| It is the appearance of drug-eluting stent that has opened the new page of Percutaneous transluminal Coronary Intervention (PCI) since 2003. The rate of in-stent restenosis(IRS) has decreased, the incidence of stent thrombosis, however, has been increasing, especially in complex coronary lesions. Meanwhile, no-reflow phenomenon has also seen more often. So it is important to conduct anti-thrombosis therapy during peroperative period. Tirofiban hydrochloride, representative GP Ⅱb/Ⅲa receptor antagonists, has been applied wildly to treat Acute Myocardial Infarction (AMI). This research aims at estimating the clinical value of tirofiban hydrochloride in PCI of complex coronary lesions.1.Materials and Methods:1.1 General data:We have continuously and randomly selected104 patients (56 males and 48 females,aged 61.73+/-6.43 years old) who were diagnosed ischemic heart disease and confirmed for complex coronary artery lesions by coronary angiography from April 2013 to April 2014. According to The WHO diagnostic criteria of ischemic heart diseases was applied to this study,we classified 104 patients to three types:15 cases of stable angina pectoris,61 cases of unstable angina pectoris,28 cases of Non-ST segment Elevated Myocardial Infarction. Exclusion criteria:1. Older than 80 years old; 2.ST-elevation myocardial infarction; 3.The recent bleeding (1 year), including gastrointestinal bleeding or clinical significance of urinary tract hemorrhage; 4.Left main lesion; 5. Cardiac function grade Ⅲ-Ⅳ (NYHA classification); 6. Serious uncontrolled hypertension (systolic blood pressure is greater than 180 mmHg, and/or diastolic blood pressure is greater than 110 mmHg); 7.the known blood coagulation disorders; 8. History of abnormal platelet or thrombocytopenia, preoperative platelet count is less than 100×109/L; 9. Severe renal insufficiency (creatinine clearance is less than 30 ml/min).10. Severe hepatic insufficiency; 11. History of cerebrovascular disease within one year; 12. big surgery or severe physical trauma within one month; 13. Acute pericarditis; 14. Hemorrhagic retinopathy; 15. The rheumatic valvular heart disease; Acute infection; 16.17. Dissecting aneurysm; 18 patients with tumor.Definition of complex coronary lesion:According to the complex degree, panel from ACC/AHA classified lesion of coronary artery into type A B1 B2 and C, and defined type B1 and type C as complex coronary artery lesion in 1998. If there is only one type B lesion, that will be defined as type B1. If there are two or more than two type B lesions, that will be called type B2.104 cases have been chosen into this research.50 type B2 cases(strengthened group 23,control group 27) and 54 type C cases (strengthened group 29, control group 25).1.2 Method1.2.1 Medication:For the control group, conventional dual antiplatelet therapy is conducted before operation. Heparin is given in 80-100 u/kg during the operation by intravenous administrration. After operation, conventional dual antiplatelet therapy is also needed accompanied with low molecular heparin (1 mg/kg 12h,5 to 7 days) and statin. As to beta blockers and/or ACEI, it depends on disease. Intensive treatment group:In addition to what were administrated in control group tirofibanhydrochloride (5 mg/100 ml, made in GrandPharma Company in WuHan)were continuous given to intensive treatment group via injecting 10μg/kg tirofiban hydrochloride into coronary artery in 5 minutes and continuous intravenous pumping with the speed of 0.15μg (kg·min) for 24 to 36 hour.1.3 Observation Indexes1.3.1 Serum index:Venous blood extracted at 24 hours after PCI was used to detect TNI level with chemiluinescence method. The normal value was less than 0.04ng/ml.24 hours after the operation and preoperative venous blood were needed for the determination of hsCRP by particle enhanced immunonephelometry, then calculating the delta hsCRP. Delta hsCRP was divided into two type (<3mg/l and>3mg/l) Venous blood at 6 hours after PCI were collected to detect blood routine with a tube whichrcontained citrate.1.3.2 Postoperative angina pectoris:Chest pain, duration less than 15 minutes, with ST dynamic changes in ECG or exercise load test positive.1.3.3 Major adverse cardiac events (MACE):all-causes death, stent thrombosis, target vascular reconstruction or newly myocardial infarction are included.Definition of stent thrombosis:due to the effect of various factors in stent thrombosis. This study applies for definite stent thrombosis, defined as referring to confirmed by angiography or pathology confirmed clear stent thrombosis. Stent thrombosis were classified into four types with the time of thrombosis after PCI according to the Academic Research Consortium (ARC):①Actue stent thrombosis:Stent thrombosis within 24 hours after stent implantation;②Subacute stent thrombosis:Stent thrombosis at 1 to 30 days after stent implantation;③Late stent thrombosis:Stent thrombosis at 30 days to 1 year after stent implantation;④Late late stent thrombosis:Stent thrombosis over 1 year after stent implantation;1.3.4 TIMI flow grade:TIMI 0:no perfusion, vascular occlusion, no contrast agent through;TIMI 1:a small amount of contrast agent through the narrow site, but insufficient distal vascular bed developmentTIMI 2:narrow parts by contrast, can make the distal vascular enhancement, but the contrast agent through the proximal blood vessels speed faster than the speed of a narrow place, or narrow distal contrast emptying delay than the severe stenosis site;TIMI 3:contrast filling distal vascular quickly, the speed of the proximal to the flow within the vascular bed and reach the speed of the distal vascular bed.1.3.5 Bleeding:ACS and bleeding events of PCI from relative experts of European Society of Cardiology Working Group on thrombus (TIMI bleeding grade):①Major hemorrhage:intracranial hemorrhage or clinical visible hemorrhage (including imaging hemorrhage) with decrease of hemoglobin concentration no less than 5g/dL;②Small hemorrhage:clinical visible hemorrhage (including imaging hemorrhage) with decrease of hemoglobin concentration ranging from 3g/dL to 5g/dL;③Moderate hemorrhage:clinical visible hemorrhage with decrease of hemoglobin concentration no more than 3g/dL.(decrease amplitude of hemoglobin concentration replaced by AHb).1.3.6 Platelet-Judgment standard on glycoprotein Ⅱb/Ⅲa receptor antagonists induced thrombocytopenia (GIT):Check the platelet account 24 hours after receiving glycoprotein Ⅱb/Ⅲa receptor antagonists.Mild thrombocytopenia:The platelet count< 100* 109/L; Severe thrombocytopenia:The platelet count< 50* 109/L; Extremely severe thrombocytopenia:The platelet count< 20 x 109/L.1.4 Statistical Method:We use SPSS version 19.0 to analysis statistics,we also regard the mean+/-standard deviation (x±s) as the expression of measurement data,and compare the different means among different groups via t test. The count data is analyzed by X2 test, if the p is less than 0.05, it means there is significance detected.2.Results:2.1 Patients clinical condition:For age, sex ratio, high blood pressure, diabetes, LDL-C and creatinine of two groups, there was no statistically significant difference (p> 0.05). And for NSTMI, UAP and SAP there were also no statistically significant difference (p>0.05).2.2 Coronary artery intervention:From the results of coronary angiography, there was no statistical significance (p>0.05) on the composition proportion of type B2 and type C, and the number of placing stents between the two groups.2.3 Validity comparison2.3.1 TNI and AhsCRP:Increasing amplitude of TNI and AhsCRP in the intensive therapy group was obviously lower than the control group’s. There were significant statistic difference (P<0.001).2.3.2 Postoperative angina pectoris and MACE 30 days afteroperation.MACE was not occurred in the intensive therapy group, while there was one case death of unexplained sudden death on the 15th day in control group. One case with subacute stent thrombosis recovered after stent replacement and strengthening anti-platelet therapy. But there was no obvious statistical significance between the two groups (P=1.000).Angina pectoris have occurred in both groups, but the rate of intensive therapy group was lower than the control group’s (1.9% vs 15.4%). Statistical significance were detected (P=0.031).1 case with angina pectoris have been confirmed without stent thrombosis and restenosisvia coronary angiography, and eased after drug treatment. In the control group, there were 8 cased observed. Two cases with mild stenosis developed into myocardial ischemia,and turned to be better after intensive stain therapy and anti-platelet therapy.2 cases considered for coronary artery spasm, improved after giving diltiazem hydrochloride 1 cases with clopidogrel resistance 1 case was considered for the consequence of anxiety symptoms,and eased after anti-anxiety therapy.2.3.3 TIMI flow after operationIntensive therapy group was higher than the control group (100% vs 88.5%) for TIMI flow level 3 after operation. And intensive therapy group was lower than the control group (0% vs 11.5%) for TIMI flow level 2 after operation.The differences were statistically significant (P<0.05).2.4 safety comparison:In the intensive therapy group, the number of bleeding point in 1 case with moderate hemorrhage gradually reduced after discontinuation of tirofiban.2 cases with small hemorrhage, was the hematuria and nasal bleeding respectively Hematuria was treated by discontinuation of tirofiban and bladder irrigation.After three times bladder washing in 24 hours, the hematuria has never occurred again. For the view of specialist, nasal bleeding was considered for the nasal mucosa dry, and stopped after nasal local treatment.In the control group, there were 2 cases with moderate bleeding, conjunctival congestion and gingival bleeding and diagnosed as conjunctivitis after clinical consultation,which had no correlation with the drug.They were both improved after giving eye drops. Gingival bleedingeased after local treatment with cotton ball compression.1 cases with small hemorrhage was bleeding at the puncture sites and improved after discontinuation of low molecular heparin. No massive hemorrhage has observed, little hemorrhage and micro hemorrhage common occurrence rate was 5.8%,there was no statistical difference (p= 1.000). Decrease amplitude of hemoglobin concentration in the intensive therapy group was more than the control group (1.81±0.565 vs 1.62±0.530), but no significant difference was detected (P=0.78). Slightly thrombocytopenia (GIT) only occurred in the intensive group occurred and eased at the 6th hours after discontinuation of tirofiban. Although there was no hemorrhage detected in the control group, this difference had no statistical significance (p=1.00).3.Main conclusionThe decrease of TNI and delta hs CRP meant lower degree of microembolization and myocardial injury, which may corresponded with the improvement of TIMI flow after receiving tirofiban hydrochloride. But there was no significant different for MACE, the result need further research. In intensive therapygroup, hemorrhage and declination of platelet did not occur, which indicated tirofiban hydrochloride therapy was safety. And none MACE have been observed in the intensive therapy group, which might be related with drug delivery within coronary artery, without increasing the risk of hemorrhage. The consequence also suggested tirofiban hydrochloride therapy was safety. It seems that tirofiban hydrochloride therapy has a certain value, good curative effect and security in complex coronary artery lesions PCI therapy. We suggested there was need to continue to focus on tirofiban hydrochloride therapy in complex coronary artery lesions PCI therapy in future clinical practice. |
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