Forty‐two consecutive patients were checked for profiles of platelet aggregability before, during, and 10 and 30 minutes after catheter ablation. They were randomized into Group A (n = 20) who accepted intravenous aspirin (in 0.015 g/kg body weight) and Group P (n = 22) who accepted only placebo treatment. Blood samples were drawn from ascending aorta (Ao) and main pulmonary artery (MPA) simultaneously at each time period. In Group P, the EC50 of substrate induced platelet aggregability decreases significantly during (for ADP, from 1.72 to 0.78/mol/L for samples from Ao, P ± 0.0001; and from 1.68 to 0.69 μmol/ Lfor MPA, P ± 0.0001; for collagen, from 2.26 to 1.34 μg/mLfor Ao, P ± 0.005, and from 2.40 to 1.64 μg/mL, P ± 0.0001) and 10 minutes after successful ablation (for ADP, to 0.70 μmol/L for Ao, P ± 0.000, and to 0.61 μmol/L for MPA, P ± 0.0001; for collagen, to 1.54 μg/mL for Ao, P ± 0.01, and to 1.63 μg/ mL, P ± 0.0001), and then returned to baseline levels 30 minutes later (all P = NS) compared with comparative baseline levels. The levels of thromboxane B2 (TXB2) had the similar evolution. The evolution of platelet aggregability profiles was not associated with total energy dose, duration of energy application, duration of procedure, impedance, and ablation site. However, there were moderate positive correlations between the TXB2 levels and tip temperatures (r = 0.56, P ± 0.05 for Ao and r = 0.65, P ± 0.01 for MPA). These results suggest that increased platelet aggregability can occur during and 10 minutes after radiofrequency current ablation and antiplatelet therapy can maintain “flat” response of platelet aggregability to radiofrequency energy, which may provide possible benefits in preventing the occurrence of the complication.
|頁（從 - 到）||1980-1990|
|期刊||Pacing and Clinical Electrophysiology|
|出版狀態||已發佈 - 1月 1 1995|
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