The Relationship And Possible Mechanism Between NPY And Coronary Heart Disease

Objectives:To explore the relationship between NPY and the occurrence and development of coronary heart disease（CHD）,as well as the role and possible mechanism of smoking in promoting the progression of CHD.Methods:128 patients with CHD diagnosed by coronary angiography were included,including 87 male patients and 41 female patients.According to the results of angiography,the patients in CHD group with intimal thickening,thrombosis and collateral formation were divided into complex group,and the others were divided into simple group.Besides,the CHD group was divided into smoking group and non-smoking group.According to the time of smoking,the smoking group of CHD group were divided into group A and group B.Patients whose smoking age was more than 20 years were divided into group A and those whose smoking age was less than 20years were divided into group B.Control group 62 cases are from the physical examination center without obvious organ injury of physical examination personnel,including 40 males and 22 females.The plasma concentrations of endothelial nitric oxide synthase（e NOS）,endothelin（ET）,thromboxane A2（TXA2）and neuropeptide Y（NPY）were measured by enzyme-linked immunosorbent assay.Results（1）The NPY,ET,TXA2 level in CHD group were significantly higher than that in control group[（58.76±17.63）ng.m L^-1vs.（37.48±11.36）ng.m L^-1,P=0.000,P<0.05;（36.16±10.04）pg.m L^-1vs.（27.80±7.18）pg.m L^-1,P<0.001;（27.69±6.91）pg.m L^-1vs.（24.32±7.28）pg.m L^-1,P=0.003,P<0.05].The e NOS level in CHD group was significantly lower than that in control group[（3.00±0.94）ng.m L^-1vs.（4.05±1.44）ng.m L^-1,P=0.003,P<0.05].（2）Subgroup analysis of CHD group:plasma NPY leve in complex group was significantly higher than that in simple group group[（74.26±14.98）ng.m L^-1vs.（51.06±13.65）ng.m L^-1,P<0.001],there was no significant difference in plasma e NOS,ET,TXA2 level between the two groups.Besides,the NPY,ET level in smoking group were significantly higher than that in control group[（62.91±16.32）ng.m L^-1vs.（53.93±18.11）ng.m L^-1,P=0.004,P<0.05;（37.92±9.85）pg.m L^-1vs.（34.33±10.27）pg.m L^-1,P=0.047,P<0.05],there was no significant difference in plasma e NOS and TXA2 level between the two groups.Furthered study find the NPY level in group A was significantly higher than that in group B[（74.59±14.59）ng.m L^-1vs.（46.54±8.79）ng.m L^-1,P<0.001].Plasma ET level in group B was significantly higher than that in group A[（39.58±10.65）pg.m L^-1vs.（34.54±9.14）pg.m L^-1,P=0.037,P<0.05],there was no significant difference in plasma e NOS and TXA2 level between the two groups.Complex coronary lesions and smoking have no interaction effect on NPY（P=0.769）.（3）Correlation analysis between two variations showed that plasma NPY had positive correlations with smoking,mean arterial blood pressure,the ET and TXA2 level[（r=0.17,P=0.021）,（r=0.26,P<0.001）,（r=0.46,P<0.001）,（r=0.24,P=0.001）],while having negative correlations with HDL and the e NOS level[（r=-0.22,P=0.002）,（r=-0.26,P<0.001）].Conclusions（1）NPY may be involved in the occurrence and development of coronary heart disease,and the mechanism may be closely related to the changes of NPY on vascular endothelial function.Related.（2）Smoking in patients with coronary heart disease is related to the concentration of NPY and endothelial dysfunction,and the mechanism may involve endothelial dysfunction caused by NPY.