Objective To investigate the effect of nucleotide-binding oligomerization domain-like receptor protein3 (NLRP3) inflammasome on coronary artery vascular endothelial function in patients with coronary heart disease. Methods 50 CHD patients and 25 controls were recruited according to the inclusion criteria. The clinical data including sex, age, smoking history, body mass index (BMI), mean arterial pressure (MAP), fasting plasma glucose (FPG) and blood lipids were collected for analysis. The transcription and expression of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC) and caspase-1 mRNA as well as protein in peripheral blood mononuclear cells (PBMCs) in all the groups were evaluated by real-time qPCR and Western blot respectively, and the levels of plasma interleukin-1β (IL-1β), interleukin-18 (IL-18), nitric oxide synthase (NOS) and endothelin-1 (ET-1) in all the groups were detected by ELISA assay. Results The expression levels of ASC mRNA, NLRP3, ASC, caspase-1 and IL-1β, IL-18, NOS and ET-1 were significantly different between the two groups (P<0.05). In the CHD group, ASC was positively correlated with IL-1β, IL-18 and ET-1 (r=0.508, 0.543, 0.411, P=0.006, 0.003, 0.030), caspase-1 was positively correlated with MAP, IL-1β, IL-18, ET-1 and smoking (r=0.424, 0.470, 0.430, 0.382, 0.474, P=0.025, 0.012, 0.022, 0.045, 0.011), NLRP3 mRNA was positively correlated with IL-18 (r=0.340, P=0.016). In control group, ASC and caspase-1 were positively correlated with FPG (r= 0.654, 0.403, P=0.000, 0.046). There was a negative correlation between IL-18 and NOS in CHD group (r=-0.304, P=0.032), and a positive correlation between IL-1β and ET-1 (r=0.301, P=0.034). There was no correlation between IL-1β, IL-18, NOS and ET-1 in the control group. Conclusion In patients with coronary heart disease, NLRP3 inflammasome activation leads to downstream excess IL-1β and IL-18 production, which further increases the release of ET-1 and decreases the release of NO from coronary vascular endothelial cells, leading to coronary vascular endothelial dysfunction and promoting the occurrence and development of coronary heart disease