缺血性脑卒中患者CYP2C19基因多态性与个体化用药的相关性

目的:探讨根据CYP2C19代谢分型进行的个体化用药调整对于氯吡格雷治疗缺血性脑卒中的指导作用,为临床个体化用药提供参考。方法:纳入80例脑梗死患者,根据是否行CYP2C19基因检测分为经基因检测的个体化用药指导组40例和非基因检测的对照组40例。个体化用药指导组根据CYP2C19代谢分为:慢代谢型、中间代谢型、快代谢型及超快代谢型。快代谢型及超快代谢型按照常规使用氯吡格雷75 mg,每天1次。中间代谢型采用双倍氯吡格雷剂量150 mg,每天1次。慢代谢型患者氯吡格雷更换为替格瑞洛90 mg,每天2次或停用氯吡格雷,改用阿司匹林肠溶片100 mg每天1次;对照组按照常规使用氯吡格雷75 mg,每天1次。对所有入组患者出院后进行为期3个月的门诊或电话随访。比较两组血管事件发生率和改良Rankin量表(mRS)(0-1)发生率。结果:个体化用药指导组血管事件发生率明显低于对照组,mRS评分(0-1)发生率明显高于对照组,差异均有统计学意义(P<0.05)。结论:经CYP2C19基因检测对缺血性脑卒中患者进行的个体化用药,能显著降低血管不良事件发生率,同时对于患者预后生活能力改善也有显著提高。     

缺血性脑卒中患者CYP2C19基因代谢型、联用药物与氯吡格雷抵抗关系的研究

目的 探讨CYP2C19基因代谢型、联用药物与氯吡格雷抵抗的关系.方法 选择缺血性脑卒中患者102例,连续口服氯吡格雷75 mg/d,共7d.检测患者CYP2C19各基因型及血小板聚集率,以1年内发生缺血性脑卒中复发终点事件为观察指标.结果 CYP2C19基因弱代谢型15例,中间代谢型39例,强代谢型48例,氯吡格雷抵抗发生率在弱代谢型较中间代谢型高,中间代谢型较强代谢型发生率高,差异均有统计学意义(P＜0.05);氯吡格雷联用阿司匹林、他汀类药可明显减少卒中复发事件(P＜0.05).结论 采用基因分型法可预测缺血性脑卒中患者氯吡格雷疗效,指导临床个体化给药.氯吡格雷联用阿司匹林、他汀类药的应用效果较好.     

替格瑞洛与氯吡格雷在CYP2C19等位基因功能缺失患者中的抗血小板疗效比较

目的比较替格瑞洛与氯吡格雷在细胞色素P450 C19(CYP2C19)等位基因功能缺失的行冠状动脉介入治疗(PCI)的急性冠状动脉综合征(ACS)患者中应用的抗血小板疗效。方法选取行PCI的ACS患者,筛选CYP2C19等位基因功能缺失患者,包括*2/*2、*2/*3以及*3/*3。共入选患者52例,随机分为两组,每组26例。替格瑞洛组于PCI术前给予替格瑞洛180 mg负荷量后90 mg,po,bid;氯吡格雷组术前给予氯吡格雷300 mg负荷量后75 mg,po,qd。若是急诊PCI手术,替格瑞洛组于术前给予替格瑞洛180 mg负荷量后90 mg,po,bid;氯吡格雷组术前给予氯吡格雷600 mg负荷量后75 mg,po,qd维持。观察患者术后1年的主要心脑血管不良事件(MACCE)、出血情况及其他药物不良反应。结果两组患者基线资料无显著差异(P>0.05),应用血管紧张素转换酶抑制药/血管紧张素受体拮抗药、肾上腺素β受体阻滞药比例无显著差异(P>0.05)。术后1年,替格瑞洛组MACCE发生率为8%(2/26),低于氯吡格雷组(31%,8/26,P<0.05)。两组出血事件发生率分别为12%和8%,组间差异无显著意义(P>0.05)。结论 CYP2C19等位基因功能缺失患者给予替格瑞洛治疗可改善临床预后,基于CYP2C19基因型的个体化方案可考虑在行PCI术的ACS患者中实施。     

CYP2C19基因多态性指导下的抗血小板个体化治疗急性脑梗死的临床观察

目的 探讨CYP2C19基因多态性指导下的抗血小板个体化治疗对急性脑梗死病人疗效的影响.方法 前瞻性纳入非心源性急性脑梗死的病人100例,根据CYP2C19基因多态性分为常规治疗组、慢代谢个体化治疗组和慢代谢常规治疗组,常规治疗组和慢代谢常规治疗组给予阿司匹林+氯吡格雷治疗,慢代谢个体化治疗组给予阿司匹林+氯吡格雷+西洛他唑治疗.三组病人疗程均为15 d,比较各组病人疗效、美国国立卫生院卒中量表(NIHSS)评分及主要出血事件的发生率.结果 各组病人性别、年龄、原发性高血压、糖尿病、高脂血症等方面,均差异无统计学意义(P>0.05);常规治疗组与慢代谢个体化治疗组的有效率分别为84.00%和76.67%,差异无统计学意义(P>0.05),两组的出血事件及其他不良反应均差异无统计学意义(P>0.05);慢代谢常规治疗组对血小板的抑制率低于慢代谢个体化治疗组,差异有统计学意义(P<0.05).结论 联合使用西洛他唑可以克服氯吡格雷抵抗,根据基因指导抗血小板治疗急性脑梗死的疗效良好.     

氯吡格雷对冠心病患者PCI术后CYP2C19、PON1 基因多态性与FIB、D-二聚体水平的相关性研究

目的：分析冠心病患者经皮冠状动脉介入治疗(PCI)术后,规律服用氯吡格雷治疗时CYP2C19、PON1基因多态性与血浆纤维蛋白原（FIB）、D-二聚体水平的相关性研究。方法：选取在某三甲医院确诊为冠心病且行PCI术的患者217例,对217例患者行CYP2C19*2、CYP2C19*3、CYP2C19*17、PON1基因监测,观察患者在规律服用氯吡格雷治疗（75 mg·d-1）1个月以上的血浆FIB、D-二聚体指标。结果：在217名患者中CYP2C19* 17基因未检测出突变型等位基因,因此对超快代谢型基因不做统计分析。CYP2C19基因的快代谢型、中间代谢型、慢代谢型之间的FIB指标对比均无统计学差异（P>0.05）;快代谢型与中间代谢型、快代谢性与慢代谢型之间的D-二聚体指标均无统计学差异（P>0.05）;中间代谢型与慢代谢型之间D-二聚体指标有统计学差异（P<0.05）。PON1基因GG型与GA型、GG型与AA型、GA型与AA型的FIB和D-二聚体指标水平均无统计学差异（P>0.05）。结论：携带CYP2C19慢代谢基因型的患者使用常规氯吡格雷剂量治疗,增加血栓风险,可考虑适当增加氯吡格雷服药剂量或改服替格瑞洛进行溶栓治疗。PON1基因多态性与氯吡格雷治疗血小板反应性差异并无关联性。     

CYP2C19和ABCB1基因检测指导患者氯吡格雷个体化给药

目的利用CYP2C19和ABCB1基因检测结果指导患者氯吡格雷个体化用药。方法选取某院2018年8月~2019年6月30例使用氯吡格雷的患者,采用荧光原位杂交法检测患者氯吡格雷相关基因(CYP2C19*17、CYP2C19*3、CYP2C19*2和ABCB1)的基因型,根据检测结果为患者提供给药建议。另选取1例冠状动脉粥样硬化心脏病PCI术后患者,测定氯吡格雷相关基因型,为患者提供个体化给药建议。结果CYP2C19基因检测结果显示,30例患者中1例为超快代谢型,8例为快代谢型,18例为中间代谢型,3例为慢代谢型;ABCB1 CC野生型13例,CT突变杂合型14例,TT突变纯合型3例。1例冠状动脉粥样硬化心脏病患者PCI术后规律双联抗血小板治疗仍反复胸闷胸痛,CYP2C19基因检测为CYP2C19*1/*2中间代谢型,无ABCB1突变,药物代谢减慢,建议氯吡格雷更换为替格瑞洛。结论通过基因检测指导患者氯吡格雷个体化给药,促进临床合理用药。     

CYP2C19基因多态性及患者主要临床资料与氯吡格雷药物抵抗的相关性研究

目的观察药物代谢酶系统中CYP2C19基因多态性及患者主要临床资料与服用氯吡格雷前后血小板聚集率变化(氯吡格雷药物抵抗)的相关性。方法入选拟行冠脉造影检查或支架植入治疗患者35例,根据围手术期应用氯吡格雷前后血小板聚集率变化,将患者分为氯吡格雷抵抗组和非抵抗组。检测CYP2C19基因型,并记录患者年龄、性别、烟酒史、高血压、糖尿病等主要临床资料,分析基因水平及临床水平各因素对血小板聚集及氯吡格雷药物抵抗的影响。结果检测出氯吡格雷抵抗的患者15例,CYP2C19慢代谢基因型患者4例,Logistic回归分析显示,CYP2C19基因型是氯吡格雷抵抗的危险因素(OR=1.236,95%CI:0.273~5.599,P=0.049)。结论 CYP2C19基因型在基因水平与氯吡格雷抵抗相关,临床水平资料未见明显相关性。     

CYP2C19基因多态性与氯吡格雷ADP抑制率的临床研究

目的探讨CYP2C19基因多态性与氯吡格雷ADP抑制率间的临床关系,以期为个体化的抗血小板治疗方案提供用药参考。方法选取本院2014年10月至2015年10月收治的120例急性冠状动脉综合征患者作为临床研究对象,患者术前均进行CYP2C19基因型测定并完成经皮冠状动脉介入术治疗,患者按基因型分为慢代谢组、中等代谢组及快代谢组,每组40例。入院当天给予患者过量氯吡格雷和标准剂量阿司匹林,之后按规律常规给予氯吡格雷75 mg/d,于第1天和第7天测定患者ADP抑制率,并根据结果筛选出抗氯吡格雷患者,加大氯吡格雷用量后7 d再次测定患者ADP抑制率,并进行前后差异比对。结果与服用前相比,服用氯吡格雷7 d后3组患者的血小板聚集率均明显下降,其中快代谢型患者显著优于中间代谢型和慢代谢型者(P<0.05)。氯吡格雷抵抗患者增加药物剂量后7 d,ADP抑制率无明显改变,差异无显著性(P>0.05)。结论针对急性冠状动脉综合征患者,采用适时的CYP2C19基因多态性检测对于指导选用药物治疗具有一定临床意义,但仅通过基因分型还无法完全预测氯吡格雷的给药剂量,对于氯吡格雷抵抗患者单纯增加氯吡格雷剂量不能同时达到提高血小板抑制率的效果,治疗方案还需进一步探讨和深入研究。     

CYP2C19代谢型对ACS患者PCI术后氯吡格雷临床应用的疗效分析

目的：本研究通过回顾性分析ACS患者CYP2C19酶代谢型对抗血小板聚集药物药效的影响,以期为患者制订PCI术后个体化抗血小板聚集治疗方案提供依据。方法：选择经冠脉造影确诊为急性冠脉综合症、已行PCI术,同时进行了CYP2C19基因多态性检测的患者130例。根据代谢类型不同,将患者分成快、中、慢代谢3组,分析3组患者氯吡格雷及替格瑞洛两种抗血小板药物的使用情况、心血管不良事件发生率、出血不良反应以及院外用药情况。结果：①CYP2C19基因检测快代谢型46例,中代谢型62例,慢代谢型22例;②在不同代谢型患者中,慢代谢组氯吡格雷的使用率显著低于快代谢组和中代谢组,而替格瑞洛的使用率显著高于快代谢组和中代谢组;③在慢代谢组中,使用氯吡格雷的患者心血管缺血事件发生率显著高于替格瑞洛,慢代谢组使用氯吡格雷患者心血管缺血事件发生率显著高于快代谢组和中代谢组;④出血不良反应在3组间比较无明显差异;⑤快代谢组质子泵抑制剂的使用率显著高于中、慢代谢组,其余合并用药的使用率在3组间无明显差异。结论：在临床治疗中,检测CYP2C19代谢类型将有助于减少心血管不良事件的发生,使患者获得更大益处。     

高维持剂量氯吡格雷对急性心肌梗死患者急诊经皮冠状动脉介入术后血小板聚集率及超敏C反应蛋白的影响

目的 探讨高维持剂量氯吡格雷对急性心肌梗死患者急诊经皮冠状动脉介入术(PCI)后血小板聚集率和炎性反应的影响.方法 选取符合标准的76例诊断为急性ST段抬高型心肌梗死(STEMI)的急诊患者,且所有患者均予以氯吡格雷600 mg以及阿司匹林300 mg顿服,后予以行PCI术,并采用随机数字表法分为观察组(高维持剂量组)38例和对照组(常规剂量组)38例,观察组予以氯吡格雷150mg·d-1 ×7d,后改为75 mg·d-1,对照量组予以75 mg·d-1维持治疗,术前及术后7d分别测1次血小板聚集率和超敏C反应蛋白(hs-CRP),并进行比较.结果 两组7d后的血小板聚集率、hs-CRP较前均明显降低,且观察组的血小板聚集率、hs-CRP降低更为明显,差异有统计学意义(P＜0.05).结论 STEMI患者急诊PCI术后予以高维持剂量的氯吡格雷可更进一步降低血小板聚集率以及炎性反应.     

回顾性分析氯吡格雷弱代谢患者的抗血小板治疗现状

目的筛查氯吡格雷弱代谢型急性冠脉综合征患者,回顾性分析其抗血小板治疗现状。方法选取医院收治的285例陕西汉族急性冠脉综合征患者,通过焦磷酸测序技术检测CYP2C19*2和CYP2C19*3基因多态性筛查氯吡格雷弱代谢患者,分析其抗血小板治疗现状。结果在285例患者中,快代谢型占38.6%,中间代谢型占49.1%,慢代谢型占12.3%,后两者为弱代谢型(61.4%)。中间代谢型患者,53.6%应用氯吡格雷75mg·d~(-1);46.4%调整治疗方案,如氯吡格雷剂量加倍至150mg·d~(-1),更换替格瑞洛或三联疗法(加用西洛他唑)。慢代谢型患者,54.3%应用氯吡格雷75mg·d~(-1),45.7%调整为上述治疗方案,其中28.5%更换替格瑞洛。结论在陕西汉族急性冠脉综合征患者中,氯吡格雷弱代谢型发生率高,目前个体化抗血小板治疗方案并无统一规范。     

负荷剂量氯吡格雷治疗短暂性脑缺血发作的疗效观察

目的:观察负荷剂量氯吡格雷治疗短暂性脑缺血发作(TIA)的疗效及安全性。方法:108例TIA患者,随机分为负荷剂量组和常规剂量组。负荷剂量组58例,在常规治疗的基础上给予首剂氯吡格雷300mg,24h后维持75mg.d-1治疗;常规剂量组50例,在常规治疗的基础上给予氯吡格雷75mg.d-1,2组均用药14d。观察服药前、服药后2、5、10h2组患者血小板聚集率及服药后2组的疗效及安全性。结果:负荷剂量组的疗效显著优于常规剂量组,2组比较差异有统计学意义(P<0.05);2组用药后血小板聚集率均显著低于治疗前(P<0.05),且负荷剂量组显著低于同期常规剂量组(P<0.05)。治疗过程中未见有危及生命的出血现象。结论:2组患者在常规治疗的基础上加用氯吡格雷均可使患者TIA得到不同程度的控制,但采用负荷剂量氯吡格雷治疗可取得更好效果。     

替格瑞洛对急性冠脉综合征经皮冠状动脉介入治疗围术期血小板聚集率的影响

目的 探讨替格瑞洛对急性冠脉综合征(ACS)经皮冠状动脉介入治疗(PCI)围术期血小板聚集率(MPAR)的影响.方法 80例确诊为ACS行PCI术患者为研究对象,术前采用随机数字表法分为替格瑞洛治疗组(观察组)和氯吡格雷治疗组(对照组),每组40例.所有研究对象入院前已连续服用氯吡格雷(泰嘉) 75 mg·d-1持续7 d以上者维持原剂量,未曾服用过氯吡格雷者予以300 mg负荷剂量后75 mg·d-1维持.观察组入院前已连续服用替格瑞洛每次90 mg,2次/天,持续7 d以上者维持原剂量,未曾服用过替格瑞洛者予以180 mg负荷剂量后改标准剂量替格瑞洛(每次90 mg,2次/天)治疗.分别于治疗前、术后5 d抽取空腹外周血标本进行MPAR的测定.结果 治疗前观察组和对照组患者MPAR比较,差异无统计学意义 (P>0.05);术后5 d外周血MPAR均明显低于治疗前(P<0.05);观察组MPAR明显低于对照组(P<0.05).结论 替格瑞洛较氯吡格雷能更好地抑制ACS血管病变患者PCI围术期MPAR,降低早中期不良心血管事件的发生率,对重度冠状动脉血管病变的患者具有更好抗血小板聚集的治疗效果.     

Genetic polymorphisms of CYP2C19 influences the response to clopidogrel in ischemic heart disease patients in the South Indian Tamilian population

Background

The antiplatelet activity of clopidogrel is variable among patients suffering from ischemic heart disease. Variation in the cytochrome P450 2C19 (CYP2C19) gene coding for the CYP2C19 enzyme is one of the major determinants of this variable response to clopidogrel. The activity of the CYP2C19 enzyme, which plays a role in the conversion of the prodrug clopidogrel to its active metabolite, is genetically influenced by polymorphisms in its gene. The aim of our study was to evaluate the association of CYP2C19 polymorphisms and the antiplatelet effect of clopidogrel in the South Indian Tamilian population.

Materials and methods

Genotyping and platelet aggregation results of 149 ischemic heart disease patients on clopidogrel maintenance therapy (75 mg daily dose) were analyzed in this study. CYP2C19 polymorphisms were genotyped by the PCR-restriction fragment length polymorphism method. We measured residual platelet activities in these patients on clopidogrel therapy in terms of impedance (expressed as ohms). The study subjects were divided into two metabolizer phenotype groups [group 1: poor/intermediate metabolizers (PM/IM); group 2: extensive/ultra-rapid metabolizers (EM/URM)] based on CYP2C19 genotype, and the residual platelet activities were compared. Higher values of impedance denote increased residual platelet activity.

Results

Poor/intermediate metabolizers had significantly higher impedance values than EM/URM [(median; range) 4.0; 0–13 vs. 2.0; 0–11, respectively; p?=?0.04]. These higher impedance values denote higher residual platelet activities among the carriers of loss-of-function alleles (CYP2C19*2,*3) than among non-carriers. However, residual platelet activities were lower among the carriers of the gain-of-function allele (CYP2C19*17) than among non-carriers, although this difference was not significant.

Conclusion

Patients with CYP2C19 (*2 or *3) genetic polymorphisms had higher residual platelet activities and were associated with a reduced antiplatelet response to clopidogrel. As the South Indian Tamilian population is characterized with higher frequencies of these genetic polymorphisms, our findings mandate further studies aimed at initiating genome-based personalized antiplatelet therapy.     

Impact of CYP3A5 polymorphism on platelet reactivity at percutaneous coronary intervention and after 9 months of aspirin and clopidogrel therapy in Japanese patients with coronary artery disease

Background

High residual platelet reactivity in patients receiving clopidogrel is associated with an increased risk of a cardiovascular event after coronary stenting. The aim of our study was to evaluate the impact of the cytochrome P450 (CYP) 3A5 and CYP2C19 polymorphisms on platelet reactivity during dual antiplatelet therapy.

Methods

We determined the CYP2C19 and CYP3A5 genotypes of 101 angina patients (65 male patients, mean age 64 years) receiving dual antiplatelet therapy with aspirin and clopidogrel and evaluated the effect of these polymorphism on platelet reactivity at the early and late phases of treatment using a conventional light transmission aggregometry. Early and late phases were defined as 24 h after the loading dose and after 9 months on a maintenance dose of 75 mg daily, respectively.

Results

The distribution of the CYP2C19 genotype was 30 % in extensive metabolizers (EM; CYP2C19*1/*1), 46 % in intermediate metabolizers (IM; *1/*2, *1/*3), and 25 % in poor metabolizers (PM; *2/*2, *2/*3, *3/*3). Platelet reactivity levels in during the early and late phases were 3,793?±?1,476 and 2,960?±?1,410, respectively, in EM, 4,706?±?1,417 and 3,239?±?1,479, respectively, in IM, and 5,402?±?776 and 4,736?±?1,356 aggregation units (AU)?min, respectively in EM. The distribution of the CYP3A5 genotype was 33 % in patients carrying the wild-type or one loss-of-function allele (Expressor phenotype; *1/*1 and *1/*3, respectively) and 67 % in those carrying two loss-of-function alleles (Non-expressor; *3/*3). In total, eight patients were EM+Expressor, 22 were EM+Non-expressor, 18 were IM+Expressor, 28 were IM+Non-expressor, eight were PM+Expressor, and 17 were PM+Non-expressor. In the late phase of PM with the CYP2C19 polymorphism, the levels of platelet reactivity according to CYP3A5 genotype were 3,963?±?1,436 and 5,100?±?1,190 AU?min in Expressor and Non-expressor, respectively (P?<?0.05), however, there was no difference in platelet reactivity between Expressor and Non-expressor in EM and IM.

Conclusions

Our results suggest that antiplatelet response to clopidogrel in the late phase depends on the CYP3A5 polymorphism in PM with CYP2C19.     

Non‐antiplatelet effect of clopidogrel: improving endothelial function in Chinese healthy subjects with different CYP2C19 genotype

Clopidogrel has been shown to improve endothelial function in vitro and in patients with coronary artery disease. However, it remains unclear whether such an effect of clopidogrel is associated with CYP2C19 polymorphisms that determine the antiplatelet effect of clopidogrel. After genotyping, 12 healthy participants were enrolled in the study. Among them, six participants were CYP2C19*1/*1 (extensive metabolizers; EM) and the other six participants were CYP2C19*2/*2 or *3 (poor metabolizers; PM). All participants received 300 mg clopidogel orally. Endothelial function was assessed by measurement of flow‐mediated dilation of the brachial artery, and adenosine diphosphate‐induced platelet aggregation was determined by using optical aggregometry at 0, 4 and 24 h after administration of 300 mg clopidogrel. Flow‐mediated dilation was significantly higher at 4 and 24 h after a loading‐dose administration of clopidogrel in both the CYP2C19 EM and PM groups, but showed no significant difference between the two groups. Adenosine diphosphate‐induced platelet aggregation was significantly inhibited at 4 and 24 h after administration of clopidogrel in the CYP2C19 EM group. However, there was no statistical correlation between the change in flow‐mediated dilation and adenosine diphosphate‐induced platelet aggregation in the two CYP2C19 groups. This is the first study to report that clopidogrel improves endothelial function in healthy Chinese subjects, which is unrelated with the CYP2C19 genotype and independent of antiplatelet action.     

高龄急性冠脉综合征患者双联抗血小板治疗的疗效及安全性探讨

目前,双联抗血小板治疗(dual antiplatelet therapy,DAPT)仍然是急性冠脉综合征(ACS)的一线治疗方法。强化抗血小板治疗带来心血管获益的同时,由此引起的出血风险的增加也值得关注。文中通过回顾近些年来国内外几项大型临床试验,综述得出:高龄ACS患者给予DAPT有效且相对安全;对于有出血危险因素及需要长期应用阿司匹林(尤其是接受DAPT)者,可选择较低剂量阿司匹林(75～81 mg.d-1);年龄>75岁者,不推荐给予氯吡格雷负荷剂量(300 mg);服用阿司匹林和(或)氯吡格雷时,不推荐常规应用质子泵抑制剂预防胃肠道不良反应。     

CYP2C19、P2Y12基因多态性与缺血性脑卒中患者氯吡格雷抵抗的相关性研究

目的：考察CYP2C19、P2Y12受体的基因多态性与氯吡格雷抵抗的相关性研究.方法：96例中国缺血性脑卒中患者持续服用氯吡格雷75 mg,收集全血提取DNA,采用Sequenom MassARRAY iPLEX（R）基因型分析技术进行CYP2C19＊ 2（681G＞A,rs4244285）、CYP2C19＊3（636 G＞A,rs4986893）及P2Y12受体（52G＞T,rs6809699） （744T＞C,rs2046934）4个SNPs的基因型分析.采用二磷酸腺苷（ADP）诱导光比浊法测定血小板聚集功能.采用Chi-square检验或Fisher确切概率法分析相关性.结果：患者分为氯吡格雷抵抗（CR）组与非抵抗组,CYP2C19＊ 2（rs4244285）及P2Y12受体（rs2046934）基因型分布在两组间的差异有统计学意义（P=0.027,P=0.034）.其中,CYP2C19＊2 GA＋ AA基因型为CR发生的风险因素（OR=2.607,95％CI：1.062～6.399）.CYP2C19＊3（rs4986893）及P2Y12受体（rs6809699）基因型分布在两组比较中差异无统计学意义（P＞0.05）.结论：在中国缺血性脑卒中患者中,CYP2C19＊2（rs4244285） GA＋ AA型与氯吡格雷抵抗的发生密切相关,该基因型检测将有助于指导氯吡格雷的临床合理应用.