Endothelial cell (EC) dysfunction has a fundamental role in the development of atherosclerosis, which leads to myocardial infarction and stroke. The aim of this study is to investigate the effect of serum from patients with coronary atherosclerotic heart disease (CAD) on endothelial cells and investigate the possible mechanism underlying these effects. Serum from 35 patients with CAD and 35 healthy volunteers was collected. Human umbilical vein endothelial cell (HUVEC) proliferation and apoptosis were assessed by a CCK-8 assay and a flow cytometry assay, respectively. The synthesis of nitric oxide (NO) and reactive oxygen species (ROS) was measured using the nitrate reduction method and DCFH2-DA staining, respectively. The proliferation of HUVECs was inhibited by treatment with serum from CAD patients (P<0.05). Suppression of HUVEC proliferation by CAD serum occurred in a concentration-dependent manner. The synthesis of NO was also reduced in the CAD serum-treated group. Furthermore, the serum from CAD patients increased both apoptosis and intracellular ROS production in HUVECs. Moreover, treatment with tempol antagonized CAD serum-meditated HUVEC injuries. Taken together, these results suggest that HUVEC injury via CAD serum treatment is mediated by ROS production. Tempol may partly reverse this effect by abolishing HUVEC apoptosis.