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Effects of ticagrelor after PCI on myocardial microcirculation, plasma sCD40L and IL-6 levels in PATIENTS with NSTEMI

 The pathogenesis of non-ST-segment elevation myocardial infarction (NSTEMI) is that plaque rupture leads to thrombosis, which leads to complete coronary artery closure, and ST-segment elevation can be seen on electrocardiogram. Compared with ST-segment elevation myocardial infarction, the infarction scope is smaller, with almost no Q wave on electrocardiogram, and generally accompanied by a small amount of endangered myocardium [1]. The treatment of NSTEMI is mainly to dredge coronary vessels, dissolve thrombosis and improve myocardial blood supply, and percutaneous coronary intervention (PCI) is a commonly used treatment [2]. PCI can lead to vascular endothelial damage and thrombosis due to platelet adhesion, and patients are prone to dyspnea, arrhythmia, myocardial ischemia and other adverse events. Therefore, drugs should be combined to reduce platelet aggregation to treat NSTEMI[3]. Traditional antiplatelet drugs use clopidogrel, the effect is limited [4]. Tiprelor has fast onset and long-lasting antiplatelet activity, and does not need to be transformed into active products through the metabolic process of liver enzymes [5]. However, the study on its treatment of NSTEMI patients after PCI is insufficient. Therefore, this study investigated the efficacy of tiprelor in the treatment of NSTEMI after PCI. To provide more reference for the treatment of NSTEMI patients after PCI.


1. Data and methods


1.1 general data eighty-four patients with NSTEMI admitted to anshan central hospital from July 2019 to September 2020 were selected. Inclusion criteria :(1) meeting the diagnostic criteria for NSTEMI [6]; (2) Age > 18 years old; (3) All patients underwent PCI. Exclusion criteria :(1) intolerance to the drug in this study; (2) liver and kidney dysfunction, immune system, blood system, nervous system and malignant tumor diseases; (3) History of bleeding and coronary artery bypass grafting; (4) mental diseases; (5) Unstable vital signs. Patients were randomly divided into control group (42 cases) and observation group (42 cases). This study was approved by the ethics Committee of our hospital, and all patients or their families were informed and signed informed consent.


1.2 Methods The two groups were given aspirin enteric-coated tablet 300 mg orally before PCI (manufacturer: Guangdong Bangmin Pharmaceutical Co., LTD., Approval No. : H44022307, specification: 0.3 g), and aspirin enteric-coated tablet 100 mg orally once a day after PCI. The control group was given clopidogrel hydrogen sulfate tablets (manufacturer: Nanjing Zhengda Tianqing Pharmaceutical Co., LTD., Approval No. : National Drug Approval WORD H20203269, specification: 75 mg) orally, once a day, 75 mg per time. Observation group was given ticagrelor tablets (Astrazeneca Pharmaceutical Co., LTD., Approval No. : National Drug Approval H20217033, specification: 90 mg) orally, twice a day, 90 mg per time. Both groups were treated for 1 month.


1.3 Observational indicators and criteria (1) Myocardial function indicators. Fasting venous blood was collected from the two groups before and after treatment, and serum was separated. Cardiac Troponin I (cTnI) and creatine kinase isoenzyme-MB (CK-MB) were determined by enzyme-linked immunoassay (KIT was purchased from Nanjing Jianceng Institute of Biological Engineering). (2) Inflammatory response indicators. Fasting venous blood was collected before and after treatment, and plasma was separated. Soluble CD40 ligand (sCD40L) and interleukin-6 (IL-6) were determined by enzyme-linked immunoassay (ELISA kit was purchased from Nanjing Jicheng Institute of Biological Engineering). (3) Oxidative stress index. Peripheral venous blood of the two groups was collected before and after treatment, and superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by chemiluminescence assay (kit from Roche). (4) Platelet aggregation and inhibition (adenosine diphosphate pathway). Fasting venous blood of both groups was collected before and after treatment and measured by thrombus elastogram analyzer (Hamoscope, USA). (5) The occurrence of adverse reactions during treatment was recorded. (6) All patients were followed up for 1 month by telephone, wechat and home visits, and the incidence of adverse cardiovascular events in the two groups was analyzed.


1.4 Statistical Analysis SPSS 20.0 software was used for statistical analysis. Measurement data were expressed as (x± S). Independent sample T test was used for inter-group comparison, and paired T test was used for intra-group comparison. The count data were expressed as percentage (%) and the word 2 test was used for comparison. In order to P< 0.05 was considered statistically significant.


2 the results


2.1 Comparison of general data between the two groups There was no statistically significant difference between the two groups (P> 0.05), are comparable, as shown in Table 1.


2.2 Comparison of myocardial function indexes between the two groups Before treatment, there was no significant difference in the levels of cTnI and CK-MB between the two groups (P> 0.05). After treatment, the levels of cTnI and CK-MB in both groups were lower than before, and the levels of cTnI and CK-MB in observation group were lower than control group, the differences were statistically significant (P< 0.05). Are shown in table 2.


2.3 Comparison of inflammatory response indicators between the two groups Before treatment, there was no statistical significance in sCD40L and IL-6 levels between the two groups (P> 0.05). After treatment, sCD40L and IL-6 levels in both groups were lower than before, and sCD40L and IL-6 levels in observation group were lower than control group, the differences were statistically significant (P< 0.05). See table 3.


2.4 Comparison of oxidative stress indexes between the two groups Before treatment, there was no significant difference in SOD and MDA levels between the two groups (P> 0.05). After treatment, SOD level in both groups was higher than before treatment, while MDA level was lower than before treatment (P< 0.05); After treatment, SOD level in observation group was higher than control group, while MDA level was lower than control group (P< 0.05). See table 4.


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2.5 Comparison of platelet aggregation rate and inhibition rate between the two groups Before treatment, there was no significant difference in platelet aggregation rate and inhibition rate between the two groups (P> 0.05). After treatment, the platelet aggregation rate in both groups was lower than before treatment, and the platelet inhibition rate was higher than before treatment (P< 0.05); After treatment, the platelet aggregation rate in the observation group was lower than that in the control group, and the platelet inhibition rate was higher than that in the control group (P< 0.05). As shown in table 5.


2.6 Comparison of the incidence of adverse reactions between the two groups During treatment, there was no statistically significant difference in the incidence of adverse reactions between the two groups (Word 2=0.151, P=0.698), as shown in Table 6.


2.7 Comparison of the incidence of adverse cardiovascular events between the two groups During the follow-up period, there was no significant difference in the incidence of adverse cardiovascular events between the two groups (Word 2=2.477, P=0.115), as shown in Table 7.


3 discuss


NSTEMI treatment requires timely dredging of blocked blood vessels and restoration of myocardial blood reperfusion, so as to minimize the duration of myocardial ischemia [7]. PCI is widely used in NSTEMI, which can open coronary arteries and reduce mortality [8]. However, stent implantation and guide wire crossing during PCI can cause damage to vascular endothelial cells. In addition, various surgical instruments are treated as foreign bodies, resulting in platelet aggregation, thrombosis, and vascular stenosis or even occlusion [9-10]. Studies have shown that about one-third of the dilated blood vessels after PCI will become narrow again [11]. Therefore, antiplatelet drug therapy after PCI is very important. Clopidogrel can prevent platelet aggregation by reducing the binding of platelet receptors and adenosine diphosphate. The key to its efficacy lies in the generation of active products, which depends on the action of enzymes [12-13]. Studies have shown that ticagrelor may have a better anti-platelet aggregation effect, and it also has a certain role in anti-inflammatory response [14]. Therefore, this study investigated the effect of ticagrelor in the treatment of NSTEMI after PCI.


Studies have shown that cTnI will diffuse from damaged myocardial cells into the blood within 6 h after myocardial infarction, and the higher the level of cTnI in the blood, the more serious the myocardial necrosis [15]. Ck-mb is an index reflecting myocardial injury, and when cK-MB exceeds 6% of creatine kinase, it represents myocardial injury [16]. The results of this study showed that after treatment, the levels of cTnI and CK-MB in the observation group were lower than those in the control group (P< 0.05), suggesting that teprelor can improve myocardial function. Teprelor itself has an anti-platelet effect, which can reduce platelet aggregation, inhibit thrombosis, increase cardiac blood perfusion, and contribute to the recovery of myocardial function. At the same time, teprelor can regulate adenosine, maintain the degree of vasodilation and remove oxidative free radicals, so as to avoid further damage to myocardial cells. After treatment, the levels of sCD40L and IL-6 in the observation group were lower than those in the control group, suggesting that ticagrelor treatment can reduce inflammatory response, which is basically consistent with the conclusions in previous literature [17]. Ticagrelor can delay adenosine uptake by red blood cells, thereby increasing the content of adenosine in myocardium, enabling adenosine to play a full role in inhibiting the production of inflammatory factors such as sCD40L and IL-6, thereby reducing the inflammatory response. SOD is a natural antioxidant that can prevent coronary artery damage as much as possible by inhibiting oxygen free radicals [18]. MDA has the opposite effect to SOD, increasing oxide and thus destroying cardiac muscle cells. After treatment, SOD level in observation group was higher than control group, MDA level was lower than control group (P< 0.05), suggesting that ticagrelor treatment can reduce oxidative stress response. Fu Bing et al. [19] respectively used ticagrelor and clopidogrel to treat NSTEMI patients undergoing PCI surgery and found that ticagrelor could reduce oxidative stress response, which is consistent with the conclusion of this study. Wang Qian et al. [20] pointed out that ticagrelor can reduce oxidative stress response due to the role of adenosine. Ticagrelor protects adenosine, which increases SOD activity to increase SOD content. At the same time, adenosine can also dilate blood vessels, inhibit MDA production, promote blood supply in myocardium, increase oxygen content in myocardium tissue, and thus protect myocardium. In this study, after treatment, the platelet aggregation rate of the observation group was lower than that of the control group, and the platelet inhibition rate was higher than that of the control group (P< 0.05), suggesting that ticagrelor treatment can promote myocardial microcirculation. Zhang Xiumin et al. [21] studied the platelet aggregation rate before surgery, 24 h after surgery, 7 d after surgery and 1 month after surgery, and found that ticagrilor was more advantageous in reducing platelet aggregation rate in NSTEMI patients undergoing PCI. Platelet aggregation is the main cause of thrombosis, which continuously blocks blood vessels and affects the microcirculation of the heart muscle. Clopidogrel can not directly play the antiplatelet effect, it needs to be an active product, so the effect is slow; However, ticagrelor not only has rapid and reversible antiplatelet effects; Therefore, ticagrelor can better improve myocardial microcirculation. During treatment, there was no significant difference in the incidence of adverse reactions between the two groups (P> 0.05), and at a low level, suggesting that ticagrelor is safe for treatment. During follow-up, there was no significant difference in the incidence of cardiovascular adverse events between the two groups (P> 0.05), and at a low level, suggesting that ticagrelor has a good prognosis.


In conclusion, the treatment of NSTEMI with ticagrelor after PCI can improve myocardial function, reduce inflammatory response and oxidative stress response, and improve myocardial microcirculation, with good safety and prognostic effect, and worthy of clinical application.


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