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