Background-The recent discovery of circulating endothelial progenitor cells (EPCs) has altered our understanding of new blood vessel growth such as occurs during collateral formation. Because diabetic complications occur in conditions in which EPC contributions have been demonstrated, EPC dysfunction may be important in their pathophysiology. Methods and Results-EPCs were isolated from human type II diabetics (nϭ20) and age-matched control subjects (nϭ20).Proliferation of diabetic EPCs relative to control subjects was decreased by 48% (PϽ0.01) and inversely correlated with patient levels of hemoglobin A1C (PϽ0.05). Diabetic EPCs had normal adhesion to fibronectin, collagen, and quiescent endothelial cells but a decreased adherence to human umbilical vein endothelial cells activated by tumor necrosis factor-␣ (TNF-␣) (PϽ0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (PϽ0.05). Conclusions-These findings suggest that type II diabetes may alter EPC biology in processes critical for new blood vessel growth and may identify a population at high risk for morbidity and mortality after vascular occlusive events.

Ischemic complications are not uncommon after EVAR, and may exceed the incidence with open surgical repair. Limb ischemia is most often a result of limb occlusion, and can be successfully managed with standard interventions. Pelvic ischemia often results from atheroembolization despite preservation of hypogastric arterial circulation. Colonic and spinal ischemia are associated with the highest morbidity and mortality.

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