The Observation Of The Value Of Tirofiban Hydrochloride In Patients With Acute Myocardial Infarction And No/slow Reflow Phenomena After Direct Percutaneous Coronary Intervention.

IntroductionAcute myocardial infarction(AMI) is one of the main death causes in coronaryartery disease. Percutaneous coronary intervention (PCI)is the primary avenue ofimmediately liberating infarction-realated artery, restoring myocardial availabilityreperfusion, saving ischemia cardiac muscle, reducing infarct size, maintaining leftventricular function and cutting down the mortality in AMI. PCI has becomegradually advanced in recent years, increasing the therapeutic effect of AMI. But, thehypercoagulabale state like iterative thrombosis, i.e.no-reflow or slow-reflowphenomenons in PCI which resulting in more events after AMI, such as congestedcardia failure, malignant arrhythmia, cardiac sudden death, persistent left ventricularenlargement and left ventricular remodeling, is still the main cause of cardiac eventsafter the PCI. Reportedly, 2%～8% patients with PCI will experience reblunting inthe first 24 hours after PCI. Thromboplastic hypercoagulabale state is related withplatelet aggregation and platelet activation. Aspirin and clopidogrel are routinely usedin the therapies of AMI and unstable angina for their ability of inhibiting plateletaggregation. But, they only inhibite one pathway of platelet aggregation. Whileantagonist of glycoproteinⅡb/Ⅲa receptor of platelet membrane combined with theGPⅡb/Ⅲa receptor of platelet membrane and the receptor of secondary fibronectinantagonises the activation of fibrinogen and vWF, and then blocks the final route ofaggregation and activation of platelet. Meanwhile, the combination of antagonist of glycoproteinⅡb/Ⅲa receptor of platelet membrane with many ligands can preventthe combination of fibrinogen and blood coagulation factor X with Mac-1. Itdirectly adjusts blood coagulation, restrains thrombogenesis related to thrombocyteand inhibits the secretion and release of 5-HT, hence relieving the spasm ofmicrocirculation, reducing no-reflow phenomena. It has been the active drug to checkplatelet aggregation and thrombogenesis. Consequently, additionally using ofantagonist of glycoproteinⅡb/Ⅲa receptor of platelet membrane brings us the hopefor solving the tough problem of no-reflow, slowly-reflow and the thromboplastichypercoagulabale state. Therefore, we observed and analyzed patients with AMI afterdirect PCI to offer the clinical evidence for application of antagonist of glycoproteinⅡb/Ⅲa receptor of platelet membrane, which could cut down thrombogenesis andhypercoagulabale state.Materials and methods1 Materials, grouping and observing itemsSubjects were the patients from Cardiac Internal Medicine Department in thefirst hospital of the China Medical University, who suffered from acute myocardialinfarction and underwent PCI. There are 11male, (60.55±4.80) years old and 5 female, (57.4±6.58) years.The selected patients with AMI were those who underwent PCIwithin 6 hours. They were consistent with the standards of the hypercoagulabale ofno-reflow, slow-reflow,loading thrombus, were applied tirofibanhydrochloride(xinweining, produced by wuhanyuanda pharmaceuticals company), theantagonist of glycoproteinⅡb/Ⅲa receptor of platelet membrane and weredistributed to the experimental group. In the same time, another 16 patients with AMIand PCI who are 11 males with (64.18±8.69) years old, 5 females with (61.6±4.56)years old were used as control, because of no slow-reflow, loading thrombus, hypercoaguabale state and no application of antagonist of glycoproteinⅡb/Ⅲareceptor of platelet membrane in PCI. There were no obvious differences concerning age, sex, accompanied hypertension, diabetes, hyperlipemia between the two groupsof patients.2 methodsAll patients took 0.3g asprine (produced by Bayer pharmaceuticals company) and300mg clopidogrel (plavix, produced by Sanofi-Aventis pharmaceuticals company) beforePCI at a draught. The stents were inserted as rutine methods. After PCI tirofibanhydrochloride was introvenously injected with initial dose of 10μg/kg within 3minutes, pumped continuously with micro pump via the rate of 0.15μg/kg/minute for36 hours in the experimental group. The patients whose is above 70 years old takehalf loading dose at the first time. At the same time of intravenous infusion of tirofibanhydrochlorid and Heprin Sodium were introvenously injected with 0.15ng/kg/min bymicro pump for 36 hours. Drugs for oral use and drugs for hypodermic injection arethe same for the control group. The patients of control group were given heparin(Fraxiparine) 0.4ml/bid hypodermic injection for 5 days, Bayaspirin 0.3/qd po andclopidogrel(plavix) 75mg/qd po. All patients take drugs for antiangina andhyperlipemia, et al.3 observing indexes(1) Observation the related clinical index of the two groups after PCIObserving the heart function(Killip grades), improvment of angina, the incidence ofreinfarction, reangina and reperfusion arrhythmia of the two groups after PCI.(2) ST segment's returning condition of electrocardiogram The percentage ofthose who returned≥50% within the 2 hours after the PCI was calculated。(3) Biochemical indicators' detection①Both groups of patients were taken venous blood respectively before PCI and6 hours, 12 hours and 24 hours after PCI to detect the level of troponing I and the levelof CK-MB, peak amplitude and Prothrombin Time international normalized ratio(INR) with the enzymatic determination methods.②The experimental group before applying tirofiban and after applying tirofiban, were taken venous blood the same time with the control group to detect hemoglobin, hematocrit, platelet, hepatic function and renal function.③urine samples were collected in the experimental group before applyingtirofiban and after that, the control group at the same time, for urine routine controland discovering the urine occult blood.(4) the duration in hospital and major adverse cardiac events rates wereobserved.(5) Determination of the left ventricular ejection The left ventricular ejectionfraction (represent systolic function)of the two groups of patients were determinedwith ultrasonic cardiogram equipment PHILIPS SONOS-5500, prior to dischargedfrom hospital, the relative value of E/A(represent diastolic function) was Calculated.(6) adverse reaction: the adverse reaction such as bleeding and thrombopenyand so on were observed.4,statistical treatmentAll data have been analysed statistically. Measurement data was expressed by means of(?)±s.SPSS11.5 software was used for comparison, t-test and x~2 test to test interclassdifference, P＜0.05 was significant.Result1 Comparision between the two groups of the general clinical data There wasno significant difference in age, sex, risk factor, medication, duration in hospital, ischemic time and Killip grades after PCI between the two groups, P＞0.05.2 comparison of the numbers of criminal blood vessels and the TIMI grades ofthe infarct-related artery The numbers of criminal blood vessels in experimentalgroups are equal with that of the control groups. There was no significant differencebetween the two groups, P＞0.05. The TIMI grades after PCI of infarction-relatedartery isⅠ-Ⅱ, which has significant difference with that of the control group, P＜0.05. 3 The comparison of the ST segment's recovering in electrocardiogram, reperfusion arrhythmia and angina improvement between the two groups Thepercentage of the ST segment recovering≥50% accounts individually 81.25% and75% between two groups. The incidence of reperfusion arrhythmia were respectively18.75% and 12.5%. There was no statistical difference between the twogroups, P＞0.05. Angina improvement and ischemic condition were no statisticaldifference, P＞0.05.4 The comparison between the two groups before and after PCI in troponinI,MBisoenzyme of creatine kinase and their peak amplitude. Comparison the level of cTnIand CK-MB on admission between the two groups, there were no statistical differencebetween the two groups, The peak amplitudes and the average levels of cTnI andCK-MB in the experimental group the first week after PCI were lower than that of thecontrl group. The difference is significant, The cTnI is t=2.63, P＜0.05; t=3. 92, P＜0.01 respectively. The CK-MB is t=11.79, p＜0.01, ; t=9.06, P＜0.01 respectivey.5 Comparison between the two groups in hemoglobin, hematocrit, platelet, INR, hepatic function and renal function The amount of platelet in exprimental group is(170±37.00)×10~9/L and obviously decreased, t=3.99, P＜0.01.Compared with thecontrol group, the difference is significant. After 24-36 hour of withdrawlingTirofiban, the account of platelet recovered. There were no statistical difference inother index as hemoglobin, hematocrit, platelet, INR, hepatic function and renalfunction between the two groups, P＞0.05.6 Comparison between the two groups in the heart function The left ventricularejection fractions(LVEF) prior to discharge are individually 50.1±8.0% in the studygroup and 49.6±6.2% in the control group,E/Aratios＞1 prior to dischargeare individually 12 in the study group and 8 in the control group There were nosignificant difference in LVEF and E/A ratios, P＞0.05.7 Comparison between the two groups of cardiac events and adverse reactionThere were no heart events after PCI in the two groups, which included death, reinfarction revascularization. There were no intracranial hemorrhage, haematemesis, troperitoneal hemorrhage or hemorrhea in other places. There were 2 cases of urineoccult blood in experimental group. When the Tirofiban was stopped and the amountof heparin was reduced, the urine occult vanished and did not cause degression inhemoglobin and did not need blood-transfusion. In experimental group, using tirofibancaused the amount of platelet decreasing obviously, when tirofiban was stopped theamount of platelet recovered.Conclusion1 Additionally using of antagonist of glycoproteinⅡb/Ⅲa receptor of plateletmembrane, Tirofiban, can depress the levels of cTnI and CK-MB of AMI.2 Additionally using of antagonist of glycoproteinⅡb/Ⅲa receptor of plateletmembrane, Tirofiban, has become a safety and valid measure to no/slow reflow andloading thrombus after AMI with PCI.3 Additionally using antagonist of glycoproteinⅡb/Ⅲa receptor of plateletmembrane, Tirofiban, did not cause MACE such as, death, reinfarction andrevascularization in AMI and no/slow reflow and loading thrombus after direct PCI.4 Additionally using of antagonist of glycoproteinⅡb/Ⅲa receptor of plateletmembrane, Tirofiban, did not increase the incidence of serious adverse reaction, suchas bleeding after AMI with PCI...