Aim To observe the level of plasma vascular endothelial growth factor (VEGF),stromal cell-derived factor-1α (SDF-1α),whether mobilization of endothelial progenitor cells (EPC) is impaired in patients of acute myocardial infarction (AMI) with type 2 diabetics,and the pathway of SDF-1α,VEGF-EPC is abnormal. Methods Circulating CD45-/low+/ CD34+/ CD133+/ KDR+ early EPC count in peripheral blood mononuclear cells(PBMC) were quantified by flow cytometric analysis on day 1,3,5,7,14,28 after AMI. Plasma VEGF,SDF-1α and high sensitivity C-reactive protein (hs-CRP) level were mearsured at the above time points as those at EPC number counts with a standardized ELISA-kit. Results In non-diabetic patients,circulating EPC count increased after AMI,with the highest peak at day 5,following which EPC count gradually returned to baseline. In patients with type 2 diabetes,the highest peak was delayed (day 7 vs day 5),and the magnitude of EPC mobilization was decreased as compared with non-diabetic subjects [highest EPC count:(140±48)/106 vs (246±100)/106,P<0.05]. Plasma VEGF [day 5:277±95 ng/L vs 168±35 ng/L,P<0.05],SDF-1α [day 5:3 835±402 ng/L vs 3 287±384 ng/L,P<0.05]and hs-CRP[day 3:55.55±14.88 mg/L vs 36.92±14.83 mg/L,P<0.05] were significantly higher in AMI patients with diabetics than those without diabetics. Conclusion Tissue ischemia is more serious and ischemia-induced bone marrow-derived EPC mobilization is impaired in AMI patients with type 2 diabetics,and such impairment is likely due to impaired SDF-1α,VEGF -EPC mobilization pathway. This abnormal SDF-1α,VEGF-EPC mobilization pathway possibly contributes to the poor collateralization observed in diabetic patients in response to vascular occlusive disease.