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中国临床药理学与治疗学 ›› 2007, Vol. 12 ›› Issue (12): 1436-1440.

• 药物治疗学 • 上一篇    

冠心病患者生化阿司匹林抵抗的临床研究

张建华1, 叶玲丽2, 赵玮1, 陈晓曙1, 陈达开3   

  1. 1温州市第二人民医院心内科, 2检验科,温州 325000,浙江;
    3温州医学院附属第一医院心内科,温州 325000,浙江
  • 收稿日期:2007-10-13 修回日期:2007-12-15 发布日期:2020-11-10
  • 通讯作者: 陈达开,男、硕士研究生,副主任医师,研究方向:心内科临床。Tel:13587672082 E-mail:zjcdk006@sina.com
  • 作者简介:张建华,男,本科,副主任医师,研究方向:心内科临床。Tel:13706672557 E-mail:zjhbetty@126.com

Clinical research on biochemical aspirin resistance in coronary heart dis-ease patients

ZHANG Jian-hua1, YE Lin-li2, ZHAO Wei1, CHEN Xiao-shu1, CHEN Da-kai3   

  1. 1Deparment of Cardiovasology, 2Deparment of Laboratory, Third Hospital of Wenzhou 32500, Zhejiang, China;
    3Deparment of Cardiovasology First Affiliated Hospital of Wenzhou Medical College, Wenzhou 32500, Zhejiang, China
  • Received:2007-10-13 Revised:2007-12-15 Published:2020-11-10

摘要: 目的: 初步探讨冠心病(CHD)患者生化阿司匹林抵抗情况及其防治措施。方法: 经冠脉造影确诊的156例CHD患者和22例正常对照者服用阿司匹林100 mg/d(≥7 d)后,查花生四烯酸(AA)二磷酸腺苷(ADP)诱导的血小板聚集率(PAG)和血浆血栓素B2(TXB2)浓度。抽血后CHD患者加用氯吡格雷75mg/d,1周后复查PAG和TXB。AA诱导的平均PAG≥20%,同时ADP诱导的平均PAG≥70%者为阿司匹林抵抗(AR);仅符合其中一项为阿司匹林半抵抗(ASR);均不符合者为阿司匹林敏感(AS)。结果: 加用氯吡格雷前,CHD组AA诱导的PAG、AR发生率明显高于对照组(P < 0.01);CHD组AR或ASR患者ADP诱导的PAC、lg(AA诱导的PAG)、lg(TXB2浓度)显著高于AS患者(P < 0.05);CHD患者血浆TXB,浓度与ADP诱导的PAG呈正相关(r=0.497, P < 0.01),与 AA诱导的PAG呈正相关(r=0.391, P < 0.01)。加用氯吡格雷后,CHD患者AA和ADP诱导的PAG、AR和ASR 发生率、血浆TXB,浓度明显低于加用前(P < 0.01)。结论: CHD患者阿司匹林疗效降低,AR发生率升高;CHD病人AR或ASR者血浆TXB,浓度较高;氯吡格雷能加强抗血小板聚集疗效,可用于防治AR。

关键词: 冠心病, 阿司匹林抵抗, 血小板聚集率, 血栓素B, 氯吡格雷

Abstract: AIM: To investigate biochemical aspirinresistance(AR) in coronary heart disease(CHD) patientsand the preventive measures. METHODS: CHD group(156 patients with angiographically documented CHD)and control group(n = 22) whose coronary artery angio-gram were normal took aspirin 100 mg/d for ≥ 7 days, and then their blood samples were collected for determination of optical platelet aggregation index (PAG) induced byarachidonic acid (AA)andadenosinediphosphate(ADP).'The CHD patients were given clopidogrel 75 mg/d after blood collected. After 7 days the blood sampleswere collected again. AR wasdefinedas a state in whichaggregation > 20% with AA and that > 70% with ADPwasfound. Aspirin semiresistance (ASR) was defined asmeeting one of the above criteria. If both above criteriaswere not met, the condition was defined as aspirin sensi-tive(AS). RESULTS: ln CHDgroup, ADP-inducedPAG, lg(AA-induced PAG) andlg(TXB, level) in ARor ASR subgroupwere higher than those in AS subgroup 154%. respectively(P < 0.05). The incidence of AR and AA-induced PAG in CHDgroup were higher than those incontrol group respeetively (P < 0.01). The TXB, level inCHD patients correlated with ADP and AA-induced PAG,respectively (r =0.497, P < 0.0I; r=0.391, P < 0.01). The above data were collected before taking clopi-dogrel. AA and ADP-induced PAG, the incidence ofASR or AR and the plasma level of TXB, after taking clo-pidogrelwere higher than those of before taking clopi-dogrel. CONCLUSION: The antiplatelet effect of aspirinin CHDgroup was more inferior than that in controlgroup. The incidence of AR in CHD patients increased.The plasma levels of TXB, in AR or ASR subgroup werehigher than those in AS subgroup. Clopidogrel can rein-force the effect of antiplatelet, can be used to prevent orcure AR.

Key words: coronary heart disease, aspinin resis-tance, platelet agregation, TXB, elopidogrel

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