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1.
目的:评价替格瑞洛在急性冠脉综合征(acute coronary syndrome,ACS)患者经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)术后的应用价值。方法:将我院收治的565例成功行PCI的急性冠脉综合征(acute coronary syndrome,ACS)患者随机分为2组:氯吡格雷组253例,术后口服氯吡格雷75 mg、QD;替格瑞洛组312例,术后口服替格瑞洛首剂180 mg,维持量90mg、BID。两组患者术后常规口服阿司匹林100 mg、QD。研究主要终点为主要不良心血管事件(major adverse cardiovascular events,MACE),包括全因死亡、靶血管血运重建和脑梗塞;次要终点为TIMI主要出血(定义为血红蛋白下降50 g/L或颅内出血有关的临床显著出血事件)。结果:565例患者平均随访12个月,替格瑞洛组MACE发生率低于氯吡格雷组(3.8%vs.8.7%,P0.05),两组TIMI主要出血事件发生率比较,差异无统计学意义(2.9%vs.3.2%,P0.05)。结论:替格瑞洛能明显减少PCI术后主要不良心血管事件,并不增加主要出血。  相似文献   

2.
目的:探讨替格瑞洛治疗急性ST段抬高性心肌梗死(STEMI)的有效性及安全性。方法:收集西京医院心内科收治的STEMI患者196例并将其分为氯吡格雷组(n=100)和替格瑞洛组(n=96)。两组患者入院后均接受常规治疗,氯吡格雷组给予氯吡格雷负荷剂量300 mg,PCI术后给予氯吡格雷标准剂量(75 mg,1/日,口服)治疗;替格瑞洛组给予180 mg负荷剂量,PCI术后给予替格瑞洛标准剂量(90 mg,2/日,口服)治疗。于患者出院后1月、3月、6月进行随访,观察和比较两组患者不良终点事件及出血事件发生情况的差异。结果:两组患者一般情况、危险因素、临床用药及其他治疗情况比较均无统计学差异(P0.05)。两组6个月主要及次要终点事件、主要及次要出血事件的发生情况比较无显著差异(P0.05)。结论:替格瑞洛与氯吡格雷对STEMI患者近中期不良终点事件的影响相当。  相似文献   

3.
目的:探讨替格瑞洛与氯吡格雷对急性心肌梗死患者介入治疗后的心功能和炎症反应的影响。方法:选取2015年1月-2018年1月期间我院收治的行介入治疗的急性心肌梗死患者300例为研究对象。根据随机数字表法将患者分为替格瑞洛组(n=150)和氯吡格雷组(n=150),其中替格瑞洛组给予阿司匹林、替格瑞洛治疗,氯吡格雷组给予阿司匹林、氯吡格雷治疗。比较两组患者治疗前后的左心室射血分数(LVEF)、左心室舒张末期内径(LVEDd)及白介素-6(IL-6)、C反应蛋白(CRP)、可溶性CD40配体(s CD40L)、肿瘤坏死因子-α(TNF-α)水平,随访3个月,观察两组患者随访期间心血管不良事件的发生情况。结果:两组患者治疗后LVEF较治疗前升高,且替格瑞洛组高于氯吡格雷组,LVEDd较治疗前降低,且替格瑞洛组低于氯吡格雷组(P0.05)。两组患者治疗后IL-6、CRP、s CD40L、TNF-α均较治疗前升高,但替格瑞洛组低于氯吡格雷组(P0.05)。替格瑞洛组随访期间心血管不良事件总发生率为10.00%(15/150),显著低于氯吡格雷组患者的31.33%(47/150),组间比较差异有统计学意义(P0.05)。结论:相较于氯吡格雷而言,替格瑞洛治疗行介入治疗的急性心肌梗死患者效果满意,可显著改善心功能,降低炎症因子水平及心血管不良事件发生率。  相似文献   

4.
目的:通过比较奥美拉唑和泮托拉唑对冠状动脉支架术(PCI)后患者血小板功能指标和主要不良心血管事件与出血并发症发生情况,探讨不同质子泵抑制剂对PCI后氯吡格雷联合阿司匹林抗血小板作用的影响。方法:60例实施PCI后常规联合抗血小板治疗(氯吡格雷75mg/d+阿司匹林100mg/d)患者随机分为奥美拉唑组(40mg/d,20例),泮托拉唑组(40mg/d,20例)和对照组(20例),连续用药30d。分别在服药前1d及服药15d,30d用血栓弹力图检测ADP途径诱导的血小板抑制率值和比浊法检测ADP途径诱导的血小板最大聚集率(MPAR)。并观察30d各组主要不良心血管事件和出血并发症的发生情况。结果:①奥美拉唑组和泮托拉唑组与对照组相比,服药前1d及服药15d,30d用血栓弹力图检测的血小板抑制率和比浊法检测的血小板最大聚集率(MPAR)均无明显变化;奥美拉唑与泮托拉唑组间比较,差异也无统计学意义。服药15d,30d与服药前1d相比,每组血小板抑制率明显升高,血小板最大聚集率明显下降,差异有统计学意义(P0.05);但15d和30d相比较,差异无统计学意义。②三组比较心血管事件发生率相近,差异无统计学意义(P0.05);奥美拉唑组和泮托拉唑组比较,心血管事件发生率也无统计学差异(P0.05)。③与对照组比较,奥美拉唑组和泮托拉唑组胃肠道出血发生率均明显减少,有统计学意义(P0.05),但两服药组间比较,出血发生率无明显区别,差异无统计学意义(P0.05)。结论:氯吡格雷联合阿司匹林具有增强血小板抑制,降低血小板凝聚的作用,而不同机制质子泵抑制剂奥美拉唑与泮托拉唑对PCI术后氯吡格雷联合阿司匹林抗血小板治疗患者的血小板功能无明显影响,不降低对心血管事件的预防效果,同时明显降低患者胃肠出血事件的发生率。  相似文献   

5.
目的:在急性冠脉综合征( acute coronary syndromes, ACS )的治疗中,抗血小板治疗及调脂治疗是最基础的治疗方案。近来 有学者提出,氯吡格雷和他汀类药物都经过细胞色素CYP 3A4 途径代谢,二者因存在竞争性抑制,有可能降低氯吡格雷抗血小板 的活性。本试验将针对阿托伐他汀及瑞舒伐他汀进行研究。方法:选择急性冠脉综合症的患者42 例,所有患者均接受氯吡格雷治 疗(负荷剂量300 mg,维持剂量75 mg/d)。随机分配为A、B 两组,A 组(n=20)服用阿托伐他汀治疗(20 mg/d),B 组(n=22 服用瑞 舒伐他汀治疗(10 mg/d)。分别于氯吡格雷服用前、服药治疗后3 天、服药治疗后7 天后采静脉血送检,测定ADP(10 滋mol/L)诱导 的血小板聚集率。结果:阿托伐他汀组(A 组)及瑞舒伐他汀组(B 组)相比,服用氯吡格雷前ADP 诱导的血小板聚集率基线值无 统计学差异。服用氯吡格雷3 日及7 日后,ADP诱导的血小板聚集率明显降低,(3.85± 2.58)vs(3.09± 2.27),(0.65± 0.88)vs(1.05± 0.95),P>0.05,无明显统计学差异。结论:氯吡格雷的确可以降低血小板的活性。同时,短期之内氯吡格雷的抗血小板活性未受到 他汀类的影响,包括经过CPY3A4途径的他汀,如阿托伐他汀。  相似文献   

6.
目的:在急性冠脉综合征(acute coronary syndromes,ACS)的治疗中,抗血小板治疗及调脂治疗是最基础的治疗方案。近来有学者提出,氯吡格雷和他汀类药物都经过细胞色素CYP3A4途径代谢,二者因存在竞争性抑制,有可能降低氯吡格雷抗血小板的活性。本试验将针对阿托伐他汀及瑞舒伐他汀进行研究。方法:选择急性冠脉综合症的患者42例,所有患者均接受氯吡格雷治疗(负荷剂量300mg,维持剂量75mg/d)。随机分配为A、B两组,A组(n=20)服用阿托伐他汀治疗(20mg/d),B组(n=22服用瑞舒伐他汀治疗(10mg/d)。分别于氯吡格雷服用前、服药治疗后3天、服药治疗后7天后采静脉血送检,测定ADP(10μmol/L)诱导的血小板聚集率。结果:阿托伐他汀组(A组)及瑞舒伐他汀组(B组)相比,服用氯吡格雷前ADP诱导的血小板聚集率基线值无统计学差异。服用氯吡格雷3日及7日后,ADP诱导的血小板聚集率明显降低,(3.85±2.58)vs(3.09±2.27),(0.65±0.88)vs(1.05±0.95),P〉0.05,无明显统计学差异。结论:氯吡格雷的确可以降低血小板的活性。同时,短期之内氯吡格雷的抗血小板活性未受到他汀类的影响。包括经过CPY3A4途径的他汀,如阿托伐他汀。  相似文献   

7.
目的:探讨高负荷剂量氯吡格雷联合替罗非班在高危非ST 段抬高型急性冠状动脉综合征(acute coronary syndrome,ACS) 患者经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)中的作用及安全性。方法:入选208 例高危非ST 段抬高型 ACS患者,根据PCI术前氯吡格雷负荷量不同,随机分为观察组和对照组。对照组:112 例,以氯吡格雷300 mg+ 替罗非班(用法同 观察组)治疗,观察组:96例,以氯吡格雷600 mg +替罗非班0.4 滋g/(kg·min)在30 min 内静脉注射。继以0.1 g/(kg·min)由微量泵 静脉持续泵入至手术后36 h,分别测定两组最大血小板聚集率(MPAR)变化、PCI 术后TIMI心肌灌注分级(TMPG);随访住院期间 和30 d内不良心血管事件和出血事件。结果:两组临床情况、PCI前负荷剂量氯吡格雷给药时间、支架置入数目比较差异无统计 学意义(P>0.05);用药后2 h、6 h、术后24 h两组MPAR均较用药前明显降低(P<0.05);用药后6 h两组MPAR 均低于用药后2 h (P<0.05);用药后2 h时观察组MPAR 低于对照组(P<0.05)。PCI术后TMPG 3级获得率观察组高于对照组(P<0.05);30 d内复合心 血管事件发生率、出血并发症两组比较差异均无统计学意义(P>0.05)。结论:PCI术前负荷氯吡格雷600 mg可以更有效、更迅速地 抑制患者的MPAR,联合应用替罗非班时仍可改善心肌灌注,且安全可行。  相似文献   

8.
双联抗血小板治疗急性冠脉综合征临床疗效观察   总被引:2,自引:0,他引:2       下载免费PDF全文
目的:探讨双联抗血小板治疗急性冠脉综合征(ACS)的临床疗效和安全性。方法:60例ACS患者随机分为治疗组和对照组。对照组给予阿司匹林单抗血小板治疗,治疗组采用阿司匹林+氯吡格雷双联抗血小板治疗,治疗3个月后评价临床疗效。结果:治疗组临床疗效总有效率为93.3%,显著高于对照组(76.7%),相比较有显著性差异(P<0.05);治疗后,两组LVEF、CO、E/A显著上升,与治疗前比较均有显著性差异(P<0.05);且治疗组与对照组比较有显著性差异(P<0.05)。结论:阿司匹林和氯吡格雷双联抗血小板药物治疗ACS,可以强化对血小板聚集的抑制,并增强抗栓效果,值得临床应用。  相似文献   

9.
目的:探讨高负荷剂量氯吡格雷联合替罗非班在高危非ST段抬高型急性冠状动脉综合征(acute coronarysyndrome,ACS)患者经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)中的作用及安全性。方法:入选208例高危非ST段抬高型ACS患者,根据PCI术前氯吡格雷负荷量不同,随机分为观察组和对照组。对照组:112例,以氯吡格雷300 mg+替罗非班(用法同观察组)治疗,观察组:96例,以氯吡格雷600 mg+替罗非班0.4μg/(kg·min)在30 min内静脉注射。继以0.1 g/(kg·min)由微量泵静脉持续泵入至手术后36 h,分别测定两组最大血小板聚集率(MPAR)变化、PCI术后TIMI心肌灌注分级(TMPG);随访住院期间和30 d内不良心血管事件和出血事件。结果:两组临床情况、PCI前负荷剂量氯吡格雷给药时间、支架置入数目比较差异无统计学意义(P〉0.05);用药后2 h、6 h、术后24 h两组MPAR均较用药前明显降低(P〈0.05);用药后6 h两组MPAR均低于用药后2 h(P〈0.05);用药后2 h时观察组MPAR低于对照组(P〈0.05)。PCI术后TMPG 3级获得率观察组高于对照组(P〈0.05);30 d内复合心血管事件发生率、出血并发症两组比较差异均无统计学意义(P〉0.05)。结论:PCI术前负荷氯吡格雷600 mg可以更有效、更迅速地抑制患者的MPAR,联合应用替罗非班时仍可改善心肌灌注,且安全可行。  相似文献   

10.
目的:探讨电阻抗法测定血小板聚集功能在冠心病患者中的应用。方法:通过电阻抗法对486名急性冠脉综合征的患者检测,所有患者分别于服药前和服药后第4天抽取肘静脉血,采血后1小时内用全血阻抗法测定三磷酸腺苷(ADP)和花生四烯酸(AA)诱导的血小板聚集率;其中50例患者出现氯吡格雷抵抗,28例患者出现阿司匹林抵抗。结果:通过电阻抗法测定的抗血小板药物抵抗的发生率(10.29%)与文献报道的一致;在原来抗血小板药物基础增加西洛他唑或者增加氯吡格雷的剂量都能明显改善血小板药物抵抗,随着服药时间的增加血小板药物抵抗呈下降趋势;大剂量氯吡格雷组相比西洛他唑组在改善氯吡格雷抵抗更明显,差异有统计学意义(P0.05)。结论:电阻抗法测定血小板聚集功能方便快捷、安全可靠,更方便指导临床用药。  相似文献   

11.
ObjectivesComparison of Ticagrelor vs clopidogrel in antiplatelet therapeutic effect of acute myocardial infarction patients undergoing percutaneous coronary intervention.MethodsThe study focused on 2000 acute myocardial infarction patients undergoing percutaneous coronary intervention (PCI) in our hospital from January 2013 to December 2015. To reduce the formation of acute stent thrombosis caused by clopidogrel resistance, we had two options, one was to double the dosage of clopidogrel, and the other was to substitute ticagrelor for clopidogrel. Based on random number table method, the 2000 patients were divided into experimental group and control group, each containing 1,000 patients. The patients in experimental group took 180 mg ticagrelor before PCI and 90 mg ticagrelor twice a day after PCI (Gu, 2016). In contrast, the patients control group took 600 mg clopidogrel before PCI and 150 mg clopidogrel once a day after PCI. Both groups were drawn 2.7 ml of fasting venous blood for platelet aggregation rate test before PCI and 2 h, 24 h, 7 days after PCI respectively. Turbidimetric method was used to measure the ADP-induced platelet aggregation rate and observe change of platelet aggregation rate and success rate. Incidence of liver and kidney malfunction and adverse actions were monitored. All patients accepted a 6-month of follow-up examination to record and compare incidences of major adverse cardiac and cerebrovascular events. The statistical results of both groups are analyzed and compared.ResultsThe platelet aggregation rate of experimental group before PCI and 2 h, 24 h, 7 days after PCI was 59.71% ± 7.24%, 59.20% ± 7.70%, 48.66% ± 7.80% and 43.39% ± 8.28%; The control group was 58.04% ± 5.61%, 56.25% ± 6.02%, 55.68% ± 3.14%, 53.94% ± 5.30%; Comparing the platelet aggregation rate of different time, P was less than 0.05. The success rate of platelet aggregation of experimental group and control group was 80.56% and 46.86% respectively. There were significant differences between the two groups and the P was less than .05. The postoperative serum creatinine level of experimental group was higher than that in the control group (P < .05). The incidence of adverse reactions in the experimental group was significantly lower than that of the control group. There were significant differences between the two groups and the difference was of statistical significance (P < .05). According to the 5-month follow-up examination: the incidence of major adverse cardiac and cerebrovascular events in experimental group was 2.60% (52/2000) ,while the control group was 13.00% (260/2000) . There were significant differences between the two groups and the difference was of statistical significance (P < .05).ConclusionsCompared with clopidogrel, ticagrelor can achieve better n antiplatelet effect for patients with acute myocardial infarction undergoing percutaneous coronary intervention (PCI). It can effectively reduce the incidence of postoperative adverse cardiac and cerebrovascular events and control the rate of adverse reactions within the acceptable range.  相似文献   

12.
Data on the agreement between aggregometry and platelet activation by flow cytometry regarding the measurement of on-treatment platelet reactivity to arachidonic acid (AA) and adenosine diphosphate (ADP) are scarce. We therefore sought to compare three platelet aggregation tests with flow cytometry for the assessment of the response to antiplatelet therapy. Platelet aggregation in response to AA and ADP was determined by light transmission aggregometry (LTA), the VerifyNow assays, and multiple electrode aggregometry (MEA) in 316 patients receiving aspirin and clopidogrel therapy after angioplasty with stent implantation. AA- and ADP-induced P-selectin expression and activated glycoprotein (GP) IIb/IIIa were determined by flow cytometry. LTA, the VerifyNow P2Y12 assay and MEA in response to ADP correlated significantly (all p<0.001), and the best correlation was observed between LTA and the VerifyNow P2Y12 assay (r = 0.63). ADP-induced platelet reactivity by all aggregation tests correlated significantly with ADP-induced P-selectin expression and activated GPIIb/IIIa (all p<0.001). The best correlation was seen between the VerifyNow P2Y12 assay and activated GPIIb/IIIa (r = 0.68). The platelet surface expressions of P-selectin and activated GPIIb/IIIa in response to ADP were significantly higher in patients with high on-treatment residual platelet reactivity (HRPR) to ADP by all test systems (all p<0.001). A rather poor correlation was observed between AA-induced platelet reactivity by LTA and the VerifyNow aspirin assay (r = 0.15, p = 0.007), while both methods did not correlate with MEA. AA-induced platelet reactivity by all aggregation tests correlated significantly, but rather poorly with AA-induced P-selectin expression (all p<0.05), while only AA-induced platelet reactivity by LTA correlated significantly with AA-induced activated GPIIb/IIIa (r = 0.21, p<0.001). The platelet surface expression of P-selectin in response to AA was significantly higher in patients with HRPR by LTA AA and MEA AA (both p<0.02). In contrast, P-selectin expression in response to AA was similar in patients without and with HRPR by the VerifyNow aspirin assay (p = 0.5), and platelet surface activated GPIIb/IIIa in response to AA did not differ significantly between patients without and with HRPR to AA by all test systems (all p>0.1). In conclusion, ADP-induced platelet reactivity by aggregometry translates partly into flow cytometry. In contrast, AA-induced platelet reactivity correlates poorly between different platelet aggregation tests, and between aggregometry and flow cytometry. Overall, both approaches capture different aspects of platelet function and are therefore not interchangeable in the assessment of agonists´-induced platelet reactivity. Clinical outcome data are needed to determine which test systems and settings are associated with different in vivo consequences.  相似文献   

13.
李开亮  司全金  张帷 《生物磁学》2011,(7):1305-1307
目的:探讨双联抗血小板治疗急性冠脉综合征(ACS)的临床疗效和安全性。方法:60例ACS患者随机分为治疗组和对照组。对照组给予阿司匹林单抗血小板治疗,治疗组采用阿司匹林+氯吡格雷双联抗血小板治疗,治疗3个月后评价临床疗效。结果:治疗组临床疗效总有效率为93.3%,显著高于对照组(76.7%),相比较有显著性差异(P〈0.05);治疗后,两组LVEF、CO、E/A显著上升,与治疗前比较均有显著性差异(P〈0.05);且治疗组与对照组比较有显著性差异(P〈0.05)。结论:阿司匹林和氯吡格雷双联抗血小板药物治疗ACS,可以强化对血小板聚集的抑制,并增强抗栓效果,值得临床应用。  相似文献   

14.
Increased residual platelet reactivity remains a burden for coronary artery disease (CAD) patients who received a coronary stent and do not respond sufficiently to treatment with acetylsalicylic acid and clopidogrel. We hypothesized that serotonin antagonism reduces high on-treatment platelet reactivity. Whole blood impedance aggregometry was performed with arachidonic acid (AA, 0.5 mM) and adenosine diphosphate (ADP, 6.5 μM) in addition to different concentrations of serotonin (1-100 μM) in whole blood from 42 CAD patients after coronary stent placement and 10 healthy subjects. Serotonin increased aggregation dose-dependently in CAD patients who responded to clopidogrel treatment: After activation with ADP, aggregation increased from 33.7 ± 1.3% to 40.9 ± 2.0% in the presence of 50 μM serotonin (p<0.05) and to 48.2 ± 2.0% with 100 μM serotonin (p<0.001). The platelet serotonin receptor antagonist ketanserin decreased ADP-induced aggregation significantly in clopidogrel low-responders (from 59.9 ± 3.1% to 37.4 ± 3.5, p<0.01), but not in clopidogrel responders. These results were confirmed with light transmission aggregometry in platelet-rich plasma in a subset of patients. Serotonin hence increased residual platelet reactivity in patients who respond to clopidogrel after coronary stent placement. In clopidogrel low-responders, serotonin receptor antagonism improved platelet inhibition, almost reaching responder levels. This may justify further investigation of triple antiplatelet therapy with anti-serotonergic agents.  相似文献   

15.
BackgroundInadequate platelet inhibition despite aspirin and clopidogrel therapy during and after a percutaneous coronary intervention is associated with an impaired clinical outcome. Cangrelor, a direct and reversible P2Y12 inhibitor that is currently in development, has the potential to achieve higher levels of inhibition of ADP-induced platelet aggregation than clopidogrel. The aim of the present study was to compare the magnitude of platelet inhibition in clopidogrel-pretreated patients before and after the in vitro addition of a subtherapeutic dose of cangrelor. MethodsBlood samples were drawn from patients pretreated with clopidogrel and aspirin who were undergoing elective percutaneous coronary intervention (n=39). Platelet function analysis with ‘classical’ light transmittance aggregometry (both peak and late aggregation [at 6 min]) was performed before and after the in vitro addition of cangrelor (0.25 μmol/l) to platelet-rich plasma (PRP). After an incubation period of five minutes, platelet aggregation was induced by 5 and 20 μmol/l ADP. ResultsThe in vitro addition of 0.25μmol/l cangrelor to the PRP from clopidogrel-treated subjects resulted in an additional reduction in ADP-induced platelet aggregation. For ADP concentrations of 5 and 20 μmol/l, peak aggregation showed a decrease of 75 and 85%, respectively (p<0.001 for both), while late aggregation was almost completely diminished (p=0.003 and p<0.001, respectively). Furthermore, the interindividual variation in inhibition of ADP-induced platelet aggregation by clopidogrel was greatly reduced after the addition of cangrelor. ConclusionWe demonstrate that the in vitro addition of even a subtherapeutic dose of cangrelor to the PRP of clopidogrel-pretreated patients results in an additional reduction of ADP-induced platelet aggregation. Moreover, cangrelor was able to diminish the interindividual variation observed in clopidogrel-inhibited platelet aggregation. (Neth Heart J 2009;17:195–8.)  相似文献   

16.
目的:探讨替格瑞洛联合阿司匹林治疗老年急性冠状动脉综合征的效果及对血清肌钙蛋白-T(Cardiac Troponin T,cTnT)、C反应蛋白(C-reactionprotein,CRP)、脑钠素(Brain natriuretic peptide,BNP)及D-二聚体(D-Dimer,D-D)水平的影响。方法:选取2016年1月~2019年1月我院收治的急性冠状动脉综合征老年患者60例,采用随机数字表法将患者分为两组,每组30例。两组患者均行经皮冠状动脉介入(Percutaneous coronary intervention,PCI)治疗,对照组术后给予阿司匹林和氯吡格雷,观察组给予阿司匹林和替格瑞洛。比较两组患者的临床治疗效果、心功能相关指标,治疗前后血清cTnT、BNP、CRP及D-D水平的变化情况及出血事件的发生率。结果:治疗后,观察组治疗总有效率显著高于对照组(93.33%vs. 70%,P 0.05);两组左室收缩末期内径(Left ventricular end systolic diameter,LVESD)、左室舒张末期内径(left ventricular end-diastolic diameter,LVEDD)、左心房内径(Left atrial diastolic diameter,LADD)、血清cTnT、BNP、CRP及D-D水平均较治疗前显著降低(P0.05),而左室射血分数(left ventricular ejection fraction,LVEF)较治疗前明显升高(P 0.05),且观察组LVESD、LVEDD、LADD均明显低于对照组(P 0.05),而LVEF显著高于对照组(P 0.05)。此外,观察组出血事件发生率显著低于对照组(P 0.05)。结论:与阿司匹林和氯吡格雷相比,替格瑞洛联合阿司匹林可更有效改善老年急性冠状动脉综合征患者的心功能,且出血事件的发生率更低,可能与其显著降低血清cTnT、BNP、CRP及D-D水平有关。  相似文献   

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