The Dynamic Changes Of Serum P-selectin Level In Acute Coronary Syndrome And The Discussion Of Its Clinical Value

Acute coronary syndrome has intimate relation to decreasing stability of theatherosclerotic plaque induced by inflammatory reaction. The premise ofinflammatory reaction is adhesion,gathering and transfer of the leucocyte. P-selectin play an important role during this process.We design this experiment to explore the value of P-selectin in earlydiagnosing acute coronary syndrome and evaluating its curative effect .Throughdynamic estimating the patients serum P-seletin level in acute coronary syndromegroup with enzyme immunoassay, we estimate its risk stratification value incoronary heart disease. At the same time, we observe the changes of serumP-seletin during the course of implying thrombolysis treatment on the patients ofacute myocardial infarction, contrasting it to the dynamic changes of serumCK-MB levels to study the relation between P-seletin and myocardial ischemiareperfusion injury so that we can explore its value on differentiating whether theembolized vessels have been recanalized.Objective: To explore the value of adhesion molecule in diagnosing acutecoronary syndrome and evaluating the curative effect of reperfusion treatmentthrough observing dynamic changes of serum P-selectin levels in acute myocardialinfarction and unstable angina patients.Method:Assay serum concentration of P-selectin in acute myocardialinfarction group(25 case) ,unstable angina group(18 case) ,stable anginagroup(15 case) and normal control group(15 case) with the method of enzymeimmunoassay. Compare the difference of serum P-selectin levels among fourgroups. Simmultaneously, we observe dynamic serum P-selectin levels among theacute myocardial infarction patients which has been divided into recanalizalsuccess group and recanalizal failure group after accepting thrombolysis treatmentand contrast its changing trend to CK-MB.Result:The serum P-selectin level is obviously higher in acute coronarysyndrome group than its in stable angina group and normal control group.There isstill an obvious difference between acute myocardial infarction group and unstableangina .Apply thrombolysis treatment to all the acute myocardial infarctionpatients, observing dynamic serum P-selectin levels in recanalizal success groupand recanalizal failure group. In recanalizal success group,serum P-selectinconcentration first hoist then fall.However in recanalizal failure group, it continueto rise. The breakout point that two group present different trends is 3-6 hours afteraccepting thrombolysis treatment. The time that CK-MB present obviousdifference in two groups is later than P-selectin.Discussion: In recent years, more and more reaserch indicate thatinflammatory reaction play an important role during the developing process ofacute coronary syndrome and myocardial ischemia reperfusion injury. P-selectin isthe key factor that induce adhesion and gathering of the inflammatory cells whichis the premise of inflammatory reaction .P-selectin, a member of the selectin family, is localized in the membranes ofplatelet alpha granules, as well as endothelial cell Weibel-palade bodies. P-selectinis surface-expressed when platelets is activated, so it can present the activation ofplatelets. At the same time it is the earliest emerging adhesion molecule which caninduce platelet-endotheliocyte as well as platelet-neutrophil and platelet-monocyteinteractions so to trigger the activation of neutrophil and the release of vasoactivesubstances.Acute coronary syndrome occurs when an atherosclerotic plaque ruptures . From recruitment of leucocyte to rupture of plaque, inflammatory transmitter play a key role. P-selectin, as a kind of adhesion molecules, take partin this process actively. When coronary atherosclerosis happens, P-selectin issurface-expressed when vessel endothelial is injured. It absorbs quantity ofleukocytes (e.g. neutrophil ,monocyte) and triggers the activation of them.Leukocytes activated by P-selectin recruit around the atherosclerotic plaque,leading soakage reaction and the releasing of tissue active substances (e.g. oxidants,TNFα,IL-1,γ-IFN,TxA2,LTs). All these active substances cause atherosclerotic plaque ruptures ultimately. At the same time, active platelet take part in the process of atherosclerosis by virtue of P-selectin.We can observe from the experiment that the serum P-selectin level isobviously higher in unstable angina group and acute myocardial infarction than innormal control group , the t worth is 3.88,3.21,the P worth are all <0.01. We alsocompare the serum P-selectin level in stable angina group and control group, thereis no difference between them, when t-check is adopted, the t worth is 1.83, the Pworth is >0.05 .Simultaneously we find that serum P-selectin level is obviouslyhigher in acute myocardial infarction group than in unstable angina group , the tworth is 3.49, the P worth is <0.01. Now we can draw a conclusion that serumP-selectin level have obvious difference between normal people and patients whosuffering from different kind of coronary heart disease because serum P-selectinlevel is proportional to the severity of pathological changes. We can identify acutecoronary syndrome in the early course so that we can adopt intervention treatmenttimely and effectively to avoid exacerbation and reduce the mortality. Becauseunstable angina belong to one kind of severe coronary heart disease which caneasily round into acute myocardial infarction or sudden cardiac death. So dynamicobserving the serum soluble P-selectin concentration can help us detect unstableangina patients early and correctly.We also take the acute myocardial infarction patients as individualobservation object which has been divided into recanalizal success group andrecanalizal failure group after accepting thrombolysis treatment . Assay dynamicserum P-selectin levels and compare the different changing trend in two groups.The serum P-selectin level is obviously higher in recanalizal success group than inrecanalizal failure group 3h after accepting thrombolysis treatment, the t worth is2.98, the P worth is <0.01;Serum P-selectin levels begin to decrease gradually 6hafter accepting treatment and near to normal levels in 12h. However in recanalizalfailure group, serum P-selectin levels take on a gradually increasing trend at thetime 6h and 12h. after accepting treatment .So we can draw a conclusion that thebreakout point that serum P-selectin levels in two group present different changingtrend is 3-6h after accepting thrombolysis treatment. In recanalizal success group,P-selectin first hoist then fall. However in recanalizal failure group, it continue torise. This kind of dynamic P-selectin level difference has show its superioritybecause it can help us make judgement early and correctly about whether theembolized vessels have been recanalized after accepting thrombolysis treatment.;Serum CK-MB level first increase then decrease gradually whether the theembolized vessels have been recanalized. Traditional theory has proved thatCK-MB begin to increase 4h after suffering acute myocardial infarction, thenreach to peak worth within 16-24h and decrease to normal levels within 3-4 day.Through observing whether the time that CK-MB reaching to the peak worth isadvanced, we can judge whether thrombolysis treatment have achieved success.The result of our experiment is accord with traditional theory. In recanalizalsuccess group , the time CK-MB reach to peak worth is 12h after acceptingthrombolysis treatment , in recanalizal failure group, the time is 20h afteraccepting treatment. However the breakout point we can see that serum P-selectinconcentration present different trends in two group is 3-6h after acceptingthrombolysis treatment. All these datas has show P-selectin's superiority injudging whether the embolized vessels have been recanalized.When acute myocardial infarction patients accept thrombolysis treatment ,endothelial cell still in a dysfunctional state because many cell factors continue toexisting though the vessel has recover blood flow. P-selectin is surface-expressedwhen vessel endothelium is activated by many cell factors for example thrombin,histamine and oxidant. It induces endothelial cell to catch unactivated neutrophiland increases affinity between neutrophil and other kinds of adhesion molecule(e.g. ICAM-1), finally a mass of neutrophil soakage around the impairedendothelium and lead to a series of myocardial injury. Above process is the mainway to incur myocardial ischemia reperfusion injury. We discover from theexperiment that the serum P-selectin level in recanalizal success group increasetemporarily, even higher than its in recanalizal failure group at the time 3h afteraccepting thrombolysis treatment. Whether the phenomenon "abnormalincreasing" has some relation to excessive inflammatory reaction induced bymyocardial ischemia reperfusion injury, we still need farther explorement andprovement.It is obvious that dynamic serum P-selectin level measurement not only candifferentiate each kind of coronary heart disease and filter acute coronarysyndrome in the early process, but also it can be used as a indirect indexrepresenting whether thrombolysis treatment acquire success among the patientssuffering from acute myocardial infarction. When comparing to CK-MB, its effectis even superior .It is obvious that P-selectin concerns nearly not only to the developingprocess of atherosclerosis and acute coronary syndrome but also to myocardialischemia reperfusion injury because it plays an important role in inflammatoryreaction and thrombosis. Measuring series of serum P-selectin level can bring anew way to acute coronary syndrome in early diagnosis,treatment effectevaluation and prognosis judgement.Conclusion: The changes of serum P-selectin level have imitate relation bothto the severity of acute coronary syndrome and to the recanalized degree ofaccording obstructive vessel when acute myocardial infarction patients acceptingthrombolysis treatment. So dynamic serum P-selectin level measurement not onlycan differentiate the severity of acute coronary syndrome, but also can used as aindirect index representing whether thrombolysis treatment acquire success amongthe patients suffering from acute myocardial infarction.