Activated Platelets And Its Clinical Significance In Patients With AMI Treated By PCI

Objective:Activated platelets play an important role in the course of occurrence and development of AMI.In the normal circulation,platelets are in the resting state.In the course of PCI. platelets are activated by balloon dilatation,stimulation of stent and vascular endothelium injury.As aboved reason,PCI has become the main cause of acute vascular occlusion,coronary micro-embolization,vascular restenosis.The objective of this article is to study the state of platelets after PCI and effect of antiplatelet drugs by the randomized controlled method. Through this study,we can get reliable theoretical basis for prevention and treatment of AMI.Material and methods:The study was performed in thirty patients(17 males and 13 females,mean age 55±9)with first AMI admitted to our hospital from March 2007 to April 2008 and thirty healthy volunteers(18male and 12female,average age was 53±8).All patients were diagnosed as AMI corresponding by 1999 criterion of AHA/ACC:(1)All patients had typical persistent angina for more than thirty minute;(2)The cardiac enzyme(CK CK-MB)peak increased beyond more than two folds of normal range and troponin was positive;(3)the electrocardiographic evidence of ST-segment elevation evolved in two or more bordering leads and existing mobile changes;(4)all patients were diagnosed within 12 hour from AMI.Defining the exclusion criteria:(1) Variability angina;(2)Serious liver and kidney function disease;(3) Ischemic encephalopathy;(4) Blood system diseases;(5)Patients are resistant-anti platelets drug and sensitive to anti platelets drug.(6) Patients has taken platelet function impact the drug before operation,such as aspirin,low molecular weight heparin.All patients was divided two groups:trial group n=30,control group n=30.we collected blood cholesterol,blood triglyceride,electrocardiographic information.All patients were accepted emergence CAG and PCI treatment.All the patients in trial group have taken aspirin 300mg and clopidogrel 300mg before PCI and persist in taking aspirin 300 mg and clopidogrel 75mg.During the intervention,we gave trial group unfractionated heparin 10000 U.we gave low-molecular-weight heparin calcium 5000U/12h,3-5d.All the patients and volunteers were taken venous blood sample by vacuum blood collection needle within two days before taken aspirin.The trail group would be taken venous blood sample again after 2 weeks when the state of patients get well.Dont take tourniquet when taken the blood sample.Drop the first 2 ml blood mixed by tissue fluid.A sample is directly inhaled through the suction tube CTAD,gently mixing, avoiding violent shaking and impact on the platelet activation.We would fluorescent label,fix,and detect the platelets within 20 minutes.Control tube add Mouse IgM FITC, Mouser-PE,CD61 PerCP the 10μL,test-tube add PAC-1 FITC, CD62 P PE,CD61 PerCP the 10μL,then two tubes all add precooling 2～8℃1%polyformaldehyde 0.5 mL and blending, two tubes then all were placed in 2～8℃refrigerator 30 minutes.The above steps are completed within 2h in order to decrease the activation of platelets.Preparation of specimens will detected on machine in 24 hours.SPSS13.0 statistic software was used to analysis all the data.The numerical variable was pretented as mean+SD,the categorical variable was pretented as rate or percentage.We used analysis of variance between trial group and control group.Two groups were analysed by paired t-test between pre-PCI and post-PCI respectively:statistical significance was indicated by P value＜0.05.Results:(1)There was no significant difference of the baseline characteristics between the two groups,including the age,sex,history of smoking,weigh index(P＞0.05).Acute myocardial infarction group pre-treatment platelet surface glycoprotein PAC1,CD62P expression rates were(17.26±5.36)%,(4.01±2.78)%respective,healthy control group, respectively(2.15±0.55)%,(1.06±0.53)%,acute myocardial infarction group was significantly higher(P＜0.05).(3)Acute myocardial infarction group after treatment by the anti-platelet PAC1,CD62P expression rate decreased to(4.32±0.82)%and (2.14±0.72)%,compared with pre-treatment have decreased significantly(P＜0.05).(4) Acute myocardial infarction group after treatment by the anti-platelet PAC1,CD62P expression rate decreased to(4.32±0.82)%and(2.14±0.72)%,still higher than the healthy control group(P＜0.05).(5) Platelet count PLT (×10~9 / L) before and after the experimental group,no significant changes in medication,medication before and after the trial group compared with the control group no significant change.Conclusion:The research showed that the level of PAC1,CD62P is visible higher in the patients of AMI than in the healthy human(P＜0.05),there is a clear platelet activation in the patients with AMI,platelet activation participated in the occurrence and development of AMI.At the same time,the research showed that the patients with AMI have marked improvement of their clinical symptoms.The fact that the level of PAC1,CD62P visible decrease showed anti-platelet therapy for patients with acute myocardial infarction are effective,also provides a theoretical basis for acute myocardial infarction in patients with anti-platelet-activating drug.