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The Relationship Between The Change Of Plasma Level Of Homocystein With Tissue Factor In Patients With Unstable Angina Pectoris

Posted on:2006-08-23Degree:MasterType:Thesis
Country:ChinaCandidate:T H WangFull Text:PDF
GTID:2144360152481665Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: The incidence of coronary heart disease (CHD)is increasing gradually. CHD had been a main fatal disease thatinfluenced mankind health. Etiopathogenisis of CHD is not yetcomplete certain . Researchs have showed that CHD is a diseaseof multi-liability factor .To discover its risk factors andinterven its pathogenesis is important pointer nowadays formedical study in the world. It was considered that occurrenceand development of CHD is a kind of pathophysiological procesthat development of coronary artery atherosclerosis under actionof many kinds of risk factor leads to Coronary artery stenosiseven total occlusion. The dysfunction of endothelium, smoothmuscle cell proliferation, activation and aggregation of bloodplatelet and thrombosis are main mechanisms. Though, as main,independent risk factor of CHD , age, sex,smoking, lipiddisorders ,blood pressure, diabetes have been acknowledged,some patients have no thoses risk factors.It shows thatoccurrence and development of CHD have relation to other riskfactors possiblely. Homocysteine is a new risk factor of CHD,which differ from other conventional risk factors such asage,sex,smoking, blood pressure, lipid disorders ,diabetes .Themechanism of HCY inducing CHD have relation toVEC( vascular endothelial cell) injury, lipid metabolismdisorder,promoting VSMC(vascular smooth musclecell )proliferation ,blood coagulation and fibrolysis systemunbalance possiblely. However, it is not demonstrated clearly.The aim of this study is to alter plasma level of homocystein byfolic acid 5mg/d and VitaminB12 0.25mg/d in patients withuntable angina pectoris ,and investigate the relationship betweenlevel of HCY and TF in plasma.To explore the possiblepathogenesis mechanisms of homocystein to cause CHD andsignificance of folic acid and VitaminB12 and to providetheoretical evidence for clinical treatment .Methods: The study group comprised 72 consecutivepatients with unstable angina pectoris(UAP)who underwentcoronary angiography in cardiac center of the people,s Hospitalof HeBei Province, 36 patients in medical treat group which addfolic aid and vitaminB12 and 36 patients as contrle group who betreat as normal conronary heart disease patient.Exclusion criteria: acute myocardial infarction within fourweeks, left ventricular ejection fraction<30%, valvular heartdisease, recent operation and injury, renal or liver dysfunction,acute or chronic inflammation, disease of hematological system,acute cerebrovasular disease, bronchial asthma, von Willebranddisease, cancer, oral vitamins, lack of estrogen, organtransplantation, self immunity disease.Age, sex, hypertension, diabetes, TC,TG, HDL-C, LDL-C,VLDL-C, lipoprotein a ,smoking and CHD family history inevery subjects were recorded in detail.Blood sampling: Peripheral blood samples were taken onthe second day after the patients came into hospital .Then wetake the blood samples again after 4 weeks,8 weeks and12weeks respectively. Coded samples were stored at ~80℃andanalyzed in a single batch for the study, thus, patientmanagement was independent of these results. Levels of HCYand TF-Ag were measured with ELISA.Statistics analysis: SPSS11.0 software pack was used tomake statistical analysis. Initially the homogeneity of variancebetween all the groups was analyzed. All the numerical data wasshown as mean±standard deviation ,students t test or analysisof varience was used to establish significance. Chi-square testwas used for analysis of categorical data. Linear Correlationanalysis was used to measure the coefficient of correlation aboutthe correlation data. Logistic Regression Analysis was used topredict the main factors and also Hosmer-Lemeshowgoodness-of fit to confirm the data.P value < 0.05 wasconsidered statistically significant.Results:1 There was no significant difference in clinical or laboratoryvalues beween patients with treatment group and controlgroup,beween patients with normal level of HCY in treatmentgroup and control group.2 The comparisons of HCY and TF levels in each groups.2.1 The rate of hyperhomocysteinemia is 45.8% in all patients.There was no significant difference in Rate ofhyperhomocysteinemia beween patients with treatment andcontrol group(47.22% vs 44.44%, respectively, P=0.477),andwas no significant difference beween patients with treatmentand control group in the HCY and TF levels ofpre~treatment(17.09±7.00μmol/l vs 15.37±5.30μmol/l,P=0.356;202.35±78.73 pg/ml vs 175.77±70.82 pg/ml,P=0.137, respectively).2.2 The HCY levels of post-treatment(4 weeks,8 weeks,12weeks)were significantly lower than those of pre-treatment intreatment group(15.18±4.66μmol/l,12.65±3.29μmol/l,11.45±3.17μmol/l,p<0.05).The HCY levels of post~treatment(4 weeks,8 weeks,12weeks)is 13.57±4.69μmol/l,11.29±3.41μmol/l,9.92±2.71μmol/l respectively in control group,andthe difference is not significant(p>0.05).2.3 The TF levels of post-treatment(4 weeks,8 weeks,12weeks)were significantly lower than those of pre-treatment in twotreatment and control group(4.50±33.78 pg/ml,69.52±30.64pg/ml,63.31±29.99 pg/ml,p<0.01;114.83±47.42 pg/ml,103.09 ±46.18 pg/ml , 92.14 ±40.44 pg/ml , p<0.01,respectively),but the lowering degree of TF level in treatmentgroup were higher than those in control group significantlydifferent (p>0.05).2.4 These patients with nomal plasma HCY level in treatmentgroup and control group ware named as A group and B grouprespectively.There was no significant difference in HCY and TFlevels of pre-treatment beween A group and B group(11.36±2.48μmol/l vs11.75±2.71μmol/l,p=0.618;160.01±50.89 pg/mlvs 148.57±55.75 pg/ml ,p=0.510, respectively). There was nosignificant difference in HCY level of post-treatment beweenpatients with A and B group (A: 11.36±2.48μmol/l vs 11.06±2.51μmol/l ,p=0.129;B:11.68±2.67 μmol/l vs 11.75±2.71μmol/l p=0.144 respectively).TF levels of post-treatment(3months later) were lower than those of pre-treatment in A andB groups (A: 151.56 ±42.21 pg/ml vs 160.01 ±50.89pg/ml ,p=0.04;B:143.45±51.77 pg/ml vs 148.57±55.75pg/ml ,p=0.02, respectively), but the lowering degrees of bothgroups were not significantly different (p=0.600).3 There were positive relations between HCY and TF in allpatients(r=0.571, p<0.001).4 The pro-treatment level of HCY (relative risk RR=3.892,confidence internal CI=3.113-5.665, P=0.002) was theindependent predictor of TF level elevation in patients withUAP (percentage of correct classification=86%,Hosmer-Lemeshow Goodness-of-Fit, P=0.847).Conclusions:1 Plasma HCY level enhanced in patients with UAP,taking folicand vitminB12 could lower the HCY level efficiently in patientswith UAP.But it is only effective in patients withhyperhomocysteinemia.
Keywords/Search Tags:unstable angina pectoris, homocysteine, tissue factor, folic acid, vitamin B12
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