不稳定型心绞痛患者联合应用氯吡格雷与复方丹参滴丸治疗对其血小板功能影响

目的探讨不稳定型心绞痛患者联合应用氯吡格雷与复方丹参滴丸对其血小板功能的影响。方法选择2014年1月~2017年1月本院收治的不稳定型心绞痛患者96例,所有患者均给予常规治疗,按照随机原则把所有患者分为单一用药1组、单一用药2组和联合用药组,每组32例。其中,单一用药1组给予患者氯吡格雷,单一用药2组给予患者复方丹参滴丸,联合用药组同时给予患者氯吡格雷与复方丹参滴丸,观察并对比3组患者的血小板功能情况。结果单一用药1组总有效率为93.76%,单一用药2组总有效率为90.63%,联合用药组总有效率为96.88%,组间比较无明显差异(P0.05),每组患者治疗后的TXB2水平及血小板聚集率均比治疗前明显降低(P0.05),且联合用药组的TXB2水平及血小板聚集率均明显低于其他两组(P0.05)。结论不稳定型心绞痛患者联合应用氯吡格雷与复方丹参滴丸,对抗血小板聚集的影响明显优于单用氯吡格雷或复方丹参滴丸。     

复方丹参滴丸协同阿司匹林对冠心病患者血小板聚集功能的影响

目的 探讨复方丹参滴丸协同阿司匹林对冠心病患者血小板聚集功能的影响.方法 将60例急性冠脉综合征(ACS)患者随机分为阿司匹林组(对照组)与阿司匹林加复方丹参滴丸组(试验组).于用药前及用药1周、用药1月后测定血小板最大聚集率(PAGM)、血栓素B2(TXB2)含量.结果 治疗1月后试验组PAGM、TXB2含量均明显低于对照组(P<0.05和P<0.01).结论 ACS患者联合应用复方丹参滴丸和阿司匹林能显著降低PAGM、TXB2水平,优于单独应用阿司匹林.     

复方丹参滴丸对冠心病患者阿司匹林抵抗的作用

目的:探讨复方丹参滴丸对冠心病阿司匹林抵抗患者二磷酸腺苷(ADP)、花生四烯酸(AA)诱导的血小板聚集率的影响。方法:根据AA和ADP作为诱导剂测定的血小板聚集功能,将39例阿司匹林抵抗患者随机分为2组。A组为常规阿司匹林治疗组(n=19),B组为阿司匹林联合复方丹参滴丸治疗组(n=20)。分别在治疗前以及治疗1个月后测定由ADP、AA诱导的血小板聚集率,比较2组治疗前后及治疗后不同组别上述指标的差异。结果:阿司匹林联合复方丹参滴丸治疗1个月后,可使冠心病阿司匹林抵抗患者血小板聚集率下降,与治疗前比较有显著性差异[(49.46%±5.18%)比(73.81%±2.86%),P=0.048 9];可使冠心病患者血尿酸水平下降,B组治疗后血尿酸水平为(421.69±34.01)μmol/L,较治疗前[(444.69±50.88)μmol/L]明显下降(P=0.038 9),与A组治疗后[(444.88±21.32)μmol/L]相比明显下降(P=0.042 2)。2组患者在治疗中未出现不良临床事件。结论:复方丹参滴丸对冠心病阿司匹林抵抗患者有抗血小板聚集作用,并且治疗后可降低血尿酸水平。     

复方丹参滴丸联合阿司匹林对冠心病患者的治疗效果及血小板聚集功能的影响

目的探究复方丹参滴丸协同阿司匹林对冠心病患者的临床效果及血小板聚集功能的影响。方法将我院2017年1月至2018年4月收治的80例冠心病患者,随机分成两组,每组40例。对照组使用阿司匹林治疗,观察组在对照组基础上加用复方丹参滴丸治疗,比较两组治疗3个月后的临床效果及血小板聚集功能的指标。结果观察组的甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL),明显优于对照组(P0.05);观察组的血小板最大聚集率(PAGM)、血栓素水平(TXB2),明显低于对照组(P0.05);观察组的不良反应发生率为5.00%,明显低于对照组的35.00%(P0.05);观察组总有效率为95.00%,明显高于对照组的75.00%(P0.05)。结论复方丹参滴丸协同阿司匹林对冠心病患者的临床效果良好,有较好的抑制血小板聚集作用,有利于调节血脂水平,降低不良反应的发生,安全性高,值得临床进一步推广。     

曲美他嗪与复方丹参滴丸对冠心病心肌缺血的影响

曲美他嗪(TMZ)是抗心肌缺血新药；复方丹参滴丸具有扩张心脑血管、抗血小板聚集、清除氧自由等作用。2001年10月至2003年8月，我们用两药治疗冠心病取得一定疗效。现报告如下。     

复方丹参滴丸对不稳定型心绞痛患者血浆内皮素和血小板α-膜颗粒蛋白的影响

目的 观察复方丹参滴丸对不稳定型心绞痛患者的临床疗效及血浆内皮素(ET)和血小板α-膜颗粒蛋白(GMP-140)水平的影响.方法 168例不稳定型心绞痛患者分为常规治疗组(79例)和复方丹参滴丸组(89例).所有入选患者均接受硝酸酯类、美托洛尔(或钙拮抗剂)及阿司匹林治疗,复方丹参滴丸组在上述治疗基础上加用复方丹参滴丸10粒,每日3次,连用8周.观察统计两组治疗前1周和治疗结束后1周心绞痛发作次数及自拟的疼痛强度及持续时间记分值,检测治疗前后患者血浆ET和 GMP-140水平的变化.结果 复方丹参滴丸组和常规治疗组比较,治疗后疼痛发作频率、疼痛强度及持续时间记分均有明显减少,而复方丹参滴丸组的降低程度比常规治疗组明显(P<0.05). 两组可改善不稳定型心绞痛患者心电图ST段的偏移,而复方丹参滴丸组的疗效比常规治疗组显著(P<0.05).两组治疗后血浆ET和GMP-140水平均明显减低,而复方丹参滴丸组的疗效比常规治疗组显著(P<0.01).结论 复方丹参滴丸治疗不稳定型心绞痛患者疗效明显高于常规治疗,可能与改善血管内皮功能、抑制血小板聚集密切相关.     

国产和进口氯吡格雷对经皮冠状动脉介入术后血小板功能的影响

目的观察国产氯吡格雷和进口氯吡格雷对冠心病患者经皮冠状动脉介入治疗(PCI)术后血小板功能的影响。方法将450例冠心病患者随机分为2组,其中国产氯吡格雷组230例,进口氯吡格雷组220例。另选健康对照组220例。两治疗组分别于PCI术前3天开始服用氯吡格雷,服用氯吡格雷前、PCI术前、术后10min及PCI术后1周检查血小板聚集率及血小板活化指标。结果冠心病患者血小板聚集率及血小板活化状态较健康对照组明显增高。治疗前国产和进口氯吡格雷组的血小板聚集率及血小板活化指标差异无统计学意义。两治疗组PCI术后10min血小板聚集率及血小板活化状态均较术前明显增高,PCI术后1周两治疗组之间差异无统计学意义。结论PCI术后血小板聚集率及血小板活化状态明显增高,国产和进口氯吡格雷均有良好的抗血小板作用,两者抗血小板聚集和活化的作用相似。     

高龄老年应用氯吡格雷与阿司匹林抗血小板治疗的临床研究

目的对比研究高龄老年应用氯吡格雷与阿司匹林抗血小板治疗的效果及安全性。方法91例高龄老年冠心病患者随机分为氯吡格雷组(50 mg/d)、阿司匹林组(100 mg/d)及对照组(复方丹参滴丸10粒3次/d),药物治疗8周后,观察实验前后血小板聚集率改变、胃黏膜出血、对中性粒细胞及血小板的影响以及凝血三项的改变。结果与对照组比较,氯吡格雷组与阿司匹林组对血小板聚集率均有确切的抑制作用;在血小板聚集率抑制方面,氯吡格雷组优于阿司匹林组;各组实验前后均未出现中性粒细胞及血小板的显著变化;在胃黏膜损伤方面,虽然阿司匹林组发生例数较多,但各组均无显著差异;阿司匹林组及对照组实验前后凝血指标未发生变化,氯吡格雷组用药后活化部分凝血酶时间延长,与对照组比较有显著差异,而用药前两组无显著差异。结论高龄老年应用氯吡格雷与阿司匹林均能获得确切的抗血小板聚集效果,且较安全,其中氯吡格雷效果优于阿司匹林。     

复方丹参滴丸对冠心病患者血液流变学的影响

复方丹参滴丸 (DSP)是一种治疗冠心病的纯中药制剂 ,已广泛应用于临床。本研究旨在探讨 DSP对冠心病患者血液流变学的影响。1　对象和方法1.1　对象　符合 WHO冠心病诊断标准者 81(男 6 0 ,女 2 1)例 ,年龄 42～ 6 5岁 ,稳定型心绞痛 (AP) 5 2例 ,不稳定型心绞痛 (UAP) 2 9例。1.2　方法　复方丹参滴丸每次 10粒 ,3次 / d,口服 ,疗程 2个月。同时服用消心痛等基础药。停止服用抗血小板聚集等改善血液流变学的药物 (如阿斯匹林等 )。治疗前后观察心绞痛发作情况 ,ECG,血液流变学 ,血小板聚集率等。血小板聚集率测定采用 ADP为诱导剂 …     

国产和进口氯吡格雷对不稳定性心绞痛患者血小板功能的影响

目的　观察国产氯吡格雷和进口氯吡格雷对不稳定性心绞痛 (UAP)患者血小板功能的影响 ,比较两药抗血小板作用的优劣及其安全性。方法　 4 0例UAP患者随机分为 2组 ,其中国产氯吡格雷组 2 0例 ,进口氯吡格雷组 2 0例。另选健康对照组 10例。两治疗组分别于服用氯吡格雷前、服用氯吡格雷 30 0mg 2h后及服用氯吡格雷 75mg1次 d 1周后抽血查血小板聚集率及血小板活化指标。结果　UAP患者血小板聚集率及血小板活化状态较健康对照组明显增高。治疗前国产和进口氯吡格雷组的血小板聚集率及血小板活化指标无显著差异。治疗后两治疗组之间无显著差异。结论　血小板的活化在UAP的发生、发展过程中起着重要的作用。国产和进口氯吡格雷均有良好的抗血小板作用 ,两者抗血小板聚集和活化的作用相似 ,且无明显的不良反应。     

Inhibitory effects of cardiotonic pills on platelet function in dogs fed a high-fat diet.

Insulin resistance and the consequent metabolic disorders are associated with a state of platelet hyperactivity. Oxidative stress is responsible for the persistent platelet activation. We sought to study the inhibitory effect of cardiotonic pills, an oral herbal component, on platelet function in a dog model with insulin resistance induced by high-fat feeding. We fed 18 dogs with a high-fat diet and six dogs with normal chow as control for 6 months. Then, six dogs were fed with a high-fat diet and received additional aspirin (250 mg/day), and another six dogs received additional cardiotonic pills (1,000 mg/day) for 4 months. Time-course changes in metabolic parameters and platelet function were detected. After high-fat feeding for 6 months, 18 dogs developed a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance. In addition, a platelet hyperactivity state, characterized by increased agonist (arachidonic acid, ADP and collagen) induced platelet aggregation, platelet expression of adhesion molecules (P-selectin and GP IIb/IIIa), and platelet intracellular calcium concentration, was indicated. Cardiotonic pills showed a significant antioxidative activity by presenting an increase in plasma superoxide dismutase and decrease in erythrocyte glutathione, as well as a lipid-lowering effect (decrease in both plasma cholesterol and triglyceride). Either aspirin or cardiotonic pills could significantly reverse the platelet hypersensitivity and hyperfunction. Compared with aspirin, cardiotonic pills showed a more exaggerated inhibitory effect on platelet function (a significantly decreased collagen-stimulated platelet aggregation, and expression of adhesion molecules). In conclusion, cardiotonic pills inhibited platelet hyperfunction in dogs with insulin resistance. This inhibitory effect may mainly be explained by antioxidative activity and metabolic control.     

Effects of α-tocopherol (Vitamin E) on the Ultrastructure of Human Platelets In Vitro

Washed human platelets were incubated with increasing concentrations of α-tocopherol. Spontaneous aggregation was induced by tocopherol (0.5 mM or above). Aggregation was inhibited by ethylenediaminetetraacetate and platelet activation was reduced by prostaglandin E(1). Using electron microscopy, it was confirmed that tocopherol caused platelet disruption to some extent and the released components may have generated aggregation. These effects were not observed in platelet-rich plasma. Spontaneous activation was not observed when the concentration of tocopherol was 0.03 mM or lower. Concentrations of tocopherol between 0.075 mM and 0.0075 mM had inhibiting influences on activation of washed platelets by thrombin. Tocopherol (between 0.1 mM and 0.005 mM) changed activation of washed platelets by cationized ferritin in that it facilitated the first phase of aggregation but reduced the second phase in an indirect proportional manner. The results show that the effects of tocopherol in washed platelet preparations are not comparable to those observed in plasma and that the platelet membrane must be regarded as a crucial target for vitamin E.     

Antiplatelet effects of clopidogrel compared with aspirin after myocardial infarction: enhanced inhibitory effects of combination therapy

OBJECTIVES: We sought to compare the inhibitory effects of the combination of two doses of aspirin plus clopidogrel with either drug alone on platelet aggregation and activation. BACKGROUND: Enhanced platelet inhibitory effects of clopidogrel by aspirin on platelet aggregation and activation are suggested by experimental studies but have not been shown in humans. METHODS: The effects of clopidogrel 75 mg or aspirin 100 (300) mg on platelet aggregation and activation by flow cytometry after stimulation with various agonists were determined in 30 patients with a past history of myocardial infarction. RESULTS: Clopidogrel alone or in combination with aspirin markedly inhibited adenosine diphosphate (ADP)-mediated platelet aggregation compared with monotherapy with aspirin (24.6 +/- 3.3% or 26.6 +/- 2.7% vs. 44.7 +/- 2.9%; p < 0.001). Combined treatment significantly inhibited collagen-induced aggregation compared with aspirin and clopidogrel (16.4 +/- 2.4%, 36.5 +/- 4.2% and 59.3 +/- 5.1%, respectively;, p < 0.001) and resulted in considerable inhibition of aggregation induced by thrombin receptor agonist peptide (TRAP, p < 0.03). Clopidogrel with or without aspirin significantly suppressed expression of platelet activation markers CD 62p, CD 63 and PAC-1 after stimulation with ADP or thrombin (p < 0.001). In addition, the combined treatment was more effective than either agent alone after activation with low dose thrombin (p < 0.05). Both doses of aspirin equally potentiated the platelet inhibitory effects of clopidogrel. CONCLUSIONS In this prospective clinical ex vivo platelet study, clopidogrel was more effective than aspirin in inhibiting ADP-mediated platelet aggregation and activation. Clopidogrel in combination with aspirin showed synergistic inhibitory effects after stimulation with collagen and thrombin compared with monotherapies. Thus, this dual antiplatelet treatment strategy deserves further evaluation in clinical trials for secondary prevention of acute myocardial infarction or unstable angina.     

3,3',5'-Triiodothyronine inhibits collagen-induced human platelet aggregation.

To clarify further the activity of rT3, we examined the effect of rT3 on collagen-induced platelet activation as reflected by aggregation, serotonin release, and protein phosphorylation. rT3, T4, T3, and triiodothyroacetic acid inhibited collagen-induced platelet aggregation and serotonin release from platelets in a dose-dependent manner. However, thyronine did not inhibit collagen-induced platelet aggregation. The concentration at which rT3 inhibited by 50% collagen-induced platelet aggregation was 30 +/- 4 (mean +/- SE) mumol/L. rT3, T4, and T3 did not differ significantly in their abilities to inhibit platelet aggregation. Moreover, rT3 inhibited collagen-induced phosphorylation of the 20-kilodalton protein (myosin light chain) in platelets. In contrast, rT3 did not inhibit 12-O-tetradecanoylphorbol 13-acetate (TPA)- or thrombin-induced platelet aggregation and inhibited only minimally TPA-induced 40-kilodalton protein phosphorylation. These results suggest that rT3 inhibits collagen-induced platelet activation by inhibiting the activity of myosin light chain kinase and that it may be interesting to investigate some kinds of activity of rT3.     

搏心通胶囊治疗冠心病心绞痛的疗效观察

目的:观察搏心通胶囊治疗冠心病心绞痛的临床疗效及对血小板聚集率的影响。方法:将冠心病心绞痛患者60例随机分为两组,治疗组给予搏心通胶囊,对照组给予速效救心丸,两组均治疗4周,疗程结束后比较两组临床疗效、治疗前、后心电图和血小板最大聚集率。结果:治疗组在临床疗效及心电图的改善与对照组相近,在改善血小板最大聚集率方面优于对照组。结论:搏心通胶囊可明显降低血小板最大聚集率,并改善冠心病心绞痛患者的症状。     

Strawberry extract presents antiplatelet activity by inhibition of inflammatory mediator of atherosclerosis (sP-selectin,sCD40L,RANTES, and IL-1β) and thrombus formation

Cardiovascular disease prevention is of high priority in developed countries. Healthy eating habits including the regular intake of an antithrombotic diet (fruit and vegetables) may contribute to prevention. Platelet function is a critical factor in arterial thrombosis and the effect strawberries have is still unclear. Therefore, the aim of this study was to systematically examine the action of strawberries in preventing platelet activation and thrombus formation. Strawberry extract concentration-dependently (0.1–1?mg/ml) inhibited platelet aggregation induced by ADP and arachidonic acid. At the same concentrations as strawberry inhibits platelet aggregation, it significantly decreased sP-selectin, sCD40L, RANTES, and IL-1β levels. The strawberry may exert significant protective effects on thromboembolic-related disorders by inhibiting platelet aggregation. Also, this suggests that antithrombotic activity may have novel anti-inflammatory effects.     

稳定型心绞痛患者阿司匹林抵抗的相关因素及复方丹参滴丸的干预效果

目的 分析稳定型心绞痛(SAP)患者发生阿司匹林抵抗的相关因素,观察复方丹参滴丸联合阿司匹林对血小板聚集率的影响。方法 采用病例对照研究方法收集376例连续服用阿司匹林(100 mg/d) 4周以上的SAP患者,根据血栓弹力图检测结果将患者分为阿司匹林抵抗组(72例)和阿司匹林敏感组(304例),比较组间各指标的差异。随后将阿司匹林抵抗组随机分为对照组（36例）和试药组（36例）,对照组继续口服阿司匹林100 mg/d,试药组加服复方丹参滴丸10粒,3次/d。1个月后复查血小板聚集率,对结果进行统计分析。结果 阿司匹林抵抗组空腹血糖、C反应蛋白、低密度脂蛋白胆固醇显著高于阿司匹林敏感组。对照组复查血小板聚集率较前无显著差异〔(70±6)% vs.(71±4)%〕,试药组复查血小板聚集率较前显著下降〔(69±6)% vs.(44±5)%,P<0.05〕。结论 糖尿病、低密度脂蛋白胆固醇、C反应蛋白是SAP患者阿司匹林抵抗的相关因素。复方丹参滴丸在降低阿司匹林抵抗患者的血小板聚集率方面具有一定疗效。     

The effects of antiplatelet agents on platelet–leukocyte aggregations in patients with acute cerebral infarction

Background Studies have shown that platelet-leukocyte aggregates (PLA) are sensitive to platelet activation which might exist before the onset of cerebral infarction. In this study, we investigated the formation of PLA in patients with cerebral infarction and the effects of antiplatelet agents on PLA. Methods The level of soluble P-selectin, C-reaction protein, platelet aggregation rate and leukocyte-platelet aggregations were measured in 40 patients with acute cerebral infarction and 20 normal controls. The 40 patients were randomly assigned to two treatment groups: aspirin group (n = 20) and clopidogrel group (n = 20). Both groups were monitored for Scandinavian stroke scale (SNSS), soluble P-selectin, serum C-reaction protein, platelet aggregation rate and PLA before and after the treatment. Flow cytometry was used to detect the levels of PLA in the blood. Results The percentage of platelet-monocyte aggregates (PMA) in patients with cerebral infarction was significantly increased compared with the controls (P < 0.001), which was positively correlated to soluble P-selectin, C-reaction protein and platelet aggregation rate (P < 0.05). After the treatment, the levels of PMA and platelet aggregation rate were decreased in both groups (P < 0.05). The level of PMA and platelet aggregation rate in the clopidogrel group was significantly lower than that in the aspirin group (P < 0.05). Conclusions PMA are a sensitive biomarker to platelet activation in patients with cerebral infarction. In addition, although both aspirin and clopidogrel lowered the level of PMA, clopidogrel is a more effective treatment than aspirin in inhibiting platelet activation.     

Effects of Timolol on Platelets in Coronary Sinus Blood and on Myocardial Ischemia during Pacing-induced Angina

Abstract The effect of timolol on blood platelet function was studied in coronary sinus and caval vein blood at rest and during pacing-induced angina in 20 patients with coronary heart disease. During pacing-induced angina, lactate measurements confirmed that coronary sinus blood was sampled from ischemic regions in 13 men. The ischemia did not influence platelet function. In blood from non-ischemic myocardium, platelet activation was found during pacing: the ADP-induced aggregation, platelet retention and plasma β-thromboglobulin levels increased moderately but significantly. Timolol administration prevented this platelet activation, possibly by inhibiting catecholamine release from the myocardium, and reduced the ischemic response during pacing as judged from lactate measurements and ST depressions. It is concluded that timolol reduced platelet activation induced in non-ischemic regions of the heart during tachycardia stress as well as myocardial ischemia.     

Platelet aggregation in healthy women during normal pregnancy - a longitudinal study

Increased platelet activation is involved in obstetric complications such as preeclampsia and intrauterine growth retardation. It is of interest to study platelet aggregation during pregnancy, since increased aggregation theoretically could be a mechanism associated with placenta-mediated complications, which possibly could be prevented by drugs inhibiting platelet aggregation. There are, however, few robust studies describing platelet aggregation during normal pregnancy. The present longitudinal study was performed in order to study platelet aggregation during normal pregnancy resulting in a healthy child, during the puerperium and in nonpregnant, fertile women. Healthy, nonsmoking, pregnant women (n = 104), aged under 39 years and with BMI < 35, were followed during pregnancy and postpartum. Twenty-seven nonpregnant, non-puerperal, fertile women were studied for comparison. Platelet aggregation was determined with multiple electrode impedance aggregometry and analyzed at inclusion, 4 times during pregnancy and after at least 3 months postpartum. Platelet aggregation postpartum was compared with gestational weeks 8–15 and 37–40, respectively, and with nonpregnant, fertile women. Hemoglobin, leucocyte count, platelet count, prothrombin time, and activated partial thromboplastin time were determined at inclusion in order to verify normal hemostasis. Activation of platelets by arachidonic acid, adenosine diphosphate (ADP), and thrombin receptor activating peptide (trap-6) resulted in less aggregation during pregnancy, compared with postpartum (p < 0.03–< 0.001). Platelet aggregation following activation by collagen was unchanged. A minor increase in aggregation as pregnancy continued was found related to ADP (p < 0.021). Positive correlations were found between platelet counts and platelet aggregation. Postpartum platelet aggregation after activation with arachidonic acid, collagen, and trap-6 was lower than in the non-puerperal fertile state. Other hemostatic analyses were normal. In conclusion, there is a minor decrease in platelet aggregation after activation with arachidonic acid, trap-6, and ADP, measured with multiple electrode impedance aggregometry during normal pregnancy resulting in healthy babies, compared with the postpartum period. The small changes in platelet aggregation may be a consequence of a minor decrease in platelet count and probably lack clinical significance under normal conditions. Interindividual variations at certain time-points are substantial, which limits the usefulness of the multiple electrode impedance aggregometry for determining minor changes in platelet function.