As a glycosylation end product, HbA1c causes dysfunction of vascular endothelial cells, decreases endogenous fibrinolysis activity, enhances platelet agglutination, increases plasma plasminogen, quickens smooth muscle proliferation and extracellular matrix deposition, accelerates age-related endothelial dysfunction, and finally leads to a higher incidence of NSTEMI [13–18]. This evidence concerns the gene PLG and endothelial dysfunction.