射频导管消融术对血小板活性的影响及阿司匹林的干预作用

Effect of Radiofrequency Catheter Ablation on Platelet Activity and Prophylactic Aspirin Treatment

目的：探讨射频导管消融术对血小板活性的影响及术前应用阿司匹林的干预作用。方法：选择行射频导管消融术患者168例，将其随机分为两组：阿司匹林组（n=88）：术前3天口服阿司匹林；对照组（n=80）：术前不用任何药物。分别于术前（T0）、电生理检查后（T1）、放电消融成功后30分钟（T2）、术后2天（T3）测定血浆中血小板α-颗粒膜糖蛋白和血栓烷素B2的含量，并比较两组内不同时间点各指标的变化和两组间各指标的差异。结果：对照组血浆血小板α-颗粒膜糖蛋白和血栓烷素B2含量在T1时刻较T0时刻有明显升高（均P〈0．01），T2时刻进一步升高达到峰值（均P〈0．001），T3时刻虽有所下降，但仍明显高于T0时刻（P〈0．01）；阿司匹林组血浆血小板α-颗粒膜糖蛋白和血栓烷素B2在T1、T2、T3时刻与T0时刻比较无明显升高（P〉0．05），但与对照组T1、T2、T3同时间点比较升高的幅度明显降低（P〈0．01-0．001）。结论：射频导管消融术可引起血小板激活，可能致血栓形成，术前服用阿司匹林可阻止血小板激活，有防止血栓形成的效果。

Objective：To investigate the effect of radiofrequency catheter ablation（RFCA） on platelet activity and evaluate the effect of pretreatment with aspirin（ASP）. Methods：One hundred and sixty-eight patients undergoing RFCA were randomized to control group（ n = 80,without ASP）before RFCA and ASP group（ n = 88 ,pretreatment with ASP for 3 days）prior to RFCA. platelet α-granule membrane glycoprotein- 140 （ GMP-140 ） and thromboxane B2 （ TxB2 ） levels of plasma were measured at four different time points ： before RFCA （ T0 ）, after electrophysiologic studies（ESP） （T1 ） ,30 minutes after the last RFCA（ T2 ）and at 2 days after RFCA（ T3 ）. The changes at different time points were recorded and the differences between groups at each time point were compared. Results：In the control group, GMP-140 and TxB2 levels of plasma were significantly increased after EPS （P 〈 0.01 ）, and to the peak values at 30 minutes after RFCA（ P 〈 0. 001 ）, They were slightly decreased 2 days after RFCA, but were still higher than the values before RFCA （ P 〈 0.01 ） ; In ASP group, there were no remarkable elevation in the levels of plasma GMP-140 and TxB2 at different time points, compared with the values before RFCA （ P 〉 0.05 ）, but the levels were much lower at the same time points than the values in control group（ P 〈0.01 ;P 〈0. 001 ）. Conclusion ：It suggests that platelet activation may be induced by RFCA,thus enhancing thrombosis. ASP may hinder platelet activation, thus preventing thrombosis.