Different Plasma Glucose Levels To Clopidogrel Antiplatelet Active Influence

Objective：Acute coronary syndrome (ACS) is group of clinical syndromethat includes unstable angina pectoris (UAP), acute ST elevation myocardialinfarction (STEMI) and Acute Non-ST elevation myocardial infarction(NSTEMI). ACS is mainly due to coronary atherosclerotic plaque rupturedand thrombosis creates.CLARITY-TIMI-28[1]and COMMIT/CCS-2[2]experimental demonstrate that Clopidogrel can significantly reduce those thathave suffered from the acute myocardial infarction in-hospital mortality andcompound the risk of cardiovascular events.Therefore, in the modern for thetreatment of acute coronary syndrome, anti-platelet aggregation has becomedmore important initiatives.Aspirin and clopidogrel are often used.Clopidogrel is a derivative of thiophene pyridine by hepatic metabolism inbody. its active metabolism product can combined with P2Y12sites ofadenosine diphosphate ADP）which Locates in the platelet surface to preventthis receptor binding ADP sites.This process is irreversible and optional. Itmakes adenosine cyclization enzymes become activity so that restrainsfibrinogen and GPIIb/IIIa the receptors binding and inhibits plateletaggregation.Clopidogrel has half-life long and slow metabolism.When coronary heartdisease patients take clopidogrel,it may increase the risk of hemorrhage ofpatients and may increase the postoperative blood transfusion and other bloodpreparations or increases the patients the use of hospital stay and economicburden.Now many acute coronary syndrome patients have diabetes, LiuWei[3]research shows that the plasma glucose level highten can lead to increaseplatelet aggregation ability. This makes patients with acute coronary syndromein taking sulfuric acid hydrogen clopidogrel have to pay attention to dosage ofthe drug.whether dosage of the drug is too big or too small,it will give patients some hardships to imagine the consequences.But about plasmaglucose and platelet aggregation rate of the experiment was done a little,plasma glucose and acid hydrogen clopidogrel action effect are not considered.so this paper to study the problem.experimental subject：31cases with acute coronary syndrome in patientswho were treated in hospital in heart medicine was enrolled betweenNovember2010to December2011. The subjects include18male cases and13female cases, age ranges in45～73(58.74±8.13)，weight ranges in55～80kg(67.55±7.57), height ranges in155~178cm（167.41±8.06）. Inclusion criteria:All selected subjects are diagnosed acute coronary syndrome patients (withtypical clinical symptoms, electrocardiographic changes, indicated myocardialenzymes or testified by coronary angiography)； Kidney and liver function arenormal；Blood coagulation and routine blood are normal；Women are not themenstrual period (from oviposit period to menses period).Exclusion criteria:ACS are treated with clopidogrel time less than five days；Heart function islow；All kinds of blood；Hemorrhagic disease or a bleeding tendency; Plateletcount more than300x109/L or less than100x109/L; Recent use of theinfluence of clear evidence platelet aggregation drugs；Diabetics have kept ona die,but blood sugar glucose is still higher；Diabetics have been taking drugs；patients can’t tolerate high concentration of glucose.Methods: Patients with acute coronary syndrome (ACS) were admitted tothe hospital after taking conventional hydrogen sulfate clopidogrel75mg,1/day, take5days later, take75g glucose at four o’clock in the sixth daymorning to check standard glucose tolerance, are adopted vein blood to checkthe plasma glucose at five different time(before taking glucose、taking glucose30minutes later、taking glucose1hour later、taking glucose2hour later、taking glucose3hour later)。Vein blood adopted to check the plasma glucose isdetected the platelet aggregation rate at the same time, vein blood adoptedbefore taking glucose is detected glycated hemoglobin at the same time. Theplatelet aggregation is tested by the whole blood impedance.Inducers areadenosine diphosphate(10μM) and denosine diphosphate(20μM).SPSS13.0 software was used for statistical analysis.Measurement data showed a normaldistribution was expressed as the mean±standard deviation (SD),Measurement data showed a non-normal distribution was expressed as themedian（M） and interquartile range. The repeated measures engineeredvariance analysis was performed to achieve within-groups comparison atindividual time points.The difference that the platelet aggregation is inducedby10uMADP and20uMADP at the same time showed non-normaldistribution uses nonparametric test (Wilcoxon). Glycated hemoglobin andPlatelet aggregation rate induced by the same concentration ADP in differenttime of the mean value apply linear correlation analysis.P<0.05indicates thereis significant statistical difference.Results: It can be known that time has significant effect on plasma glucoseconcentration after ACS patients taking75g glucose (F=125.64, P=0.000).Time doesnot have an effect on platelet aggregation rate induced by10uMADP（F=0.591、P=0.67），time doesnot have an effect on plateletaggregation rate induced by20uMADP(F=0.843、P=0.471). Two kinds ofdifferent concentration ADP have no influence on detection of plateletaggregation rate in the same time after the patients continuous take clopidogrelup to five days.(Z respectively is-0.527、-0.654、-0.466、-1.354、-0.335，Prespectively is0.598、0.513、0.641、0.176、0.738，they have no statisticalsignificance).Platelet aggregation rate induced by10uMADP and20uMADPin different time are non-normal distribution (all the p is0.00, they are less than0.05).Between blood-glucose concentration that is tested before takingglucose、taking glucose30minutes later、taking glucose1hour later、takingglucose2hour later and taking glucose3hour later and correspondingplatelet aggregation rate induced by10uMADP have no obvious relationship.Between plasma glucose concentration that is tested before taking glucose、taking glucose30minutes later、taking glucose1hour later、taking glucose2hour later and taking glucose3hour later and corresponding plateletaggregation rate induced by20uMADP have no obvious relationship.Glycatedhemoglobin and Platelet aggregation rate induced by10uMADP in different time of the mean value have no obvious linear relationship（spearmancorrelation is-0.045，P is0.810，they have no statistical significance）.Glycated hemoglobin and Platelet aggregation rate induced by20uMADP indifferent time of the mean value have no obvious linear relationship（spearmancorrelation is-0.111，P is0.551，they have no statistical significance）.Conclusions: Immediate plasma glucose and long-term plasma glucose（byglycated hemoglobin representative） have no influence on antiplateletaggregation after Clopidogrel achieving its steady plasma drug concentration.It is not necessary that basis for high plasma glucose or low plasma glucose toadjust clopidogrel dosage in the clinical. It is no obvious difference that10uMADP and20uMADP are in the term of induction platelet aggregationrate after clopidogrel achieving its steady plasma glucose concentration.