The Effection Of Decreasing Plasm Homocysteine Level On T-PA And PAI-1 Of Unstable Angina Patients

Objective: It has been shown that homocysteine(HCY)is a independent risk factor of coronary heart disease(CHD). Homocysteine can lead to CHD and prethromboticstate by many ways.The key pathophysiology mechanism ofunstable angina pectoris is atherosclerotic plaque ruptur andthrombus following in coronary artery.The fibrinolysis systemplay a important role in preventing thrombusformation.Plasminogen activator inhibitor-1(PAI-1) and tissuetype plasminogen activator(t-PA) which secreted by endothelialcell are important factors in this system.The concentration andactivity of PAI-1 and t-PA in plasm determine the activity offibrinolysis function.Many studys show thathyperhomocysteine can increase the level of PAI-1 andpromote the developing of thrombus. Folic acid and vitaminB12 are the essential assisted factor in homocysteinemetabolism.The level of folic acid in plasm have a negativecorrelation with homocysteine.To take folic acid orally candecrease the level of homocysteine in plasm.This studyinvestigates the changes of homocysteine, tissue-typeplasminogen activator and plasminogen activator inhibitor-1 inthe UAP patients who take folic acid and vitamin B₁₂orally ,study the effect of homocysteine to fibrinolysisfunction ,explore the possible pathogenesis mechanismscausing . coronary heart disease of homocystein.Methods: The study group comprised 72 consecutivepatients with unstable angina pectoris(UAP) in cardiac centerof the people,s Hospital of HeBei Province, 36 patients inmedical treat group which add folic aid and vitaminB12,theother medications are same except folic aid and vitaminB12 incontrol group.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,lipoproteina,smoking and CHD family history in everysubjects 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 ofHCY,PAI-1 and t-PA 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 datawas shown as mean±standard deviation and students t test wasused to establish significance. Chi-square test was used foranalysis of categorical data. Linear Correlation analysis wasused to measure the coefficient of correlation about thecorrelation data. Multiple linear regression analysis was used toevaluate the main influence factor of PAI-1. We took p<0.05as statistic significance level.Results1 There was no significant difference in clinical featuresbeween treatment group and control group.The patients withnormal level of HCY is 52.6% in treatment group and 53.5% incontrol group.It is no no significant difference between them.The pre-treatment level of HCY ,PAI-1 and t-PA in plasm is nosignificant difference between treatment group and controlgroup . (17.09±7.00μmol/L vs 15.37±5.30μmol/L,P=0.356;43.01±9.12 ng/ml vs 41.76±8.77 ng/ml,P=0.143; 9.72±3.41ng/ml vs 9.96±4.12 ng/ml, P=0.310)。2. The comparisons of HCY ,PAI-1 and t-PA levels in eachgroups.2.1 HCY and PAI-1 levels of post-treatment(4 weeks,8weeks,12weeks ) were significantly lower than those ofpre-treatment in treatment group(p<0.05),the level of t-PAisn't obviously change(P>0.05). The HCY ,PAI-1 and t-PA...