Objective To analyze acute coronary syndrome patients with clinical characteristics and the sta-tus survey of the interventional treatment in the datong area.Methods 162 cases of hospitalized patients with unsta-ble angina pectoris(UA)and non ST segment elevation myocardial infarction(NSTEMI)were selected through clini-cal records,with UA78 cases and NSTEMI 84 cases.Results Clinical features:(1 )Two groups of high incidence were men,and incidence cases were 2 times than that in women.Peaks in males were 50 -60 years old,and lasted 20 years in UA group;Peaks delayed 10 years of women thanthat of men in UA group,delayed 20 years in NSTEMI group.Over the 70 -year -old,there were no gender,number differences in the two groups.Hypertension,hyperlipi-demia,diabetes,number of cases were quite in two groups.(2)The history of coronary heart disease (CHD)were respectively:in UA group,patients with 1 year or less were 48 (61.5%),30 cases (38.5%)>1 year.NSTEMI group had 67 cases (79.8%)in 1 year or less,>1 year with 7 cases (20.2%),(t =2.915,-2.743,all P <0.01).In the subgroups which the morbidity was 1 day or less,UA group had 5 cases (6.4%),NSTEMI group had 25 cases (29.8%)(t =4.066,P <0.01).(3)History of OMI respectively:UA group 18 cases (23.1%),the NSTE-MI group 8 cases (9.5%)(t =-2.533,P <0.05),the difference between the two groups had statistical signifi-cance.Coronary lesions:(1 )stents:During 78 cases of patients with UA,direct percutaneous coronary intervention (PCI)treatment were 71 cases (91.0%).During 84 NSTEMI patients,direct PCI were 63 cases (75.0%).(2)Sin-gle lesion:UA group of stents treatment were 18 cases (11.1%),the NSTEMI group were10 cases (6.2%),and had a statistically significant difference between the two groups (χ2 =26.309 P <0.01).The third.The incidence of heart for death in hospitalized patients:In the 162 cases of patients,hospital death was 3 patients (1.9%),and had occurred in NSTEMI group (3.6%),there was statistically significant difference between the two groups (χ2 =2.838 P1 -sided <0.05).Conclusion In front of coronary heart disease incidence peak,the high -risk groups:hyperten-sion,hyperlipidemia,diabetes,to carry on the curative effect of standard treatment for a long time,it is the key to avoid the risk of coronary heart disease (CHD).NSTEMI cardiac mortality,need hospital treatment.Not only secondary pre-vention of coronary artery disease focus groups of HP,hyperlipidemia,DMand also cannot ignore OMI crowd.because myocardial ischemia often,even NSTEMI.Correct myocardial ischemia is the key of the coronary heart disease treat-ment,if the drug is invalid,stents treatment should be taken into account.

Objective To investigate the effects of propofol on the release of noradrenaline ( NE) from the locus coeruleus in the brain of rabbits trying to elucidate the central mechanism of the cardiovascular inhibition induced by propofol.Methods Nine healthy male New Zealand rabbits weighing 2.0-2.5 kg were used in this study. A trocar (0.8 mm in diameter) was inserted into locus coeruleus using the stereotactic technique and fixed. Four days later push-pull perfusion of the brain was performed. 37℃ artificial cerebrospinal fluid (aCSF) was infused through the trocar at 0.1 ml?min-1 . A loading dose of propofol 2 mg?kg-1 was given i.v. followed by continuous infusion at 150 ?g?kg-1?min-1 for 30 min. The experiment was concluded at 20 min after propofol infusion. The perfusate having passed through the locus coeruleus was collected before and every 10 min during and after infusion. The NE concentration of the perfusate was measured by high performance liquid chromatography. Results The NE concentration of the perfusate from locus coeruleus significantly decreased after the loading dose and during the infusion of propofol and reached its bottom level at 10 min after loading dose. The maximal decrease was 75.5% [from (15.9 ? 3.2) pg??l-1 to (3.9?0.5) pg ? ?l-1]. Conclusion Intravenous propofol decreases the NE concentration in locus coeruleus. The cardiovascular inhibition induced by propofol may partly be explained by this central mechanism.