伴有心房颤动的急性脑梗死患者血浆溶血磷脂酸含量的变化

目的：观察伴有非瓣膜性心房颤动（NVAF）的急性脑梗死患者血浆溶血磷脂类分子（LPA／AP）含量的变化特点，探索NVAF相关性卒中的病理生理学机制，为临床进行抗栓治疗提供依据。方法：经临床和辅助检查确诊的235例未接受抗栓治疗的NVAF患者、119例伴有NVAF的急性脑梗死患者以及120例不伴有NVAF的急性脑梗死患者纳入本研究。测定其血浆溶血磷脂酸（LPA）及其相似总磷脂（AP）的含量变化，年龄匹配的健康体检者作为对照组。同时观察不同年龄组NVAF患者血浆LPA含量的差异。结果：与对照组比较，各年龄组NVAF患者血浆LPA含量均显著增高，其中≥76岁年龄组增高最为显著，且显著高于≤60岁年龄组（P〈0．01）。发病24h，伴有NVAF的急性脑梗死组患者血浆LPA含量显著高于NVAF组（P〈0．01）和对照组（P〈0．001）。NVAF组和伴有NVAF的急性脑梗死组患者血浆AP含量均显著高于对照组（P〈0．01）。发病24h，伴有NVAF的急性脑梗死组血浆LPA含量显著高于不伴NVAF的急性脑梗死组（P〈0．01）和对照组（P〈0．001）。不伴NVAF的急性脑梗死组血浆LPA含量显著高于对照组（P〈0．01）。至发病后1周，伴有NVAF的急性脑梗死组患者血浆LPA含量仍高显著于不伴NVAF的急性脑梗死组和对照组（P〈0．05）。发病后2周和1个月时，三组间LPA含量无显著性差异。结论：NVAF患者血浆LPA含量显著增高，提示其体内血小板处于活化状。NVAF相关性脑梗死患者血小板活化状态持续时间较长，故其抗栓治疗的时间窗应较长。LPA可作为一种理想的分子标记物，并可用于判断NVAF患者体内血栓形成或血栓形成前状态。     

脑出血患者血浆溶血磷脂类分子含量变化的研究以及微创血肿清除术的疗效

目的 观察脑出血患者血浆溶血磷脂类分子（LPA/AP）含量变化的特点以及微创血肿清除术联合镁制剂的影响，探索脑出血后病理生理学机制及有效的干预方法。方法 选取脑出血患者328例，测定其血浆溶血磷脂酸（LPA）及其相似磷脂（AP）的含量变化，并与359例脑梗死患者进行比较，年龄匹配的健康体检者作为对照组。同时观察微创血肿清除术及镁制剂对脑出血患者血浆LPA、AP含量及预后的影响。结果 发病24h脑梗死组血浆LPA的含量[（4.23±0.61）μmol/L]显著高于脑出血组[（2.66±0.44）μmol/L，P <0.01]及对照组[（2.54±0.39）μmol/L，P <0.01]。脑出血组血浆AP含量[（6.65±0.76）U]显著高于脑梗死组[（5.35±0.57）U，P <0.01]及对照组[（4.09±0.48）U，P <0.01]。发病1周、2周，脑出血组血浆AP含量仍高于脑梗死组和对照组（P <0.01）。微创钻颅血肿清除术及镁制剂治疗能够显著降低脑出血患者血浆AP含量（P <0.01），改善患者预后。结论 脑出血患者血浆AP含量显著升高，提示脑出血后2周内均存在膜损伤；微创钻颅血肿清除术联合镁制剂治疗能够有效降低血浆AP含量，改善患者预后，具有神经保护作用。     

阿托伐他汀对家兔动脉粥样硬化血管细胞粘附分子-1基因表达的影响

目的 探讨家兔动脉粥样硬化病变中血管细胞粘附分子-l（VCAM-1）的表达和阿托伐他汀的抗动脉粥样硬化作用。方法 24只大耳白兔随机分为常规饲料组、胆固醇饲料组和阿托伐他汀组，饲养l6周。实验前后检测（血清胆固醇TC）、甘油三酯（TG）、低密度脂蛋白（LDL），采用免疫组化和逆转录多聚酶链式反应（PCR）方法测定主动脉壁VCAM-1阳性表达百分比和mRNA的表达。结果 阿托伐他汀显著降低TC和LDL水平（P〈0．01）。胆固醇饲料组和阿托伐他汀组病变局部VCAM-1的阳性染色百分比和mRNA的表达量明显高于对照组（P〈0．01）,但阿托伐他汀组动脉粥样硬化病理改变较胆固醇饲料组明显减轻。VCAM-1阳性染色百分比及mRNA的表达量较胆固醇饲料组明显降低（P〈0．01）。结论 动脉粥样硬化的发生伴有血管细胞粘附分子的高度表达。阿托伐他汀不但有调脂作用，而且具有抑制粘附分子和抗动脉粥样硬化的作用。     

奥扎格雷钠联合阿司匹林对急性脑梗死患者血浆溶血磷脂酸和酸性磷脂水平的影响及意义

目的探讨奥扎格雷钠联合阿司匹林对急性脑梗死患者血浆溶血磷脂酸（LPA）和酸性磷脂（AP）水平的影响及临床疗效。方法将131例脑梗死患者随机分为奥扎格雷钠组（66例）和阿司匹林组（65例）,两组均给予拜阿司匹灵、丹参注射液治疗,奥扎格雷钠组加用奥扎格雷钠治疗1个疗程（15d）。分别于治疗前后测定患者血浆LPA和AP水平并与健康对照组比较。应用中国脑卒中量表（CSS）进行神经功能转归评价。结果急性脑梗死患者治疗前血浆LPA和AP水平显著高于健康对照组（P〈0.01）,治疗后奥扎格雷钠组与健康对照组比较差异无统计学意义,血浆LPA、AP水平及CSS评分均较阿司匹林组明显改善（分别为P〈0.05,P〈0.01）。结论奥扎格雷钠联合阿司匹林可显著降低急性脑梗死患者血浆LPA和AP水平,抑制血小板聚集,促进神经功能恢复。     

PAS三联疗法对脑梗死患者踝臂指数的影响及机制

目的 探讨普罗布考＋阿司匹林＋阿托伐他汀（PAS）三联疗法对急性脑梗死患者踝臂指数（ABI）的影响,评估其抗动脉硬化的作用.方法 选择大连市第五人民医院神经内科自2010年9月-2011年10月收治的96例急性脑梗死患者为研究对象,并分为阿托伐他汀＋阿司匹林（AS）组48例（阿司匹林100 mg/d、阿托伐他汀20 mg/d,口服）和PAS组48例（阿司匹林100 mg/d、阿托伐他汀20 mg/d、普罗布考0.25/次,2次/d,口服）,观察治疗前及治疗1年后ABI变化.结果 治疗1年后AS组和PAS组ABI值均有明显提高,差异均明显（P＜0.01）.治疗后PAS组ABI值较AS组升高（P＜0.05）.结论 PAS三联疗法具有更强的抗氧化降脂作用,改善动脉硬化.     

心房颤动患者体内溶血磷脂类分子含量与无症状性脑梗死的相关性

目的 观察非瓣膜性心房颤动(NVAF)患者中无症状性脑梗死(SBI)的发病率及其血浆溶血磷脂类分子(LPA/AP)含量的变化,探索房颤相关性脑卒中的病理生理学机制,为临床进行抗栓治疗提供依据.方法 选取经临床和辅助检查确诊的235例未接受抗栓治疗的NVAF患者、116例无NVAF的SBI患者及120名年龄大于60岁的健康体检者纳入本研究.测定其血浆溶血磷脂酸(LPA)及其极性相似总磷脂(AP)的含量变化.同时观察NVAF合并SBI时体内血小板的活化状态.结果 235例NVAF患者中,SBI的发生率为31.5%,其中年龄大于60岁的157例NVAF患者中,SBI的发生率为37.6%.NVAF合并SBI患者血浆LPA含量[(3.78±0.61)μmol/L]显著高于对照组[(2.66±0.49)μmol/L,95%CI 3.47～4.21,P=0.000]、NVAF无SBI组[(3.29±0.57)μmol/L,95%CI 3.01～3.76,P=0.008]及无NVAF的SBI组[(3.17±0.54)μmol/L,95% CI2.86～3.54,P=0.004].NVAF无SBI组及无NVAF的SBI组血浆LPA含量也显著高于对照组.NVAF合并SBI患者血浆AP含量显著高于对照组、NVAF无SBI组及无NVAF的SBI组.NVAF无SBI组及无NVAF的SBI组血浆AP含量也显著高于对照组.与对照组相比,年龄大于60岁的NVAF患者合并存在SBI的比率显著升高.NVAF患者合并存在SBI时体内血小板的活化程度显著升高.结论 NVAF是SBI的重要危险因素.NVAF患者合并存在SBI时体内血小板的活化程度升高.NVAF或NVAF合并SBI患者均存在缺血性膜损伤.对于NVAF或合并SBI患者在进行抗栓治疗时应充分考虑抗血小板治疗的重要性.LPA可作为一种理想的分子标记物用于判断NVAF或NVAF合并SBI患者体内血小板的活化状态.     

抗血小板药物对急性非心源性脑梗死患者血浆溶血磷脂酸的影响

目的 观察抗血小板药物阿司匹林和氯吡格雷对急性非心源性脑梗死患者血浆溶血磷脂酸（lysophosphatidic acid,LPA）水平的影响。方法 选取急性脑梗死患者180例,随机分为阿司匹林组和氯吡格雷组,阿司匹林组在常规治疗的基础上加用拜阿司匹林0.1g,每天一次,氯吡格雷组在常规治疗的基础上加用氯吡格雷75mg,每天一次。两组分别于治疗前和治疗后第12～14天测定血浆LPA。另设正常对照组50名,均为我院健康体检者。结果 脑梗死组LPA水平明显高于对照组（3.80±0.87μmol/L vs 2.85±0.65μmol/L,P <0.01）;与治疗前相比,阿司匹林组和氯吡格雷组治疗后LPA水平均明显降低（3.26±0.50μmol/L vs 3.79±0.83μmol/L,P <0.01;3.06±0.69μmol/L vs 3.82±0.90μmol/L,P <0.01）,但氯吡格雷组降低更明显（P <0.01）。结论 急性脑梗死患者血中LPA水平高于正常人;抗血小板药物阿司匹林、氯吡格雷均能显著降低急性脑梗死患者LPA,其中氯吡格雷较阿司匹林更明显。     

阿托伐他汀对自发性高血压大鼠动脉血压和血管内皮功能的影响

目的探讨阿托伐他汀对自发性高血压大鼠(SHR)动脉血压和血管内皮功能的影响。方法选用8周龄SHR12只,随机分为阿托伐他汀治疗组(ATV组,n=6)、蒸馏水组(DW组,n=6),另选6只WKY大鼠作为正常对照。ATV组大鼠给以阿托伐他汀50mg/(kg·d)加适量蒸馏水灌胃。DW组和WKY组每天同时用等量蒸馏水灌胃。观察给药前后大鼠尾动脉血压的变化,测定大鼠血清总胆固醇(TC)、甘油三酯(TG)和高密度脂蛋白胆固醇(HDL-C)浓度,观察血浆内皮素1(ET-1)水平、主动脉组织一氧化氮合酶(NOS)活性的变化特点。结果ATV组大鼠动脉血压显著低于DW组(P＜0．01)；与DW组和WKY组比较,ATV组血清TC、TG和HDL-C浓度显著降低(P＜0．01,P＜0．05)；DW组血清ET-1水平显著高于WKY组(P＜0．05),主动脉组织NOS活性显著低于WKY组(P＜0．05),经ATV治疗后血清ET-1水平明显降低(P＜0．05),而主动脉组织NOS活性显著增高(P＜0．01)。结论长期应用阿托伐他汀可以显著降低动脉血压。阿托伐他汀通过改善血管内皮功能延缓高血压的病理过程。     

阿托伐他汀治疗脑梗死患者颈动脉粥样硬化斑块的临床研究

目的观察阿托伐他汀对脑梗死患者颈动脉粥样硬化斑块的治疗作用。方法选择有颈动脉粥样硬化斑块的脑梗死患者82例，随机分为阿托伐他汀治疗组（42例）和对照组（40例）。分别于入院时、治疗第3个月、6个月、12个月动态监测2组患者的血脂水平，并进行颈动脉超声检查评估颈动脉粥样硬化斑块内膜-中层厚度（IMT）。结果2组间血脂变化无显著性差异（P〉0．05）；颈动脉斑块IMT在6个月后治疗组厚度缩小，对照组厚度增加，2组与初诊时比较差异有统计学意义（均P〈0．05）。结论阿托伐他汀除有良好的降脂作用外，还有稳定甚至减轻动脉粥样硬化的作用。     

阿托伐他汀对老年急性脑梗死患者治疗效果及影响

目的探究阿托伐他汀对老年急性脑梗死患者的治疗效果及影响。方法选取老年急性脑梗死(发病48h内)患者68例,男46例,女22例,平均年龄(61.0±7.5)岁。随机数字法均分为阿托伐他汀治疗组与对照组,对照组予硝苯地平缓释片、阿司匹林肠溶胶囊、甘露醇行降颅内压、抗凝治疗;治疗组在对照组基础上给予阿托伐他汀,观察2组治疗后的血清指标。结果治疗12周末,2组患者血浆hs-CRP及血清MMP-9水平较本组治疗前均显著下降,且组间比较,阿托伐他汀组比对照组下降更显著(P0.05);阿托伐他汀组较治疗前TC、TG、LDL-C、IMT有所下降,HDL-C升高(P0.05),与对照组治疗12周末组间比较,显著低于对照组,HDL-C显著高于对照组,P0.05;NIHSS评分阿托伐他汀组重型(17.11±3.01)、中型(7.13±2.48)、轻型(2.66±0.99)显著低于对照组,MBI评分(96.31±7.53)显著高于对照组(87.22±6.21);2组有不同程度的不良反应,如恶心、头晕、便秘等(对照组分别为1、1、3例,阿托伐他汀组分别为1、2、1例,P0.05),患者未停止给药或特殊治疗,不良症状耐受。结论在老年脑梗死患者治疗中,阿托伐他汀疗效明确、能降低血脂、抑制动脉粥样硬化、减轻机体炎症反应,改善血管内皮功能及改善患者脑梗死早期预后,能有效减轻神经功能损伤、且安全不良反应小,作为治疗老年急性脑梗死的核心药物值得基层医院、门诊推广应用。     

Influence of acetylsalicylate on plasma lysophosphatidic acid level in patients with ischemic cerebral vascular diseases

BACKGROUND AND PURPOSE: Lysophosphatidic acid (LPA) is released from activated platelets. Acetylsalicylate (aspirin) is the most commonly used antiplatelet drug. The purpose of this study is to observe whether treatment with acetylsalicylate decreases the LPA level in patients with ischemic cerebrovascular diseases. METHODS: We performed a study examining LPA level in fresh plasma in cases and controls enrolled in the LPA and Stroke Prevention Study. Level of LPA was assayed by measuring its inorganic phosphorus after separation by chromatography. RESULTS: An elevated LPA level was seen in cases (n = 254) with ischemic cerebrovascular disease (3.11+/- 1.55 micromol/l) compared with 136 healthy controls (1.77 +/- 1.04 micromol/l) (p < 0.001). Administration of aspirin (100 mg q.d.) for 1 month significantly lowered LPA level in patients (n = 142) (2.41 +/- 1.03 mu mol/l) compared with that before taking acetylsalicylate (4.06 +/- 1.03 micromol/l) (p < 0.001). However, the LPA level in patients (n = 36) who stopped acetylsalicylate after taking it for 1 month was re-elevated. Before and after taking acetylsalicylate for 1 month, their LPA levels were 4.23 +/- 1.15 and 1.93 +/- 0.85 micromol/l, respectively. After 1 month withdrawal, level was 3.90 +/- 1.09 micromol/l (p < 0.001 compared that before taking acetylsalicylate). CONCLUSION: Our findings support a close association between increased plasma LPA level and platelet activation. Acetylsalicylate could decrease plasma LPA levels, which may be used as a mechanism for acetylsalicylate in the prevention of ischemic stroke.     

通心络胶囊对急性脑梗死患者血浆溶血磷脂酸含量的影响

目的 探讨通心络胶囊对急性脑梗死患者血浆溶血磷脂酸(LPA)的影响及其治疗作用机制,分析达到预防脑梗死复发效果所需强化治疗的最短时间.方法 选取经临床和CT/MRI确诊的发病72 h内的急性脑梗死患者70例,采用随机数字表法分为治疗组和对照组.2组患者均给予常规治疗,包括阿司匹林片11服,每次100mg,每天1次.治疗组加用通心络胶囊口服,每次4粒,每天3次,连服60d.全部患者于发病72 h内及治疗30、60 d时测定血浆LPA含量.观察通心络胶囊对脑梗步匕患者血浆LPA含量变化的影响,并随访2个月内腩梗死的复发率.结果 2组患者治疗后较治疗前血浆LPA含量均明显降低,治疗组更为明显.治疗30 d时血浆LPA含量则已降至正常,与对照组比较,差异有统计学意义(P<0.05).治疗组治疗60 d内脑梗死复发率较对照组明显降低,差异有统汁学意义(P<0.05).结论 通心络胶囊可以显著降低脑梗死患者血浆LPA含量,与阿司匹林合用可能有较好的预防脑梗死复发的效果.建议急性脑梗死发病后的强化治疗时间不少于1个月.     

厄贝沙坦对急性脑梗死患者血浆溶血磷脂酸、内皮素-1和血清一氧化氮含量的影响

目的研究厄贝沙坦对急性脑梗死患者血浆溶血磷脂酸（LPA）、内皮素-1（ET-1）和血清一氧化氮（NO）含量的影响。方法将53例急性脑梗死患者随机分为厄贝沙坦治疗组（25例）和常规治疗组（28例）,并以23例非脑血管病患者和7名健康志愿者作为对照组。厄贝沙坦治疗组给予厄贝沙坦150mg＋阿司匹林100mg,常规治疗组给予阿司匹林100mg,每天1次,其余治疗方法相同,连续治疗14d。分别在治疗前后抽取静脉血检测LPA、ET-1和NO含量,并对两脑梗死组治疗前后进行神经功能缺损程度评分（NDS）。结果（1）脑梗死患者血LPA、ET-1含量较对照组显著升高（均P〈0.05）,NO含量显著降低（P〈0.05）;NDS与NO含量呈负相关（r=-0.4345,P〈0.05）。（2）厄贝沙坦治疗组和常规治疗组治疗后血LPA、ET-1含量和NDS较治疗前显著降低（均P〈0.05）,NO含量显著升高（均P〈0.05）。（3）治疗后厄贝沙坦治疗组与常规治疗组相比,血LPA、ET-1、NO含量改善更为明显（均P〈0.05）。结论厄贝沙坦能显著降低急性脑梗死患者血LPA、ET-1含量,提高血NO水平,显示其有抗血小板活化及内皮保护作用。     

阿托伐他汀钙对血脂水平正常的短暂性脑缺血发作患者的影响

目的观察阿托伐他汀钙合用阿司匹林治疗血脂水平正常短暂性脑缺血发作(transient ischemic attack,TIA)患者的疗效和安全性。方法 66例血脂水平正常的TIA患者随机分为治疗组(n=34)和对照组(n=32)组,治疗组口服阿托伐他汀钙20mg/d,阿司匹林100mg/d;对照组口服阿司匹林100mg/d。所有患者分别于入院后第1天及6个月检测血脂水平、谷草转氨酶、血清磷酸肌酸激酶,并行颈动脉超声检测内膜—中膜厚度,并观察2组6个月内TIA复发或进展为脑梗死的病例数。结果治疗6个月时与对照组相比甘油三脂、总胆固醇、低密度脂蛋白胆固醇水平、颈动脉内膜-中层厚度显著降低,高密度脂蛋白胆固醇则明显升高,脑血管疾病发生率明显降低,差异有统计学意义(P<0.05)。结论阿托伐他汀不仅有助于减少血脂水平正常的TIA患者脑血管疾病的发生,而且具有良好的安全性,同时还可以提高动脉粥样硬化斑块稳定性,具有抗粥样硬化作用。     

Effects of fixed low-dose warfarin, aspirin-warfarin combination therapy, and dose-adjusted warfarin on thrombogenesis in chronic atrial fibrillation

BACKGROUND AND PURPOSE: Recent clinical trials have established that adjusted-dose warfarin (international normalized ratio [INR] 2.0 to 3.0) is highly effective in the reduction of ischemic stroke in patients with nonvalvular atrial fibrillation (AF). We hypothesized that the introduction of fixed low-dose warfarin alone or in combination with aspirin (300 mg) could normalize hemostatic markers, namely plasma fibrin D-dimer (an index of thrombogenesis), plasminogen activator inhibitor-1 (PAI-1, an index of fibrinolysis), fibrinogen, and von Willebrand factor (vWf, an index of endothelial dysfunction), in a manner comparable to adjusted-dose warfarin (target INR 2.0 to 3.0). METJODS: Sixty-one patients with AF (44 men, mean+/-SD age 64+/-19 years) who were not receiving any antithrombotic therapy were prospectively randomized into 1 of 3 treatment groups: warfarin (2 mg) (n=23; group 1), combination 1 mg warfarin plus 300 mg aspirin (n=21; group 2) or combination 2 mg warfarin plus 300 mg aspirin (n=17; group 3). Subjects from all 3 AF groups were matched for sex, age, and blood pressure. Blood samples were taken for sequential measurements for changes in plasma fibrin D-dimer, PAI-1, fibrinogen, and vWf before and at 2 and 8 weeks after randomization (phase 1). All patients were subsequently offered adjusted-dose warfarin therapy (phase 2), and an additional blood sample was taken 6 weeks later. RESULTS: When pretreatment results were compared with those from 60 age- and sex-matched healthy control subjects in sinus rhythm, there were significant elevations in levels of fibrinogen (P=0.025), vWf (P<0.0001), and fibrin D-dimer (P<0.0001) in patients with AF compared with control subjects. There were no significant changes in the levels of various indices measured after 2 and 8 weeks of therapy in all 3 groups, except for an increase in PAI-1 level (P=0.024) in group 3. After 6 weeks of therapy with dose-adjusted warfarin (INR 2.0 to 3.0), there was a significant decrease in plasma fibrinogen (P=0.023) and fibrin D-dimer (P=0.0067) levels. There were no significant changes in the levels of PAI-1 (P=0.198) or vWf (P=0.33). CONCLUSIONS: The present results confirmed that high levels of vWf, fibrinogen, and fibrin D-dimer levels were present in patients with AF compared with control subjects. Moreover, the introduction of 300 mg aspirin plus low-dose warfarin (1 mg/d), low-dose warfarin alone (2 mg/d), or 300 mg aspirin plus low-dose warfarin (2 mg/d) did not significantly reduce any of the hemostatic markers studied (except PAI-1 levels), whereas conventional full-dose warfarin (INR 2.0 to 3.0) significantly reduced levels of fibrin D-dimer and fibrinogen. These results are in keeping with the disappointing ineffectiveness of low-intensity warfarin therapy, aspirin-warfarin combination, and ultralow-dose warfarin therapy in the recent prematurely terminated clinical trials and the established benefits of conventional adjusted-dose anticoagulation therapy.     

急性脑梗死患者血清HMGB1、OPG和MIF水平的变化及PAS三联疗法的干预作用

目的 探讨急性脑梗死患者血清高迁移率族蛋白BI( HMGB1)、骨保护素(OPG)及巨噬细胞移动抑制因子(MIF)水平的变化以及普罗布考、阿司匹林、他汀类药物(PAS)三联疗法对其干预作用.方法 选择150例急性脑梗死患者,根据颈动脉超声检查结果分为颈动脉稳定斑块组(50例)和颈动脉易损斑块组(100例).将稳定斑块组作为对照组,易损斑块组抽血检查后按随机数字法分为AS组50例(阿司匹林100 mg/d,阿托伐他汀20 mg/d,口服)和PAS组50例(阿司匹林100 mg/d,阿托伐他汀20 mg/d,普罗布考0.25/次,2次／d,口服).比较治疗前和治疗后4周血清HMGB1、OPG和MIF水平.结果 治疗前,易损斑块组中两亚组血清HMGB1、OPG和MIF含量均明显高于稳定斑块组,差异有显著统计学意义(均P＜0.01);两亚组中血清HMGB1、OPG和MIF含量差异无统计学意义(均P＞0.05).治疗后4周,PAS组中血清HMGB1,OPG和MIF含量均明显低于AS组,且各指标下降幅度均高于AS组,差异有显著统计学意义(均P＜0.01).结论 血清HMGB1、OPG和MIF均参与脑梗死患者动脉粥样硬化的进程,可作为评估颈动脉粥样硬化斑块不稳定性的预测因子,PAS三联疗法可有效降低其血清浓度,具有更强的抗炎作用,可提高易损斑块的稳定性.     

水蛭素合用阿司匹林与单用阿司匹林或氯吡格雷治疗短暂性脑缺血发作的随机对照研究

目的：探讨水蛭素合用阿司匹林治疗短暂性脑缺血发作（TIA）的疗效和安全性。方法：89例TIA患者随机分为3组：（1）氯吡格雷组（n=29），口服氯吡格雷75mg／d：（2）阿司匹林组（n=30），口服阿司匹林100mg／d；（3）水蛭素合用阿司匹林组（n=30），口服水蛭素0．32g，3次／d，阿司匹林100mg／d。观察治疗后90d内TIA复发或进展为脑梗死的病例数，观察出血等不良事件发生率。结果：治疗后90d内总的脑梗死发生率为4．5％，3组之间无显著差异。水蛭素合用阿司匹林组和氯吡格雷组90d内的TIA复发风险分别较单用阿司匹林降低69％（P=0．0078）和65％（P=0．0170）。总的出血发生率为2．25％，均发生在水蛭素合用阿司匹林组。结论：水蛭素合用阿司匹林可降低90d内TIA复发率的效果优于单用阿司匹林，与单用氯吡格雷相似，但出血风险增高。     

Comparative studies on the effects of different doses of atorvastatin combined with aspirin on inflammatory cytokines and carotid plaques in patients with ischemic cerebrovascular disease

Abstract

Objective: To make comparative studies on the effects of different doses of atorvastatin combined with aspirin on inflammatory cytokines, blood lipids, blood glucose, other biochemical indexes and carotid plaques in patients with ischemic cerebrovascular disease (ICVD) and carotid plaques.

Method: One hundred and twenty patients with ICVD and carotid plaques admitted by Renmin Hospital, Hubei University of Medicine Hospital from December 2016 to December 2017 were selected and randomly divided into experimental group and control group, 60 cases in each group. Patients in the control group was asked to orally take standard dose of atorvastatin (20?mg/d) combined with aspirin enteric-coated tablets (100?mg/d). Patients in the experimental group was asked to orally take high-dose atorvastatin (40?mg/d) combined with the same amount of aspirin enteric-coated tablets. Patients in two groups were treated for 6?months averagely. The levels of inflammatory factors, changes in blood biochemical parameters and carotid plaque degrees of patients in two groups before and after treatment were inspected and compared.

Results: The levels of serum high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF-a), interleukin-6 (IL-6) and homocysteine (Hcy) in patients of the experimental group after treatment were higher than those in the control group, difference with statistical significance (p?<?.05). The total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) in patients of the experimental group after treatment were lower than those in the control group and before treatment. The high-density lipoprotein cholesterol (HDL-C) was higher than that of the control group and before treatment, the levels of fasting blood glucose (FBS) and glycosylated hemoglobin (HbAIc) in patients of the experimental group significantly increased compared to those before treatment, difference with statistical significance (p?<?.05). There was no significant change in the control group. The carotid intima-media thickness (IMT) and plaque area in patients of the experimental group were lower than those in the control group and before treatment, difference with statistical significance (p?<?.05).

Conclusion: High-dose atorvastatin combined with aspirin for treatment of patients with ICVD can effectively reduce inflammatory inflammatory cytokine levels in serum and reduce IMT and carotid plaque area. With more obvious effect than lower dose of atorvastatin combined with aspirin, it is easy to cause blood glucose abnormality. So, it is necessary to pay attention to monitoring blood sugar during medication period.     

氯吡格雷对急性脑梗死患者血浆溶血磷脂酸水平的影响

目的研究急性脑梗死患者血浆溶血磷脂酸(Lysophosphatidic acid,LPA)水平的变化及氯吡格雷对急性脑梗死患者血浆溶血磷脂酸水平的影响,探求急性脑梗死有效的干预方法。方法所有脑梗死患者随机分为氯吡格雷组及实验对照组,氯吡格雷组除给予脑梗死常规治疗外,加用氯吡格雷75mgqdpo,实验对照组只给予常规治疗。对急性脑梗死患者分别在治疗前、治疗3d及21d后进行血浆LPA水平的检测。结果氯吡格雷组治疗前及治疗21d后血浆LPA水平为:(4.82±1.10)和(2.23±0.96)μmol/L,两者相比有显著性差异(P<0.01);实验组治疗前及治疗21d后血浆LPA水平为(4.79±1.24)和(3.26±1.20)μmol/L,2者相比差异有显著性(P<0.01),两组治疗21d后血浆LPA水平相比差异有显著性(P<0.01)。皮层支氯吡格雷组治疗前及治疗21d后血浆LPA水平为:(5.59±1.08)和(2.62±1.03)μmol/L,2者相比差异有显著性(P<0.01);皮层支实验对照组治疗前及治疗21d后血浆LPA水平为:(5.55±0.96)和(4.01±0.75)μmol/L,2者相比差异有显著性(P<0.01),两组治疗21d后血浆LPA水平相比差异有显著性(P<0.01)。深穿支氯吡格雷组治疗前及治疗3d后血浆LPA水平为:(3.98±1.02)和(2.77±0.98)μmol/L,2者相比差异有显著性(P<0.01);深穿支实验对照组治疗前及治疗3d后血浆LPA水平分别为:(3.95±1.17)和(3.83±1.56)μmol/L,2者相比差异无显著性(P>0.01),两组治疗3d后血浆LPA水平相比差异有显著性(P<0.01)。结论氯吡格雷可降低急性脑梗死患者血浆LPA水平,对皮层支及深穿支梗死均有效,深穿支效果更佳。