冠心病患者生化阿司匹林抵抗的临床研究

Clinical research on biochemical aspirin resistance in coronary heart disease patients

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B_2(TXB_2)浓度。抽血后CHD患者加用氯吡格雷75 mg/d,1周后复查PAG和TXB_2。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PAG、lg(AA诱导的PAG)、lg (TXB_2浓度)显著高于AS患者(P<0.05);CHD患者血浆TXB_2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_2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_2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。

AIM： To investigate biochemical aspirin resistance（AR ） in coronary heart disease（CHD） patients and the preventive measures. METHODS： CHD group （156 patients with angiographically documented CHD） and control group （ n = 22） whose coronary artery angiogram were normal took aspirin 100 mg/d for ≥-7 days,and then their blood samples were collected for detenrfination of optical platelet aggregation index （PAG） induced by arachidonic acid （AA） and adenosine diphosphate （ADP）. The CHD patients were given clopidogrel 75 mg/d after blood collected. After 7 days the blood samples were collected again. AR was defined as a state in which aggregation 320% with AA and that 3 70% with ADP was found. Aspirin semiresistance （ASR） was defined as meeting one of the above criteria. If both above criterias were not met, the condition was defined as aspirin sensitive （AS）. RFSULTS： In CHD group, ADP-induced PAG, lg（AA-induced PAG） and lg（TXB2 level） in AR or ASR subgroup were higher than those in AS subgroup respectively（ P 〈 0.05）. The incidence of AR and AA- induced PAG in CHD group were higher than those in control group respectively （P 〈 0.01 ）. The TXB2 level in CHD patients correlated with ADP and AA-induced PAG respectively （r=0.497, P〈0.01; r=0.391, P〈 0.01 ）. The above data were collected before taking clopidogrel. AA and ADP -induced PAG, the incidence of ASR or AR and the plasma level of TXB2 after taking clopidogrel were higher than those of before taking clopidogrel. CONCLUSION： The antiplatelet effect of aspirin in CHD group was more inferior than that in control group. The incidence of AR in CHD patients increased. The plasma levels of TXB2 in AR or ASR subgroup were higher than those in AS subgroup. Clopidogrel can reinforce the effect of antiplatelet, can be used to prevent or cure AR.