氯吡格雷联合阿托伐他汀对脑血栓患者血小板和血流动力学参数的影响

探讨氯吡格雷联合阿托伐他汀对脑血栓患者血小板和血流动力学参数的影响。将126例脑血栓患者随机分为对照组和观察组各63例。在常规治疗基础上,对照组口服氯吡格雷,观察组同时口服氯吡格雷和阿托伐他汀。观察两组患者治疗前后的血小板参数以及血流动力学参数变化。治疗后,两组血小板聚集率和血小板粘附率均显著降低,且观察组低于对照组,差异均有统计学意义(P0.05)。治疗后,两组血浆粘度、高切全血粘度、低切全血粘度、血沉、纤维蛋白原和D-二聚体水平均显著降低,且观察组低于对照组(P0.05),差异均有统计学意义(P0.05)。氯吡格雷联合阿托伐他汀可有效改善脑血栓患者血小板和血流动力学参数。     

瑞舒伐他汀对急性冠脉综合征行经皮冠状动脉介入治疗患者心功能的影响

目的探讨瑞舒伐他汀对急性冠脉综合征行经皮冠状动脉介入(PCI)治疗患者心功能的影响。方法选取700例急性冠脉综合征患者。随机分成观察组和对照组各60例。所有患者均接受PCI治疗,对照组患者在PCI治疗的基础上给予常规抗血小板、抗凝、扩血管治疗,观察组患者则在对照组的基础上给予瑞舒伐他汀强化治疗。比较2组患者治疗前后的心功能状况、心肌损伤情况、血清炎症因子水平及不良心血管事件发生率。结果 2组患者治疗后左室射血分数(LVEF)显著提高,且观察组显著高于对照组(P0.05);2组患者治疗后的左心室舒张末期内径(LVDD)以及左心室收缩末期内径(LVSD)显著下降,且观察组显著低于对照组(P0.05);2组患者治疗后的肌酸激酶同工酶(CK-MB)和心肌肌钙蛋(c Tnl)均显著提高,且观察组显著高于对照组(P0.05);2组患者治疗后的超敏C反应蛋白(hs-CRP)和脑尿钠肽(BNP)水平均显著下降,且观察组显著低于对照组(P0.05);观察组患者心脏不良事件和再狭窄的发生率显著均低于对照组患者(P0.05)。结论瑞舒伐他汀可保护急性冠脉综合征行PCI治疗的患者的心功能,减轻心肌损伤和炎症水平,降低术后心脏不良事件、再狭窄的发生率。     

阿托伐他汀联合氯吡格雷治疗脑梗塞的临床观察

目的探索阿托伐他汀与氯吡格雷联合治疗脑梗塞的疗效。方法选取2015年5月~2017年5月在我院就诊的脑梗塞患者160例。随机分为观察组和对照组各80例。两组均给予常规对症治疗,对照组患者在此基础上加用氯吡格雷治疗,观察组患者在对照组基础上加用阿托伐他汀治疗,对比两组患者的治疗效果。结果观察组治疗3个月后NIHSS评分、IRS评分均低于对照组,BI评分显著高于对照组,差异有统计学意义(P0.01);两组MAR比较差异无统计学意义(P0.05);观察组斑块厚度、斑块面积等指标均优于对照组,差异有统计学意义(P0.01)。结论阿托伐他汀联合氯吡格雷治疗脑梗塞效果确切,可以有效促进患者神经功能及颈内动脉斑块状况改善,值得推广应用。     

阿托伐他汀与氯吡格雷对急性冠状动脉综合征患者血小板聚集率的影响

目的 探讨阿托伐他汀和氯吡格雷对急性冠状动脉综合征（ACS）患者血小板聚集率的影响.方法 选择66例ACS患者作为ACS组,25例健康志愿者作为对照组.ACS组患者在常规药物治疗基础上均予阿司匹林（100 mg/d）、氯吡格雷（75 mg/d）和阿托伐他汀（20 mg/d）治疗.对照组志愿者均予阿司匹林肠溶片、氯吡格雷和阿托伐他汀口服,药品来源、剂量与ACS组相同.采用流式细胞仪测定上述受试者的血小板聚集率.结果 对照组志愿者分别采用双联抗血小板联合阿托伐他汀治疗以及双联抗血小板治疗,血小板聚集率分别为（44.27±16.37）%、（47.61±16.67）%,二者差异无统计学意义（P〉0.05）.ACS组患者采用上述2种方法治疗,血小板聚集率分别为（47.70±15.07）%、（47.03±15.45）%,二者差异无统计学意义（P〉0.05）.结论 氯吡格雷与阿托伐他汀联合治疗不影响氯吡格雷的抗血小板作用,二者无相互作用.     

阿托伐他汀强化治疗对冠心病患者PCI术后血小板活化及心肌损伤的影响

目的观察阿托伐他汀强化治疗对冠心病患者PCI术后血小板活化及心肌损伤的影响。方法选择2015年8月~2017年2月于我院行PCI手术的冠心病患者80例,根据入院顺序分为对照组40例和观察组40例。观察组在术前给予患者口服80mg阿托伐他汀,术后维持20mg/d用药剂量,连用4w;对照组仅在术后连服4w阿托伐他汀,20mg/d。观察两组治疗效果。结果治疗后,对照组术后4w P-选择素及血小板膜糖蛋白Ⅱb/Ⅲa水平、术后24h血清肌酸激酶同工酶及肌钙蛋白水平均高于观察组,差异有统计学意义(P0.05)。结论在行PCI术的冠心病患者中应用阿托伐他汀进行强化治疗效果显著,可有效抑制术后血小板活化,减轻心肌损伤。     

阿托伐他汀对急性冠脉综合征患者PCI围术期的治疗效果影响

目的针对急性冠脉综合症患者在PCI围术期应用阿托伐他汀强化治疗,并探究分析其对治疗效果的价值。方法选择2016年5月~2017年1月经由本院治疗的136例急性冠状动脉综合征患者,随机分为对照组和观察组各68例,对照组PCI围术期采用常规治疗,观察组围术期采用阿托伐他汀强化治疗,对比两组患者治疗前后的各项血清生化指标及术后随访期间不良心血管事件发生情况。结果治疗后,两组患者hs-CRP、LDL-C与TC指标均有所降低,但观察组的降低幅度显著优于对照组,差异有统计学意义(P0.05);治疗后,两组患者Cr与ALT指标均有所升高,但差异无统计学意义(P0.05);两组术后随访12月,观察组心血管不良事件发生3例(4.41%),对照组发生21例(30.88%),差异有统计学意义(P0.05)。结论 PCI围术期应用阿托伐他汀加强治疗可显著改善各血清指标,减少不良事件发生情况,建议广泛应用。     

阿托伐他汀对急性心肌梗死冠脉介入治疗后炎性因子水平的影响

目的 评价阿托伐他汀对急性心肌梗死冠脉介入治疗(PCI)后炎症因子水平的影响 方法 将2017年5月至2018年5月在我院治疗的60例急性心肌梗死患者随机分为对照组和实验组,每组30例,在PCI手术常规治疗基础上,对照组给予辛伐他汀,实验组给予阿托伐他汀。分别于治疗前和治疗后测定总胆固醇、甘油三酯、低密度脂蛋白、hs-CRP和PCT水平,比较患者PCI术后一个月心血管事件发生情况。结果 治疗前两组甘油三酯( Triglyceride,TG)、血清总胆固醇(Total cholesterol,TC)和低密度脂蛋白(Low-density lipoprotein,LDL-c)水平相比无统计学差异(P＞0.05),治疗后两组TG、TC和LDL-c水平较治疗前均显著降低(P＜0.05);其中,实验组治疗后TG、TC和LDL-c水平均明显低于对照组(P＜0.05)。 两组治疗前后hs-CRP、PCT水平相比无统计学差异(P＞0.05),两组治疗后hs-CRP、PCT水平较治疗前显著降低(P＜0.05),实验组治疗后hs-CRP、PCT水平明显低于对照组(P＜0.05)。实验组患者心血管事件发生率明显低于对照组(6.67%和23.33%,P＜0.05)。结论 阿托伐他汀能显著降低急性心肌梗死冠脉介入治疗后患者的血脂、炎症因子水平,减少心血管事件发生率。     

阿托伐他汀联合氯吡格雷治疗脑梗塞的临床疗效

目的分析阿托伐他汀联合氯吡格雷治疗脑梗塞的临床疗效。方法选取2018年10月～2019年9月我院收治的脑梗塞患者78例,采用随机数字表法分为对照组和观察组各39例。对照组给予氯吡格雷治疗,观察组给予阿托伐他汀联合氯吡格雷治疗。对比两组临床疗效。结果观察组临床总有效率分别为92.31%,显著高于对照组的71.80%,差异有统计学意义(P0.05)。两组治疗后NIHSS评分均显著低于治疗前,且观察组显著低于对照组(P0.05)。两组治疗后ADL评分均显著高于治疗前,且观察组显著高于对照组(P0.05)。结论阿托伐他汀联合氯吡格雷治疗脑梗塞能显著提高临床疗效,改善患者神经功能和日常生活活动能力。     

首次负荷剂量阿托伐他汀对AMI急诊介入术中无复流及hs-CRP的影响

目的 观察急性心肌梗死急诊经皮冠状动脉介入(PCI)治疗前首次服用80 mg阿托伐他汀能否预防术中无复流的发生及降低hs-CRP水平.方法 73例急性心肌梗死急诊PCI患者随机分为观察组(37例)及对照组(36例).2组患者PCI术前均嚼服阿司匹林300 mg,氯吡咯雷600 mg.观察组予冠心病基础药物治疗,在PCI前首次给予负荷剂量阿托伐他汀80 mg,后给予阿托伐他汀40 mg/d;对照组仅予基础药物治疗,并给予阿托伐他汀40mg/d.观察PCI术中无复流的发生及术前、术后12 h hs-CRP的变化.结果 观察组术中无复流的发生率稍低于对照组(8.1％vs22.2％)但差异无统计学意义(P＞0.05);术后12h阿托伐他汀组hs-CRP水平低于对照组[(10.29±9.15)vs(13.77±10.41 )mg/L,P＜0.01].结论 对于急性心肌梗死急诊PCI患者,介入术前首次给予负荷剂量的阿托伐他汀能够降低炎症反应,能否确实降低PCI术中无复流的发生有待进一步研究.     

阿托伐他汀联合硫酸氯吡格雷片及阿司匹林治疗老年急性脑梗死的效果观察

目的：探究阿托伐他汀联合硫酸氯吡格雷片及阿司匹林治疗老年急性脑梗死的效果。方法：将2018年5月~2019年10月收治的86例急性脑梗死患者,采用随机数字表法分为对照组和观察组,各43例。对照组接受硫酸氯吡格雷片联合阿司匹林治疗,观察组在对照组基础上联合阿托伐他汀治疗,均治疗2个月。比较两组治疗效果。结果：治疗后,两组美国国立卫生研究院卒中量表评分均较治疗前下降,且观察组低于对照组（P＜0.05）;治疗后,两组三酰甘油、总胆固醇以及超敏-C反应蛋白水平均较治疗前降低,且观察组低于对照组（P＜0.05）;治疗后两组颈动脉内膜中层厚度、斑块厚度、斑块面积以及斑块数量均较治疗前下降,且观察组低于对照组（P＜0.05）;两组不良反应发生率比较无显著差异（P＞0.05）。结论：阿托伐他汀联合硫酸氯吡格雷片及阿司匹林治疗老年急性脑梗死,可改善患者神经功能缺损程度,调节血脂水平,控制炎症介质,降低颈动脉粥样硬化程度,安全可靠。     

冠状动脉粥样硬化性心脏病血小板参数变化

目的探讨冠心病患者血小板参数变化的临床意义。方法采用深圳迈瑞BC5800血细胞分析仪测定60例冠心病患者和50例健康对照者外周血中血小板计数(PLT)、血小板平均体积(MPV)、血小板体积分布宽度(PDW)和大血小板比率(P-LCR),并进行统计分析。结果冠心病患者与健康对照组的PLT、MPV、PDW及P-LCR比较,差异均有统计学意义(P<0.05),其中MPV、PDW和P-LCR明显高于健康对照组,而PLT则明显低于健康对照组。结论临床上动态监测冠心病患者的血小板参数变化,对冠心病的预防、诊治及预后有一定的参考意义。     

The association of depression with platelet activation: evidence for a treatment effect

Summary. Background: Depression is associated with an increased risk of cardiovascular disease (CVD). Although the mechanism is uncertain, prothrombotic and inflammatory factors may play a role. Objectives: As platelets play a key role in CVD, we determined first, whether depressed individuals had more activated platelets than non‐depressed individuals and second, whether treatment of depression reduced platelet activation levels. Patients/methods: We recruited 108 depressed outpatients and 45 control subjects all without a history of CVD. After psychological assessment, the depressed patients were offered treatment with medication and/or psychotherapy. Flow cytometric markers of platelet activation and level of depression were assessed at baseline and at 4 weeks and 6 months after treatment. Results: Depression was associated with increased platelet activation with a higher number of circulating CD62p (0.76 × 10⁹ L^?1 vs. 0.46, P = 0.019) and CD63 (P = 0.05) positive platelets compared with controls. Patients with depression also had more circulating platelet‐leukocyte aggregates than controls (P < 0.001). There was a positive correlation between the severity of depression and the level of platelet activation. Platelets from depressed patients were also hyperreactive to adenosine 5´‐diphosphate (ADP) stimulation with increased CD62p and CD63 exposure (P = 0.003 and 0.019, respectively). Six months of treatment resulted in a reduced number of circulating CD62p and CD63 positive platelets (29.84% and 53.38% decrease) and a 20.9% reduction in CD63 exposure after ADP activation. Conclusions: Depression is associated with increased in vivo platelet activation and resolution of depression using psychotherapy and/or medication reduces platelet activation. These findings provide insights into the link between depression and cardiovascular risk.     

Effect of platelet turnover on whole blood platelet aggregation in patients with coronary artery disease

Summary. Background: Previous studies have demonstrated considerable variation in the antiplatelet effect of aspirin. Objectives: To investigate the impact of platelet turnover on the antiplatelet effect of aspirin in patients with stable coronary artery disease (CAD) and to identify determinants of platelet turnover. Methods: Platelet turnover was evaluated by measurements of immature platelets and thrombopoietin in 177 stable CAD patients on aspirin monotherapy, including 85 type 2 diabetics and 92 non‐diabetics. Whole blood platelet aggregation was determined using the VerifyNow^® Aspirin test and multiple electrode aggregometry (MEA, Multiplate^®) induced by arachidonic acid (AA) (1.0 mm ), adenosine diphosphate (ADP) (10 μm ) and collagen (1.0 μg mL^?1). Results: Immature platelet levels significantly correlated with MEA (r = 0.31–0.36, P‐values < 0.0001) and the platelet activation marker sP‐selectin (r = 0.19, P = 0.014). Contrary to the VerifyNow^® test, MEA significantly correlated with variations in platelet count (r = 0.45–0.68, P‐values < 0.0001). Among patients with residual platelet reactivity according to AA, there were significantly more diabetics (61% vs. 41%, P = 0.027) and higher levels of sP‐selectin (77.7 ± 29 vs. 70.2 ± 25 ng mL^?1, P = 0.070) and serum thromboxane B₂ (0.81 [0.46; 1.70] vs. 0.56 [0.31; 1.12] ng mL^?1, P = 0.034). In a multivariate regression analysis, immature platelet levels were determined by thrombopoietin levels (P < 0.001), smoking (P = 0.020) and type 2 diabetes (P = 0.042). Conclusions: The antiplatelet effect of aspirin was reduced in CAD patients with an increased platelet turnover. Once‐daily dosing of aspirin might not suffice to adequately inhibit platelet aggregation in patients with an increased platelet turnover.     

Dual antiplatelet therapy unmasks distinct platelet reactivity in patients with coronary artery disease

Summary. Background: Platelet‐induced thrombosis is a major risk factor for recurrent ischemic events, although platelet function in patients with cardiovascular disease taking aspirin and clopidogrel is very poorly characterized. The aim of this study was to assess platelet reactivity in patients with cardiovascular disease taking aspirin and clopidogrel. Methods: We developed a rapid assay to measure platelet aggregation in response to arachidonic acid, collagen, adenosine diphosphate (ADP), epinephrine and thrombin receptor activating peptide (TRAP) in 80 healthy volunteers. We then recruited 200 consecutive patients from outpatient clinics and the cardiac catheterization laboratory and tested platelet function. Platelet aggregation induced by epinephrine is a marker of global platelet reactivity. We tested platelet function in 146 patients compliant with antiplatelet therapy. Platelet aggregation to epinephrine was divided into quartiles. The platelet response to the other agonists was analysed based on the response to epinephrine. Results: Platelet reactivity increased significantly across the quartiles in response to epinephrine in healthy volunteers and patients (P < 0.0001). A significant increase in response across quartiles was seen with all agonists in healthy volunteers (P < 0.001). In contrast, a significant increase in response across quartiles was only seen with ADP in patients (P < 0.0001). Hypertension, smoking and diabetes were significantly associated with increasing platelet reactivity to epinephrine (P < 0.05). Conclusion: This study shows that platelet response differs between healthy volunteers and patients on dual antiplatelet therapy. In patients with cardiovascular disease, dual antiplatelet therapy unmasks a distinct type of platelet reactivity in response to epinephrine and ADP but not other agonists.     

川崎病患儿血小板α-颗粒膜蛋白及血小板参数变化的观察与探讨

目的探讨川崎病(Kawasaki Disease,KD)患儿急性期血小板α-颗粒膜蛋白(CD62P)、血小板参数的动态变化与本病发病机制及冠状动脉并发症之间的关系.方法应用荧光标记单克隆抗体和流式细胞仪以及自动血球记数仪分别对30例KD急性期患儿血清CD62P及50例KD急性期患儿血小板参数进行了检测,并与20例健康体检儿童进行对照.结果 KD组急性期血浆CD62P表达明显高于对照组(P<0.01),血小板计数(PLT)、血小板压积(PCT)、血小板分布宽度(PDW)水平也明显高于对照组(P<0.01).结论 KD急性期患儿血浆CD62P呈高表达,PLT、PCT、PDW水平明显增高,提示急性期KD患儿体内血小板代谢旺盛,释放因子较多,活化程度显著增高,表现为高聚集、高黏附,高凝固及低血浓度的血液流变特点;而此期也正是临床KD患儿动脉血栓及冠状动脉瘤形成的高峰期,提示活化的血小板参与或促发了冠状动脉血栓的形成;因此动态检测CD62P、血小板参数的变化,及时采取有效抗炎抗凝措施,对于减轻KD患儿血管炎症,防止血栓形成,预防冠状动脉并发症的发生具有重要的临床意义.     

未成熟血小板比率在急性冠状动脉综合征的早期诊断价值

目的探讨未成熟血小板比率（IPF）在急性冠状动脉综合征（ACS）中的早期诊断价值。方法入选浙江大学医学院附属第一医院221例ACS患者（研究组）和同期60例健康体检者（对照组）。检测外周血IPF、平均血小板体积（MPV）、血小板计数及其他各项生化指标,将研究组患者按纽约心脏病协会（NYHA）分级对上述指标进行比较,并对研究组患者IPF水平作秩相关及偏相关分析。结果研究组IPF及MPV水平明显高于对照组,且血小板计数明显低于对照组（P均〈0．05）。研究组患者NYHA分级后三组间年龄、血浆脑利钠肽前体、IPF、血小板计数、MPV、红细胞分布宽度、低荧光强度网织红细胞比率、甘油三酯、总蛋白及白蛋白比较,差异均具有统计学意义（P均〈0．05）。秩相关显示,IPF与MPV、甘油三酯、总胆固醇、NYHA分级呈正相关（r=0．697、0．432、0．466、0．318,P均〈0．05）,与血小板呈负相关（r=-0．587,P〈0．05）。且控制性别、年龄后的偏相关分析显示,IPF与血小板仍呈负相关（r=-0．463,P〈0．05）。结论外周血IPF是预测ACS患者近期临床预后的有效指标。     

冠心病患者血尿酸水平与血小板参数的关系探讨

目的探讨冠心病(CHD)患者血尿酸(SUA)水平与血小板参数的关系。方法对77例CHD患者及51例体检健康者进行SUA与血小板参数[血小板计数(PLT)、大血小板比率(P-LCR)、平均血小板体积(MPV)及血小板体积分布宽度(PDW)]检测。根据SUA水平另将CHD患者分为CHD伴高尿酸血症(HUA)组和CHD正常尿酸组。并对各组检测结果进行统计学分析。结果 CHD患者与健康对照组比较,SUA、P-LCR、MPV、PDW显著增高(P<0.01、P<0.05),PLT显著减低(P<0.01)。CHD伴HUA组与CHD正常尿酸组比较,P-LCR、MPV、PDW显著增高(P<0.05),PLT显著减低(P<0.01)。CHD正常尿酸组与健康对照组比较,血小板参数差异均无统计学意义(P>0.05)。CHD患者SUA与P-LCR、MPV、PDW呈显著正相关(r=0.207、0.213、0.238,P<0.05),与PLT无显著相关性(P>0.05)。结论 CHD患者SUA水平与血小板参数关系密切,HUA可能通过促进血小板活化、增强血小板黏附、聚集和释放功能而参与CHD的发生发展。     

Dynamics of platelet thrombus formation

Summary.  Platelet aggregation and thrombus formation at sites of atherosclerotic plaque rupture is a dynamic process that can lead to intermittent or permanent obstruction to blood flow, resulting in ischemic tissue injury and organ dysfunction. There is a growing body of evidence suggesting that the dynamics of platelet aggregation and initial thrombus development are regulated by two distinct, complementary processes, involving: (i) rheological (biomechanical) and (ii) soluble-agonist -dependent mechanisms. Rheological-dependent platelet aggregation occurs between discoid platelets and requires the biomechanical adhesive and signaling function (mechanotransduction) of the major platelet adhesion receptors, GPIb and integrin α_IIbβ₃. Soluble agonists further potentiate platelet activation, stimulating global platelet shape change and degranulation, and play a major role in stabilizing formed aggregates. Unraveling the dynamics of platelet aggregation and thrombus formation in vivo requires consideration of the cooperative interplay between rheological- and soluble agonist-dependent platelet aggregation mechanisms.     

冠状动脉介入治疗术后三联抗血小板治疗对冠心病合并糖尿病患者的影响

目的 探讨冠心病合并糖尿病患者冠状动脉介入治疗(percutaneous coronary intervention,PCI)术后阿司匹林、氯吡格雷及西洛他唑三联抗血小板治疗对血小板功能及短期预后的影响.方法 318例患者分为双联抗血小板组和三联抗血小板组,于术前、术后7天及术后30天测定p-选择素及血小板聚集率(platelet aggregation rate,PAR),并且统计1个月内主要心血管不良事件(major adverse cardiovascular events,MACE)发生率.结果 术后7天、术后30天三联组较双联组P-选择素表达率均显著降低,差异均有统计学意义[(5.25±2.09)％ vs(6.03±2.12)％,(2.67±1.67)％ vs (3.24±1.98)％,P＜0.05].术后7天、术后30天三联组较双联组PAR均显著降低,差异均有统计学意义[(22.02±6.02)％ vs (29.06±5.71)％,(20.03±4.62)％ vs (26.78±4.35)％,P＜0.05].随访1个月,三联组及双联组MACE发生率分别为1.85％(3/162)、7.05％(11/156),差异有统计学意义(P＜0.05).出血的发生率分别为9.26％(15/162)、7.05％(11/156),差异无统计学意义(P＞0.05).结论 三联抗血小板治疗能够更有效地抑制冠心病合并糖尿病患者血小板的活化和聚集,降低PCI术后MACE事件发生率且不增加出血风险.