺) were independently, inversely correlated to AAA diameter. Proliferation, adhesion, migration, tube formation, and senescence of late EPCs were significantly impaired in AAA patients.

Conclusion

The number and function of EPCs were impaired in AAA patients, suggesting their potential role in AAA.