Platelet thromboxane(11-dehydro-Thromboxane B_2) and aspirin response in patients with diabetes and coronary artery disease

Aspirin(ASA) irreversibly inhibits platelet cyclooxygenase-1(COX-1) leading to decreased thromboxane-mediated platelet activation. The effect of ASA ingestion on thromboxane generation was evaluated in patients with diabetes(DM) and cardiovascular disease. Thromboxane inhibition was assessed by measuring the urinary excretion of 11-dehydro-thromboxane B2(11dhTxB2), a stable metabolite of thromboxane A2. The mean baseline urinary 11dhTxB2 of DM was 69.6% higher than healthy controls(P = 0.024): female subjects(DM and controls) had 50.9% higher baseline 11dhTxB2 than males(P = 0.0004), while age or disease duration had no influence. Daily ASA ingestion inhibited urinary 11dhTxB2 in both DM(71.7%) and controls(75.1%, P < 0.0001). Using a pre-established cut-off of 1500 pg/mg of urinary 11dhTxB2, there were twice as many ASA poor responders(ASA "resistant") in DM than in controls(14.8% and 8.4%, respectively). The rate of ASA poor responders in two populations of acute coronary syndrome(ACS) patients was 28.6 and 28.7%, in spite of a significant(81.6%) inhibition of urinary 11dhTxB2(P < 0.0001). Both baseline 11dhTxB2 levels and rate of poor ASA responders were significantly higher in DM and ACS compared to controls. Underlying systemic oxidative inflammation may maintain platelet function in atherosclerotic cardiovascular disease irrespective of COX-1 pathway inhibition and/or increase systemic generation of thromboxane from non-platelet sources.

Evaluation of the Effect of Aspirin on Platelet Aggregation: Methodological Recommendations for Aspirin-Drug Interaction Studies

Given the broad application of aspirin as antiplatelet drug, availability of standardized methodology to assess potential interaction with any co-medication on platelet aggregation is desired. We characterized the effect of aspirin (ASA) therapy on collagen-induced platelet aggregation in whole blood to define such methodology. Collagen-induced platelet whole blood aggregation was assessed in 6 healthy male volunteers on 2 occasions (Day 1, Day 7) using the Chronolog aggregometer. From Day 2 up to Day 7, subjects received a daily oral dose of 75 mg ASA. The relationship between collagen dose and platelet aggregation response was assessed. On Day 1, maximal aggregation was observed at 1 μg/mL collagen (15.3 ± 4.6 Ω) and higher. Reproducible results were obtained without any indication of intra-subject fluctuations. ASA treatment decreased maximal aggregation by 80% and 38% at 0.5 and 2.0 μg/mL collagen, respectively. Power calculations were performed based on the observed intra-subject variability and demonstrated minimal sample sizes of 9 - 11 subjects for future cross-over ASA-drug interaction studies exploring effects on platelet aggregation, which demonstrates that the proposed collagen-induced ex vivo whole blood platelet aggregation is a feasible methodology to evaluate ASA-drug interactions in healthy volunteers.

Effect of pretreatment with aspirin and ticlopidine on the change of platelet aggregability after radiofrequency catheter ablation

Eighty-two patients with supraventricular tachycardia undergoing radiofrequency catheter ablation (RFCA) were studied to observe the inhibition effect of aspirin and ticlopidine on platelet aggregability(PAG) and thromboxane B2(TXB2) of the blood samples.Patients were divided into aspirin group A.ticlopidine group B.aspirin+ticlopidine group C and control group D.PAG and TXB2 were increased clearly after RFCA in all groups(P<0.001).Treatment with aspirin or ticlopidine before operation could reduce the patelet aggregability caused by RFCA and the joint effect of two drugs(change rate of group A:52.51±12.51%;group B:54.78±11.27%;group C:30.51±10.59%;group D:91.75±21.43%;(P<0.05)was studied .The much decreased platelet aggregability after antiplatelet therapy was evidence of the potential benefit of the treatment in preventing thromboembolism after ablation.Pretreatment with aspirin and ticlopidine together is a good way to decrease palateler aggregability after RFCA.

Clinical importance of aspirin and clopidogrel resistance

Aspirin and clopidogrel are important components of medical therapy for patients with acute coronary syndromes, for those who received coronary artery stents and in the secondary prevention of ischaemic stroke. Despite their use, a significant number of patients experience recurrent adverse ischaemic events. Interindividual variability of platelet aggregation in response to these antiplatelet agents may be an explanation for some of these recurrent events, and small trials have linked "aspirin and/or clopidogrel resistance", as measured by platelet function tests, to adverse events. We systematically reviewed all available evidence on the prevalence of aspirin/clopidogrel resistance, their possible risk factors and their association with clinical outcomes. We also identified articles showing possible treatments. After analyzing the data on different laboratory methods, we found that aspirin/clopidogrel resistance seems to be associated with poor clinical outcomes and there is currently no standardized or widely accepted definition of clopidogrel resistance. Therefore, we conclude that specific treatment recommendations are not established for patients who exhibit high platelet reactivity during aspirin/clopidogrel therapy or who have poor platelet inhibition by clopidogrel.

Inhibitory effects of copper-aspirin complex on platelet aggregation

目的：研究阿司匹林铜（ＣｕＡｓｐ）对血小板聚集性的影响及其机制．方法：用Ｂｏｒｎ氏法测定ＣｕＡｓｐ对兔血小板聚集性的影响．用荧光光度法和放射免疫法观察ＣｕＡｓｐ对兔血小板５羟色胺的释放和ＴＸＢ２的产生及血浆中ＴＸＢ２和６ｋｅｔｏＰＧＦ１α水平的影响．结果：ＣｕＡｓｐ体外呈浓度依赖性抑制花生四烯酸（ＡＡ）诱导的血小板聚集和５羟色胺的释放（ＩＣ５０分别为１７和１９μｍｏｌ·Ｌ－１，９５％可信限为９－３３和１０－３０μｍｏｌ·Ｌ－１），且抑制ＴＸＢ２的产生（Ｐ＜００５）．ＣｕＡｓｐ１０ｍｇ·ｋｇ－１灌胃选择性抑制ＡＡ诱导聚集．降低血浆ＴＸＢ２，同时升高６ｋｅｔｏＰＧＦ１α的水平（Ｐ＜００５）．结论：ＣｕＡｓｐ体内外均有比Ａｓｐ更强的抗血小板聚集作用．

Effects of procainamide on adenosine diphosphate-induced platelet aggregation and thromboxane B_2 production in rabbits in vitro

Turbidimetry and radioimmunoassay were used to study the effects of procainamide (PA ) onadenosine diphosphate (ADP)-induced rabbit platelet aggregation and thromboxane B2 (TXB2) production invitro. PA 8. 5--544. 0 μmol L-1 inhibited ADP-induced platelet aggregation and TXB2 production, and theinhibition rates were 26. 7% -- 66. 7 % and 21. 4 % -- 70. 1 %, respectively. There was positive correlation between PA concentration and its efficiency in inhibiting the platelet aggregation and TXB2 production, and alsobetween the inhibition rates of platelet aggregation and that of TXB2 production. The three linear equationsand main parameters were The results indicate that PA could significantly inhibit ADP--induced platelet aggregation and TXB2 production in rabbits.

Inhibitory Effect of β-Elemene Emulsion on Platelet Aggregation and its Mechanism

为阐明β榄香烯的抗血小板作用，本文分别采用比浊法和放免法测定大鼠连续ｉｐ７ｄβ榄香烯乳６．２５～１２．５ｍｇ·ｋｇ－１·ｄ－１后对血小板聚集、血浆ｋｅｔｏＰＧＦ１α和ＴＸＢ２水平的影响。结果表明，本品分别使凝血酶、花生四烯酸和ＡＤＰ诱导血小板最大聚集率下降３８．３％～４２．６％，１４．７％～１９．１％和７．２％～１０．８％，血浆ＴＸＢ２从８８ｎｇ·Ｌ－１下降至７２ｎｇ·Ｌ－１，ｋｅｔｏＰＧＦ１α从１７．５ｎｇ·Ｌ－１增加至２０．９ｎｇ·Ｌ－１。提示ＴＸＢ２降低和ｋｅｔｏＰＧＦ１α值增加是其抑制血小板聚集的作用机制之一。

Effects of thromboxane and prostacyclin imbalance on hemodynamics and hemorrheology in severely burn patients

Fifty-seven bum patients were dosdy observed for 28 d postburn.In general,plasma levelof thromboxane B2（TXB2）,6-keto-PGFlx and TXB2/6-keto-PGFlx ratio all rose up abruptly tothe peak in the first half day after burns and then declined gradually.However the patterns of theirchanges were different:6-keto-PGFlx returned to the control level in the 2nd day postburn,remained in a higher level than the control even in the 5th day postburn,and the increase ofTXB2/6-keto-PGFlα ratio was especially pronounced in the first 3 d postbum.It was also shownthat the changes of hemodynamics and hemorrheology occurred simultaneously with the imbalanceof thromboxane and prcstacyclin in the early postburn stage.The extent of the imbalance accordedwith the severity of hemodynamical and hemorrheological changes and was closely correlated withthe changes with the stroke volume,cardiac output,systemic vascular resistance,circulatory plateletaggregate ratio,platelet count and blood vinery.These findings suggest that the imbalance be-tween thromboxane and prostacyclin plays an important role in the changes of hemodynamics andhemorrheology in severe burn cases.

Effect of polymorphism and type II diabetes on aspirin resistance in patients with unstable coronary artery disease

Background Aspirin is widely used in the secondary prevention of coronary artery diseases, including myocardial infarction, stroke, and vascular related deaths. However, the antiplatelet effect of aspirin appears to be variable and aspirin resistance （AR） is currently still controversial for Chinese patients. The aim of this study was to describe the prevalence of AR, and identify possible risk factors associated with a lack of response to aspirin treatments in patients with unstable coronary artery disease.

Inhibitiory effects of procainamide on rabbit platelet aggregation and thromboxane B_2 production in vitro

目的：研究普鲁卡因胺（ＰＡ）对凝血酶诱导血小板聚集和血栓素Ｂ２（ＴＸＢ２）产生的影响．方法：用比浊法和放射免疫分析法．结果：普鲁卡因胺８５，３４，１３６和５４４μｍｏｌ·Ｌ－１有明显抑制作用．抑制率分别为４５％±３７％，４８％±３２％，８８％±２３％，９２％±１５％和５３％±２４％，６５％±２６％，９０％±６％，９５％±６％．ＰＡ的浓度与血小板聚集和ＴＸＢ２产生的抑制效力之间，以及血小板聚集抑制率和ＴＸＢ２产生的抑制率之间均存在着正相关关系，三者的线性方程和主要参数为：＾Ｙ＝０２０７５Ｘ－４９１５７，ｒ＝０９９８５；＾Ｙ＝０９５４６Ｘ－３４６７２４，ｒ＝０９９２１；＾Ｙ＝０８２０２Ｘ＋１９７０６２，ｒ＝０９９２１．结论：普鲁卡因胺抑制凝血酶诱导血小板聚集和ＴＸＢ２产生．

Dual effects of 5-hydroxytryptamine on stable analogue of thromboxane A^(2^_) induced aggregation and release reaction in rabbit platelets

目的：研究５ＨＴ对ＳＴＡ２血小板聚集和释放反应的影响及可能的分子机制．方法：以透光法，介质中ＡＴＰ含量及荧光图像法评价血小板变形，聚集反应和［Ｃａ２］ｉ水平．结果：（１）５ＨＴ预处理可消除ＳＴＡ２的血小板变形，ＳＴＡ２０３μｍｏｌ·Ｌ－１的聚集增强，ｌ－３μｍｏｌ·Ｌ－１的聚集不变，释放反应抑制．（２）５ＨＴ预处理增加ＳＴＡ２０３μｍｏｌ·Ｌ－１的［Ｃａ２＋］ｉ，降低３μｍｏｌ·Ｌ－１的［Ｃａ２＋］ｉ降低．（３）延长加入５ＨＴ和ＳＴＡ２的间隔，ＳＴＡ２０３μｍｏｌ·Ｌ－１的聚集增强，３μｍｏｌ·Ｌ－１的聚集不变，释放反应抑制．结论：５ＨＴ对ＳＴＡ２介导的聚集和释放反应有双重影响．对ＳＴＡ２［Ｃａ２＋］ｉ的调节可能是上述反应的分子机制．

基于血小板聚集率检测的阿司匹林剂量调整方案在儿童先心病抗栓治疗中是否更优

目的 以高危血栓风险先心病儿童为对象,针对阿司匹林治疗反应多样性及近远期血栓发生率仍较高的问题,评价基于血小板功能检测目标导向的阿司匹林个体化抗栓治疗方案的临床效果是否优于传统固定剂量的给药方案。方法 采用前瞻随机对照注册研究(ChiCTR2000036446)。纳入阜外医院小儿外科中心自2020年4月~2021年4月所有行先心病手术并且需要术后常规应用阿司匹林抗栓治疗的6岁内患儿。所有入组患儿随机分为阿司匹林固定剂量组3 mg/(kg·d)和剂量调控组。剂量调控组在3剂和6剂阿司匹林后分别行花生四烯酸诱导的血小板聚集率(PAG-AA)检测。对3剂后PAG-AA>20%者,阿司匹林加量至6 mg/(kg·d);6剂后PAG-AA仍>20%者,联用氯吡格雷0.2 mg/(kg·d)治疗。比较两组患者术后3月包括死亡在内的累计血栓事件发生率和出血事件发生率。结果 对比阿司匹林反应低下、血栓事件与出血不良事件,两组患者数据比较无统计学差异。在接受相同剂量的阿司匹林[3 mg/(kg·d),1次/d]连续3剂后,不同个体的PAG-AA存在较大差异。剂量调控组通过增加阿司匹林剂量,延长阿司匹林使用时间与联合用药,整体阿司匹林反应性得到了改善,但与固定剂量组比较无统计学差异。两组在术后3月接受随访期间以及最终复查时均无死亡病例发生,两组阿司匹林反应低下病例的血栓事件和出血事件发生率比较无明显差别。Spearman相关性检测显示阿司匹林低反应与血栓事件无明显的相关性。结论 与固定剂量阿司匹林抗栓治疗方案相比,基于血小板聚集率检测的阿司匹林剂量个体化抗栓治疗方案并不具有优越性,并不能显著降低先天性心脏病高危血栓风险患儿术后早期3月内血栓及出血事件发生率。血栓事件与阿司匹林反应低下无明显相关性。

奉贤东部地区缺血性脑卒中患者抗血小板药物抵抗现状及其影响因素分析

目的分析奉贤东部地区缺血性脑卒中患者抗血小板药物抵抗发生情况及其影响因素,为临床个体化治疗提供参考依据。方法回顾性分析奉城医院神经内科住院服用阿司匹林、氯吡格雷或二者合用的缺血性脑卒中患者282例,检测入院服药后血小板最大聚集率(MAR)。统计患者的临床资料;分析患者抗血小板药物抵抗发生情况;分析血小板药物抵抗的影响因素。结果282例患者单用阿司匹林的61例,单用氯吡格雷的23例,阿司匹林+氯吡格雷的198例;阿司匹林抵抗(AR)发生率为37.5%(97/259),氯吡格雷抵抗(CR)发生率为46.6%(103/221)。AR患者合并糖尿病比例35.1%高于阿司匹林非抵抗(NAR)患者的22.8%(P<0.05);AR患者与NAR患者年龄、性别、合并高血压、合并冠心病、吸烟史、血小板计数、血小板平均体积、血小板体积分布宽度、大血小板比率(P-LCR)、低密度脂蛋白胆固醇、总胆固醇、糖化血红蛋白、同型半胱氨酸、纤维蛋白原比较无统计学差异(P>0.05)。CR患者女性比例49.5%高于氯吡格雷非抵抗(NCR)患者的35.6%(P<0.05);CR患者与NCR患者年龄、合并高血压、合并糖尿病、合并冠心病、吸烟史、血小板计数、血小板平均体积、血小板体积分布宽度、大血小板比率、低密度脂蛋白胆固醇、总胆固醇、糖化血红蛋白、同型半胱氨酸、纤维蛋白原比较无统计学差异(P>0.05)。Logistic回归分析结果显示,合并糖尿病是AR的独立危险因素(P<0.05)。结论奉贤东部地区缺血性脑卒中患者以高于65岁的老年患者为主,抗血小板药物实验室抵抗率较高且CR率高于AR率,女性较男性更易发生CR;合并糖尿病是AR的独立危险因素,临床工作中应对老年缺血性脑卒中患者积极控制血压血糖,关注是否存在AR、CR,且给予个体化治疗。

氯吡格雷联合阿司匹林治疗女性大脑动脉狭窄所致脑梗死的临床效果

目的探讨氯吡格雷联合阿司匹林治疗女性大脑动脉狭窄所致脑梗死的临床效果。方法回顾性分析兰陵县人民医院2022年1月至2023年1月收治的84例大脑动脉狭窄所致脑梗死女性患者的临床资料,按照不同的治疗方法分为两组,各42例。对照组给予阿司匹林治疗,观察组在其基础上加用氯吡格雷治疗,比较两组临床疗效、神经功能缺损[美国国立卫生研究院卒中量表(NIHSS)]评分、血液流变学指标、血小板聚集率及不良反应。结果与对照组(80.95%)相比,观察组治疗总有效率(95.24%)更高(P<0.05);治疗后,观察组NIHSS评分[(4.12±0.35)分]低于对照组[(7.49±1.22)分],纤维蛋白原[(3.35±0.26)g/L]、血浆黏稠度[(0.67±0.13)m Pa·s]、全血高切黏度[(7.36±1.05)m Pa·s]、全血低切黏度[(8.96±0.30)mPa·s]及血小板聚集率[(28.42±6.48)%]低于对照组[(4.95±0.36)g/L、(1.36±0.15)mPa·s、(10.82±5.26)mPa·s、(11.91±4.56)mPa·s及(34.66±6.87)%],差异有统计学意义(P<0.05);两组不良反应总发生率比较,差异无统计学意义(P>0.05)。结论氯吡格雷联合阿司匹林治疗女性大脑动脉狭窄所致脑梗死的临床效果较好,有助于促进患者神经功能恢复,改善血液流变学,降低血小板聚集率,值得推广。

Effects of 5-HT released from platelets on thrombin-induced aggregation and ATP release in rabbit pla

Ｅｆｅｃｔｓｏｆ５ＨＴｒｅｌｅａｓｅｄｆｒｏｍｐｌａｔｅｌｅｔｓｏｎｔｈｒｏｍｂｉｎｉｎｄｕｃｅｄａｇｇｒｅｇａｔｉｏｎａｎｄＡＴＰｒｅｌｅａｓｅｉｎｒａｂｂｉｔｐｌａｔｅｌｅｔｓｉｎｖｉｔｒｏＬＩＢａｉＹａｎ１，ＬＩＷｅｎＨａｎ（Ｄｅｐａｒ...

RNA N^(6)-甲基腺苷甲基化对老年患者阿司匹林反应性的影响

目的探讨RNA N^(6)-甲基腺苷(m^(6)A)甲基化水平及相关基因对老年患者阿司匹林反应性的影响。方法纳入规律服用阿司匹林100 mg/d的老年患者34例,根据光比浊法检测花生四烯酸诱导的血小板聚集率分为低反应组14例(血小板聚集率>12%),高反应组20例(血小板聚集率<7%)。检测全血RNA m^(6)A甲基化水平及相关基因(YTHDF1、METTL3等)表达,血浆前列腺素H2和血栓素B2水平。结果低反应组全血RNA m^(6)A甲基化水平明显高于高反应组,差异有统计学意义(P<0.05)。低反应组YTHDF1和METTL3 mRNA表达明显高于高反应组[2.77(1.25,4.61)vs 1.32(0.75,1.84),P<0.05;1.64(1.01,2.92)vs 0.80(0.57,1.26),P<0.01]。低反应组血浆前列腺素H2和血栓素B2水平明显高于高反应组[(180.21±15.12)ng/L vs(136.48±9.32)ng/L,(213.44±10.83)ng/L vs(177.27±9.90)ng/L,P<0.05]。结论RNA m^(6)A甲基化水平在阿司匹林低反应性老年患者中升高,检测相关基因可为阿司匹林抗血小板的个体化治疗提供依据。

阿司匹林对妊娠期血小板增多症母婴结局的影响

目的探讨阿司匹林对妊娠期血小板增多症母婴结局的影响。方法选取2020年6月至2022年2月赣南医学院附属兴国医院妇产科收治的60例妊娠期血小板增多症产妇作为研究对象,采用随机数字表法分为对照组和观察组,每组各30例。对照组予以常规治疗;观察组在对照组治疗方法的基础上予以阿司匹林(50mg)治疗至孕36周。比较两组产妇治疗前后的血压、血小板计数及血小板聚集率,并统计两组产妇及新生儿不良结局的总发生率。结果治疗后,观察组的收缩压、舒张压、血小板计数和血小板聚集率均低于对照组,差异有统计学意义(P<0.05);观察组产妇的不良结局总发生率及新生儿的不良结局总发生率均低于对照组,差异有统计学意义(P<0.05)。结论阿司匹林能够改善妊娠期血小板增多症患者的凝血功能及血压,从而降低母婴不良结局的发生率,值得临床推广应用。

拜阿司匹林肠溶片、氯吡格雷单独及联合治疗急性缺血性脑卒中的效果及对血小板聚集的影响

目的 探讨对急性缺血性脑卒中采用拜阿司匹林肠溶片、氯吡格雷单独及联合治疗的临床效果及对血小板聚集影响。方法选取2022年1~12月我院收治的180例急性缺血性脑卒中患者作为本研究对象,按随机数表法将其分为3组,分别为A组、B组及C组,各60例。A组使用拜阿司匹林肠溶片联合氯吡格雷治疗,B使用拜阿司匹林肠溶片治疗,C组使用氯吡格雷治疗。对比3组神经功能、临床疗效、血小板聚集功能、血脂水平及不良反应发生率。结果 A组NIHSS评分、Barthel指数与B组、C组比较差异有统计学意义(P <0.05),且B组与C组比较差异无统计学意义(P> 0.05);A组MARAA显著低于B组、C组、MARADP显著高于B组、C组(P <0.05),且B组、C组对比差异无统计学意义(P> 0.05);A组临床总有效率为96.67%显著高于B组临床总有效率75.00%、C组临床总有效率78.33%(P <0.05),且B组、C组对比差异无统计学意义(P> 0.05);A组TG、TC、LDL-C与B组、C组比较差异有统计学意义(P <0.05),且B组与C组比较差异无统计学意义(P> 0.05);A组不良反应发生率为1.67%显著低于B组不良反应发生率28.33%、C组不良反应发生率30.00%(P <0.05),且B组、C组对比差异无统计学意义(P> 0.05)。结论 拜阿司匹林联合氯吡格雷治疗急性缺血性脑卒中较单独治疗的临床效果更为显著。

蛭龙活血通瘀胶囊与氯吡格雷联用对阿司匹林抵抗大鼠的疗效及机制研究

目的观察蛭龙活血通瘀胶囊与氯吡格雷联用对阿司匹林抵抗模型大鼠的疗效,并探索其作用机制。方法采用高脂高糖高盐饲料加乙酰水杨酸、布洛芬灌胃造模,12周后将造模成功的40只大鼠随机分为模型组、蛭龙胶囊组、氯吡格雷组和联合用药组,每组10只,各组大鼠分别以相应药物灌胃。另取10只大鼠作为正常对照组。给药4周后,各组大鼠采用血栓弹力图(thromboela-stogram,TEG)法检测血小板聚集率,ELISA法检测血栓素(thromboxane B2,TX)B2和6-酮-前列腺素(6-ketoprostaglandin,6-keto-PGF)F1α水平,荧光定量PCR法检测mi RNA-126-3p表达水平。结果与正常组比较,模型组大鼠TEG最大幅度和TXB2水平上升(P<0.05),6-keto-PGF1α和mi RNA-126-3p表达水平下降(P<0.05)。与模型组比较,各用药组大鼠TEG最大幅度和TXB2水平降低(P<0.05),6-keto-PGF1α和mi RNA-126-3p表达水平升高(P<0.05),其中联合用药效果最明显。结论蛭龙活血通瘀胶囊与氯吡格雷联合用药能降低阿司匹林抵抗大鼠血小板聚集率,且比单独使用蛭龙活血通瘀胶囊和氯吡格雷效果更好,其机制可能与调控mi RNA-126-3p的表达水平有关。

尿11-DH-TXB_(2)水平与急性冠脉综合征患者血小板聚集程度相关性分析

目的研究尿11-去氢-血栓烷B2(11-DH-TXB_(2))水平与急性冠脉综合征(ACS)患者血小板聚集程度的相关性。方法选取2019年4月至2020年12月杭州市富阳区第一人民医院收治的120例ACS患者,定义为研究组;同时选取与研究组性别、年龄相匹配的于健康体检中心体检的健康志愿者60名,定义为对照组。检测两组受试者尿11-DH-TXB_(2)水平及血小板聚集率。研究组患者根据二磷酸腺苷(ADP)诱导血小板聚集率结果分为达标组(n=30,ADP聚集率<50%)和未达标组(n=90,ADP聚集率≥50%)。采用Logistic多因素回归分析影响ACS患者血小板聚集程度的危险因素,采用Pearson相关性分析法分析尿11-DH-TXB_(2)水平与ACS患者血小板聚集率的相关性。结果研究组尿11-DH-TXB_(2)、血小板聚集率水平均高于对照组(P<0.05)。单因素分析显示,达标组性别、饮酒史、吸烟史、高血压史、糖尿病史占比,年龄、舒张压、收缩压、甘油三酯(TG)、总胆固醇(TC)、尿酸(UA)、胱抑素C(Cys C)水平与未达标组比较,差异无统计学意义(P>0.05)。未达标组体质量指数(BMI)、静息心率、D-二聚体(D-D)、低密度脂蛋白(LDL)、尿11-DH-TXB_(2)、肌钙蛋白(cTnI)、超敏C反应蛋白(hs-CRP)水平高于达标组(P<0.05)。经Logistic回归分析,静息心率、LDL、尿11-DH-TXB_(2)、hs-CRP水平均是影响ACS患者血小板聚集程度的危险因素(P<0.05)。Pearson相关性分析显示,尿11-DH-TXB_(2)水平与ACS患者血小板聚集率呈正比(r=0.552,P<0.05)。结论尿11-DH-TXB_(2)在ACS患者体内水平异常升高,与ACS患者血小板聚集程度存在一定的相关性,对判断ACS患者血小板聚集率具有临床意义。