| Objective: Variable degrees of myocardial injury can occur during the course of percutaneous coronary intervention (PCI), as reflected by rises in cardiac enzymes such as creatine kinase (CK) and creatine kinase isoenzymes. Frequent (5.0 to 30.0 percent) elevations in CK-MB had been reported. More recently, the cardiac troponin I (cTnI) has emerged as a highly sensitive and specific marker of myocardial cell injury. The prevalence of postprocedural increase of cTnI is much higher which was between 30% and 40%. It has been reported that post-PCI troponin I concentrations bore much relationship to clinical, angiographic and in-laboratory minor adverse events, indicative of myocardial injury, as well as during follow-up. Therefore, it is very important to clarify the mechanisms of post-PCI myocardial injury.Many factors reported are associated with myocardial injury following the coronary angioplasty, including transient occlusion of blood flow, distal thromboembolization, compromised lateral branches,vessel spasm resulting from the liberation of vasoactive substances, hypotension, and prolonged ischemia and so on. Most recently, researchers pay more attention to the formation of coronary microembolization during the course of PCI. Damaged endothelial cells may release thrombotic material which can activate the platelet and induce thrombus formation. Debris that are washed out of the plaque could not only dislodge into the microcirculation but also activate the platelet and then to form thrombus in the microcirculation. So myocardial injury could be induced by thrombus formation and the following microembolization. Fibrinogen as the most contained blood coagulation factor in plasma has the important functions in thrombus formation.There are several biological mechanisms through which increasing fibrinogen levels may promote thrombogenesis, including the increase of plasma and blood viscosity, facilitation to the aggregation of platelets, and so on. D-dimer as the end product of the degradation of fibrin is one molecular marker of ongoing thrombus and spontaneous thrombolysis. CK-MB and cardiac troponin I (cTnI) are the specific markers of myocardial injury. The purpose of the present study is to find out the relationship between the level of plasma fibrinogen and D-dimer and the myocardial injury during elective percutaneous coronary intervention. Another purpose of this current study is to find the high risk people of PCI. Thirdly, we also try to illuminate, with the routine adjunctive drug therapy before and during PCI, whether it is needed or not to strengthen the antiplatelet therapy and anticoagulation therapy.Methods: 122 patients who underwent elective PCI were enrolled between January to October 2006, including 86 males and 36 females, with mean age of 66.6 years. All patients received aspirin (100 mg QID) and clopidogrel (75 mg QID) for at least three days. Heparin included a 60-100IU/kg bolus injection from arterial sheath immediately before PCI, which was followed by a 2000IU every one hour. After arterial sheath removal, low molecular heparin was used for 3-5 days. In the morning of operating day and the next day (24h after PCI), blood samples were obtained through venipuncture so as to measure the levels of fibrinogen, D-dimer, CK-MB and cTnI. According to whether cTnI≥0.5ng/ml or not after PCI, patients were divided into cTnI-positive group and cTnI-negative group. Continuous variables were expressed as the mean value±SD, discrete variables were summarized as percentages. Independent Student t test was performed to determine the differences between mean values for continuous variables at baseline, and the procedural characteristics between the two groups. Groups were compared using the chi-square test for discrete variables. Plasma fibrinogen and D-dimer levels before and after procedure were compared with paired t test. The influence of clinical baseline factors, procedural variables, the levels of plasma fibrinogen and D-dimer was evaluated by stepwise logistic regression analysis. Receiver Operating Characteristics (ROC) analysis was performed on fibrinogen concentrations to define the cut-off value of sensitivity and specificity. A p value of <0.05 was considered statistically significant.Results: Among the 122 patients, 25 (20.49%) patients had elevated cTnI after elective PCI, and 97 (79.51%) patients had not elevated cTnI in 24 hours after PCI. Eighteen patients who had elevated CK-MB were all accompanied by elevated cTnI. A fair correlation was present between the postprocedural CK-MB and cTnI levels (r=0.67, P<0.05). There was no death and urgent target vessel revascularization. One patient had side branch occlusion which suffered non-ST elevation myocardial infraction and accompanied with increase of CK-MB above three times of the upper limit. The recent history of smoking, myocardial infraction, diabetes, hypertension, multivessel disease were more frequent in the cTnI-positive group, but it was not statistically significant when compared with the cTnI-negative group (P>0.05). Other baseline characteristics such as ages, gender, hypercholesterolemia, were similar in the two groups. Postprocedural cTnI-positive patients had higher level of stenosis before PCI (84.60±5.34%versus 79.88±8.12%, P <0.05) and higher maximal inflation pressure (18.68±3.47atm versus 16.87±3.12 atm, P<0.05). The patient with side branch occlusion was in the cTnI-positive group. Other procedural characteristics including transient coronary spasm, total time of dilation, total duration of stent were similar between the two groups (P >0.05). Twenty-four hours after PCI, the concentrations of fibrinogen and D-dimer were both obviously increased in cTnI-positive group (P <0.05), but not in cTnI-negative group (P>0.05). Compared with cTnI-negative group, the concentrations of fibrinogen and D-dimer in cTnI-positive group were higher either before or after PCI. Even after the patients with side branch occlusion was excluded from cTnI-positive group, comparisons between the two groups were the same as the above mentioned. By logistic regression analysis, predictors of cTnI increase post-PCI were fibrinogen level before PCI, the diameter stenosis before PCI and the maximal inflation pressure (all P < 0.05). Receiver Operating Characteristics (ROC) analysis showed a baseline fibrinogen level of≥365.35mg/dL was associated a sensitivity and specificity of 84.0% and 73.5% for predicting post-procedure cTnI elevation (P < 0.05).Conclusions: There is many factors induced postprocedural myocardial injury. Microembolization plays an important role in it which causes the disorder of microcirculation. Fibrinogen concentration before PCI is the important predictor of postprocedural myocardial injury. It could be beneficial to those patients with high risk by depressing plasma fibrinogen level. |
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