血管紧张素转换酶抑制剂抗血小板作用的研究

目的评估心血管病患者在分别接受血管紧张素转换酶抑制剂（ACEI）、阿司匹林、氯吡格雷加阿司匹林或不用上述药物时血小板的凝血活性。方法对303例心血管病患者进行全血血小板聚集功能测定。血小板聚集功能（Pag）由血小板对聚集剂ADP或胶原产生反应，通过电极的阻抗增加判定。结果在ACEI、阿司匹林、阿司匹林加氯吡格雷组Pag减弱，表现为与非治疗组相比有较低的阻抗增加。ACEI组，ADP介导的Pag下降33％（P=0．041）；阿司匹林组未见到有意义的抗血栓形成作用（17％，P=1．0）；阿司匹林加氯吡格雷组下降85％（P=0．001）。胶原介导的Pag在ACEI组下降16％（P=0．018）；在阿司匹林组和阿司匹林加氯吡格雷组分别下降23％（P=0．004）和35％（P=0．016）。结论ACEI降低Pag；阿司匹林加氯吡格雷有确切的抗血栓作用。ACEI对血小板的作用可能是该类药物在临床心血管病试验主要终点获益的原因。

Antiplatelet effect of angiotensin-converting enzyme inhibitors

Objective: To assess the coagulative activity of patients with cardiovascular disease grouped for treatment with either ACE inhibitors,aspirin,clopidogrel/aspirin,or none of these medications.Methods: Blood samples from 303 patients with cardiovascular disease were analyzed with whole-blood aggregometry.Platelet aggregation was determined by the increase in impedance across paired electrodes in response to the aggregatory agents adenosine diphosphate(ADP) or collagen.Results: Compared with no medication,platelet aggregation was attenuated by ACE inhibitors and by aspirin or clopidogrel/aspirin,which was indicated by a lower impedance increase.With ACE inhibition platelet aggregation decreased by 33%(P=0.042) after ADP induction.No significant antithrombotic effect was seen with aspirln alone(17%,P=1.0),whereas a decrease in ADP-induced platelet aggregation was extensive with clopidogrel/aspirin(85%,P=0.001).After collagen induction,platelet aggregation was reduced by 16%(P=0.028) in the presence of ACE inhibitor therapy,whereas inhibition with aspirin and clopidogrel/aspirin was 23%(P=0.004) and 35%(P=0.026) respectively,compared with participants who were not treated.Conclusion: These exvivo data on whole-blood aggregometry provide direct evidence that ACE inhibitors decrease platelet aggregation,whereas aspirin and clopidogrel are confirmed as established antithrombotics.Pleiofropic effects of ACE inhibition on platelet function may contribute to the clinical benefit observed with this drug class on major cardiovascular end points.