小剂量阿司匹林对老年缺血性脑血管病患者血小板聚集功能的影响

目的；观察小剂量阿司匹林（ASA）对老年缺血脑血管病（ICVD）患者血小板聚集功能的影响。方法：以花生四烯酸，二磷酸腺苷，肾上腺素和胶原为诱导剂检测了老年ICVD患者服用ASA（40mg/d)70例，未服ASA30例及健康对照组50例的血小板最大聚集率（MAR）。结果：40mg/d的ASA组中花生四烯酸，胶原和肾上腺素诱导MAR的变异系数较大，且70例中有25例对花生四烯酸诱导的聚集无显著抑制。此25例中随机选取10例ASA增至80mg/d后，有8例达到了对花生四烯酸聚集的显著抑制，另2例继续增至100mg/d后才达到。结论：在老年ICVD患者中，小剂量ASA作用的个体差异较大，临床ASA效果需要实验室评价并需个体化。     

多部位出血伴血小板聚集缺陷患者血小板纤维蛋白原的研究

多部位出血伴血小板聚集缺陷，特征为临床轻重不等的皮肤黏膜出血和（或）月经过多，血小板计数和凝血象正常；血小板形态无异常。血小板对二磷酸腺苷（ＡＤＰ）、血小板活化因子（ＰＡＦ）、胶原和肾上腺素等诱导的聚集反应出现不等程度的缺陷。我们对这些患者的血小板纤...     

奥美拉唑对阿司匹林抗血小板聚集作用的影响研究

目的探讨奥美拉唑对阿司匹林抗血小板聚集作用的影响。方法选择73例稳定型心绞痛患者,随机分为两组:对照组37例,服用阿司匹林肠溶片100mg+安慰剂,1次/d;实验组36例,服用阿司匹林肠溶片100mg+奥美拉唑肠溶片20mg,1次/d。两组均在给药前1d、服药后2周分别测定血小板聚集率。结果对照组及实验组治疗后较治疗前以花生四烯酸(ACA)和腺苷二磷酸(ADP)诱导的血小板聚集率均显著降低(P0.05)。以ACA为诱导剂,实验组治疗后的血小板聚集率(43.7±3.9)%较对照组的(40.2±4.2)%差异无统计学意义(P0.05);以ADP为诱导剂,实验组治疗后的血小板聚集率(76.8±6.7)%较对照组的(72.3±5.6)%差异无统计学意义(P0.05)。结论奥美拉唑对阿司匹林的抗血小板作用无明显影响。     

服用不同剂量和时间阿司匹林对急性脑梗死患者血小板聚集的影响

一般认为 ,阿司匹林抑制血小板活性的机理是通过抑制环氧化酶、阻断血栓烷合成而实现的。目前证实 ,激活血小板的途径很多 ,阿司匹林能否抑制其它激活血小板的途径尚无定论。我们观察了维持不同剂量和时间阿司匹林对急性脑梗死患者二磷酸腺苷 (ADP)、花生四烯酸 (AA)、肾上腺素     

不同氯吡格雷代谢型急性心肌梗死患者的血小板聚集率变化

目的观察不同氯吡格雷代谢型急性心肌梗死患者使用氯吡格雷后血小板聚集功能的被抑制情况。方法入选2013年3—8月急性心肌梗死患者48例,经过基因检测分为氯吡格雷慢代谢型6例、快代谢型17例和中间代谢型25例。患者均于入病房前服用负荷剂量阿司匹林300 mg和氯吡格雷300 mg,之后阿司匹林100 mg/d和氯吡格雷75 mg/d连续服用,于服药后第6天检测血小板聚集率、血细胞计数、纤维蛋白原含量和肝肾功能。结果所有患者服用氯吡格雷后第6天的血小板聚集率明显下降,二磷酸腺苷、肾上腺素诱导的抑制率分别为74%和84%。氯吡格雷快代谢型、中间代谢型和慢代谢型3组急性心肌梗死患者的二磷酸腺苷诱导的血小板聚集率分别为22.2%±13.4%、32.1%±20.1%和18.6%±13.9%(P>0.05),3组血小板抑制率分别为87%、78%和82%。结论本研究中不同氯吡格雷代谢型急性心肌梗死患者的血小板聚集功能的抑制情况无明显差异。     

血糖对稳定型心绞痛患者阿司匹林抗血小板聚集作用的影响

目的探讨血糖对稳定型心绞痛患者阿司匹林抗血小板聚集作用的影响。方法选取2012年6月—2013年12月在滨州市中心医院就诊的150例稳定型心绞痛患者,根据空腹血糖分为糖尿病A组(空腹血糖≤10 mmol/L)50例,糖尿病B组(空腹血糖10 mmol/L)50例,非糖尿病组50例。3组患者均服用相同剂量阿司匹林治疗,比较3组患者治疗前1 d、治疗后7 d二磷酸腺苷(ADP)、花生四烯酸(ACA)诱导血小板聚集率。结果 3组患者治疗前1 d ADP、ACA诱导血小板聚集率比较,差异无统计学意义(P0.05);糖尿病A组和糖尿病B组患者治疗后7d ADP、ACA诱导血小板聚集率高于非糖尿病组(P0.05),糖尿病B组患者治疗后7 d ADP、ACA诱导血小板聚集率高于糖尿病A组(P0.05)。结论血糖对稳定型心绞痛患者阿司匹林抗血小板聚集作用有明显影响。     

健康人血小板聚集率24小时节律变化研究

目的:通过检测健康人24小时固定时间点的血小板聚集率,观察其有无节律变化,为临床使用抗血小板药物时间提供合理依据.方法:30例健康年轻人入选.于1天24小时内2:00、6:00、10:00、16:00和20:00采取外周静脉血,抽血后1小时内用全血阻抗法检测血小板聚集率,诱导剂分别为胶原(2μg/ml)、肾上腺素(10μg/ml)、花生四烯酸(0.5 mM)及二磷酸腺苷(10μM及20 μM).结果:健康人血小板聚集率在24小时内,肾上腺素诱导下6:00最高,与2:00,10:00,16:00和20:00时比较,差异有统计学意义(P均<0.05);其它时间点之间比较差异均无统计学意义.胶原、花生四烯酸及二磷酸腺苷诱导下血小板聚集率各时间点之间比较差异均无统计学意义.结论:肾上腺素诱导的健康人群血小板聚集率存在24小时节律变化,早晨6:00起床后达到高峰,此后逐渐降低,夜间睡眠中达到低谷.胶原、花生四烯酸及二磷酸腺苷诱导的血小板聚集率无明显24小时节律变化.     

三七总苷对阿司匹林抵抗影响的临床观察

目的探讨三七总苷对阿司匹林抵抗（AR）病人的影响。方法选择接受阿司匹林治疗的病人318例,根据二磷酸腺苷（ADP）诱导血小板聚集率筛选出阿司匹林抵抗病人,按时间顺序分为两组。联合治疗组用三七总苷,每日3粒,加阿司匹林100mg/d;三七总苷组用三七总苷,每日3粒,疗程均为1个月。检查治疗前及治疗1个月后的血小板聚集率。结果318例病人中64例存在阿司匹林抵抗,占20.1%。联合治疗组与三七总苷组服药后1个月血小板聚集率分别为50.5%±11.7%,54.6%±10.3%,较治疗前均明显下降（P〈0.05）。结论三七总苷对ADP诱导血小板聚集率有一定的降低作用。     

老年人尿11-脱氢血栓素B2和阿司匹林抵抗的相关性研究

目的研究老年人阿司匹林抵抗（aspirin resistance,AR）的发生情况及与尿11-脱氢血栓素B2（11—DH—TXB2）的相关性。方法入选300名汉族老年人作为研究对象,所有研究对象均长期服用阿司匹林（ASA）。检测其血小板聚集率,用酶联免疫吸附法（ELISA）测定尿11-DH—TXB2浓度,并分析其与血小板聚集率的相关性。结果阿司匹林敏感（aspirin sensitive,AS）者共102例,占34．0％;阿司匹林半抵抗（aspirin semi—resistance,ASR）者共113例,占37．7％;AR者共85例,占28．3％。尿11-DH—TXB2的浓度与二磷酸腺苷（ADP）及花生四烯酸（AA）诱导的血小板平均聚集率均呈明显的正相关（P〈0．01）。结论尿11-DH—TXB2的浓度反应体内血小板聚集程度,从而可能反映老年人是否存在AR。     

野木瓜多糖对家兔血小板聚集的影响

目的研究野木瓜多糖(SCP)对血小板聚集的影响及可能机制。方法选择成年家兔30只,随机分为空白对照组、SCP 17 g/L组、SCP 34 g/L组、SCP 68 g/L组、阿司匹林组,每组6只。制备家兔富血小板及贫血小板血浆,用Born's比浊法检测17、34、68 g/LSCP对胶原、花生四烯酸(AA)、二磷酸腺苷(ADP)及凝血酶诱导的血小板聚集的影响。检测SCP对胶原诱导后血小板中5-羟色胺含量、肝素凝血酶凝固时间(HTCT)及对凝血酶作用后血小板释放丙二醛含量的影响。结果与空白对照组比较,不同浓度SCP组、阿司匹林组的胶原、ADP、凝血酶诱导的血小板聚集明显降低(P<0.05,P<0.01),SCP 1 7 g/L组AA诱导的血小板聚集无明显变化(P>0.05),SCP34 g/L组、SCP 68 g/L组、阿司匹林组AA诱导的血小板聚集明显降低(P<0.05,P<0.01)。与空白对照组比较,不同浓度SCP组丙二醛含量明显降低、HTCT延长,呈浓度依赖性(P<0.01),除SCP 1 7 g/L组外,其余各组5羟色胺明显降低,呈浓度依赖性(P<0.05,P<0.01)。结论 SCP可以抑制由胶原、ADP、AA和凝血酶诱导的血小板聚集,其机制与抑制血小板释放5-羟色胺、血小板因子Ⅳ及减少丙二醛生成有关。     

阿司匹林抵抗的临床特征分析

阿司匹林是目前应用最广的心脑血管疾病一二级预防用药.已证实阿司匹林的使用可降低致死性和/或非致死性血管事件的发生率.然而最近关注到,在长期服用阿司匹林的人群中,部分人群仍有血栓形成事件的发生,由此提出阿司匹林抵抗概念.已有多个大型多中心临床试验对阿司匹林抵抗患者的临床特征进行分析,以利于早期对该类患者进行识别.文章对阿司匹林抵抗患者的临床特征及其出现的可能原因进行综述.     

Aspirin and clopidogrel resistance: an emerging clinical entity.

Antiplatelet therapy is a cornerstone of cardiovascular medicine. Aspirin and clopidogrel have emerged as critical therapies in the treatment of cardiovascular disease. Despite their efficacy, patients on these medications continue to suffer complications. Millions of patients are currently on low-dose antiplatelet therapy but it is unknown how many of these patients are under-treated or on the wrong medication. Aspirin and clopidogrel resistance are emerging clinical entities with potentially severe consequences such as recurrent myocardial infarction, stroke, or death. The mechanism of resistance remains incompletely defined, but there are specific clinical, cellular, and genetic factors that influence therapeutic failure. These factors range from physicians who fail to prescribe these medications despite appropriate indications to polymorphisms of platelet membrane glycoproteins. Rapid and accurate diagnosis of antiplatelet resistance also remains an issue as new bedside tests are developed. By understanding the mechanism of therapeutic failure and by improving the diagnosis of this clinical entity, a new era of individualized antiplatelet therapy may arise with routine measurements of platelet activity in the same way that cholesterol, blood pressure, and blood sugar are followed, thus improving the care for millions of people.     

Aspirin administered to women at 100 mg every other day produces less platelet inhibition than aspirin administered at 81 mg per day: implications for interpreting the women’s health study

Objective We aimed to determine the relative level of platelet inhibition achieved with low-dose aspirin (81 mg daily) compared with a very low-dose (100 mg every other day). Background The Womens Health Study (WHS) found that a dose of 100 mg every other day of aspirin provided protection against stroke as primary prophylaxis, but not myocardial infarction. In the United States, the most commonly prescribed dose of aspirin for primary prophylaxis is 81 mg per day. As a result, it is important to know whether these doses are equivalent before extrapolating the results of the WHS to women in the U.S. Methods To achieve this goal, we have studied the effects of these two dosing regimens on platelet function in healthy women meeting the WHS inclusion criteria using a randomized design. We enrolled 49 healthy female volunteers and used a sequential, crossover design to compare the two regimens. The participants received a 17-day course of each aspirin-dosing regimen separated by a 7-day washout period. The degree of platelet inhibition was measured on days 14–17 of each dosing regimen using a point-of-care platelet function assay utilizing arachidonic acid to activate platelets (VerifyNow-Aspirin). Results Participants platelet response, expressed as Aspirin Response Unit (ARU) attained a significantly greater level of platelet inhibition on days 14–17 while taking aspirin 81 mg daily compared to aspirin 100 mg every other day (31.3% vs. 12.7%, P < 0.0001) with mean ± SD ARU values of 445 ± 50 and 570 ± 68, P < 0.0001. Significantly more daily readings in participants were ≥550 ARU, a value correlated with clinical outcomes in several studies, with the 100 mg every other day regimen (72.0% vs. 6.4% with 81 mg daily, P < 0.0001), and this alternate-day regimen also resulted in more day-to-day variability in platelet function (P = 0.0002). Conclusion We found significantly less inhibition of platelet function with the dose used in the WHS than the usual U.S. dose. We observed that the degree of platelet inhibition was significantly less with aspirin 100 mg every other day compared with aspirin 81 mg daily, suggesting that results of the Women’s Health Study may have underestimated both the efficacy and toxicity of aspirin as it is commonly administered. These data need to be considered when developing recommendations about the use of aspirin in the primary prevention of cardiovascular disease in women. Accumetrics is the manufacturer of the VerifyNow System, the platelet function analyzer used in this study and the authors are employees of Accumetrics.     

阿司匹林抵抗的研究

本文对阿司匹林抵抗的定义、临床意义、诊断、发生机理及对策研究作了较祥细的综述。对临床医生运用阿司匹林及如何处置阿司匹林抵抗有一定参考价值。     

Determinants of aspirin resistance in patients with type 2 diabetes

BackgroundCardiovascular disease is a leading cause of mortality among patients with type 2 diabetes mellitus (T2DM). Numerous patients with T2DM show resistance to aspirin treatment, which may explain the higher rate of major adverse cardiovascular events observed compared with non-diabetes patients, and it has recently been shown that aspirin resistance is mainly related to accelerated platelet turnover with persistent high platelet reactivity (HPR) 24 h after last aspirin intake. The mechanism behind HPR is unknown. The aim of this study was to investigate the precise rate and mechanisms associated with HPR in a population of T2DM patients treated with aspirin.MethodsIncluded were 116 consecutive stable T2DM patients who had attended our hospital for their yearly check-up. HPR was assessed 24 h after aspirin intake using light transmission aggregometry (LTA) with arachidonic acid (AA) and serum thromboxane B2 (TXB2) measurement. Its relationship with diabetes status, insulin resistance, inflammatory markers and coronary artery disease (CAD) severity, using calcium scores, were investigated.ResultsUsing LTA, HPR was found in 27 (23%) patients. There was no significant difference in mean age, gender ratio or cardiovascular risk factors in patients with or without HPR. HPR was significantly related to duration of diabetes and higher fasting glucose levels (but not consistently with HbA_1c), and strongly related to all markers of insulin resistance, especially waist circumference, HOMA-IR, QUICKI and leptin. There was no association between HPR and thrombopoietin or inflammatory markers (IL-6, IL-10, indoleamine 2,3-dioxygenase activity, TNF-α, C-reactive protein), whereas HPR was associated with more severe CAD. Similar results were found with TXB2.ConclusionOur results reveal that ‘aspirin resistance’ is frequently found in T2DM, and is strongly related to insulin resistance and severity of CAD, but weakly related to HbA_1c and not at all to inflammatory parameters. This may help to identify those T2DM patients who might benefit from alternative antiplatelet treatments such as twice-daily aspirin and thienopyridines.     

老年急性缺血性脑卒中患者早期阿斯匹林治疗的临床对照研究

目的：探讨老年急性缺血性脑卒中早期抗血小板治疗效果,以及降低致残率的临床观察,方法：采用随机双盲对照研究,对入院48小时内急性脑卒中患者,经头颅CT扫描除外脑出血,无阿斯匹林禁忌的给予160mg 1/日口服或安慰剂治疗四周,结果：共入选180例,住院期间阿斯匹林组死亡2例,对照组死亡3例,阿斯匹林组治疗期间63％基本恢复,无再发脑卒中及出血,两组治疗结果比较判别显著（P＜0．05）, 结论：阿斯匹林辅佐治疗,不影响其它常规治疗,药源方便,价廉,具有促进恢复,预防复发作用。     

Role of Helicobacter pylori eradication in aspirin or non-steroidal anti-inflammatory drug users

Helicobacter pylori(H pylori) infection and the use of non steroidal anti-inflammatory drugs (NSAIDs) including aspirin at any dosage and formulation represent well-established risk factors for the development of uncomplicated and complicated peptic ulcer disease accounting for the majority of such cases. Although the interaction between H pylori and NSAID/aspirin use in the same individuals was questioned in some epidemiological studies, it has now become widely accepted that they are at least independent risk factors for peptic ulcer disease. According to data from randomized intervention trials, naive NSAID users certainly benefit from testing for H pylori infection and, if positive, H pylori eradication therapy prior to the initiation of NSAID. A similar strategy is also suggested for naive aspirin users, although the efficacy of such an approach has not been evaluated yet. Strong data also support that chronic aspirin users with a recent ulcer complication should be tested for H pylori infection and, if positive, receive H pylori eradication therapy after ulcer healing, while they appear to benefit from additional long-term therapy with a proton pump inhibitor (PPI). A similar approach is often recommended to chronic aspirin users at a high risk of ulcer complication. H pylori eradication alone does not efficiently protect chronic NSAID users with a recent ulcer complication or those at a high-risk, who certainly should be treated with long-term PPI therapy, but H pylori eradication may be additionally offered even in this setting. In contrast, testing for H pylori or PPI therapy is not recommended for chronic NSAID/aspirin users with no ulcer complications or those at a low risk of complications.     

阿托伐他汀联合阿司匹林治疗急性脑梗死患者的临床研究

目的 探讨阿托伐他汀联合阿司匹林治疗急性脑梗死患者的疗效及其对神经功能缺损、血脂、颈动脉斑块等影响.方法 选择急性脑梗死患者80例,随机分为阿托伐他汀联合阿司匹林治疗组40例.单用阿司匹林对照组40例,比较两组神经功能缺损程度及疗效,血脂、颈部血管超声的变化,并随访6个月,观察有无再发脑梗死.结果 治疗后三酰甘油(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、颈总动脉内径、斑块体积、阻力指数、搏动指数、神经功能缺损评分在治疗组分别为(1.36±0.33)mmol/L、(5.21±0.32)mmol/L、(1.20±0.10)mmol/L、(1.31±0.37)mmol/L、(6.43±0.71)mm、(40.39±8.94)mm3、(0.70±0.06)、(2.12±0.37)、(10.24±3.31)分,低于对照组[(1.77±0.80)mmol/L、(5.80±0.37)mmol/L、(1.43±0.16)mmol/L、(1.57±0.39)mmol/L、(6.67±0.47)mm、(54.26±8.25)mm3、0.82±0.08、2.18±0.54、(14.69±3.23)分],(均P<0.05或0.01);颈动脉内中膜厚度、收缩期峰值速度治疗组分别为(1.66±0.50)mm、(71.34±15.01)an/s,高于对照组[(1.50±0.68)(68.97±18.21)an/s](均P<0.01);治疗组总有效率92.5%,高于对照组75.0%(P<0.05),6个月内未见脑梗死复发.结论 阿托伐他汀联合阿司匹林治疗急性脑梗死有利于神经功能的恢复和改善预后,对缩小颈动脉粥样斑块体积、稳定斑块、降低血脂各项指标有较好的效果,对干预脑梗死的复发起到积极作用,可作为急性脑梗死治疗的联合药物.     

Comparison of aspirin and indobufen in healthy volunteers

The aim of this study is to quantify the extent and recovery of platelet inhibition after administration of indobufen and aspirin in healthy volunteers. Indobufen inhibits platelet aggregation by reversibly inhibiting the platelet cyclooxygenase enzyme, thereby suppressing thromboxane synthesis. Twenty healthy volunteers completed the study and received aspirin (200?mg/day for 2 weeks) followed by a 4-week washout period and then indobufen (200?mg twice a day for 2 weeks). The percent (%) inhibition of platelet aggregation (IPA) was assessed using arachidonic acid (0.5?mg/ml) and adenosine diphosphate (5?µM) at 4, 12, 24 and 48 hours after last dose of each drug. IPA assessed using arachidonic acid as the agonist was similar at 4 hours after the last dose of indobufen (81.07?±?9.36%) and aspirin (96.99?±?0.29%, p?=?0.10), but significantly lower at 12 hours (74.04?±?9.55% vs. 97.94?±?0.28%, p?=?0.02), 24 hours (33.39?±?11.13% vs. 97.48?±?0.32%, p?p?p?=?0.002). Indobufen (200?mg twice a day) caused equivalent initial inhibition of platelet aggregation to aspirin (200?mg daily), and the anti-aggregation effect diminished faster than after aspirin.