Abstract
Background: The objective of this study was to investigate changes in coagulation activation and platelet activation after transcatheter closure of atrial septal defect (ASD) by determining the levels of specific markers over time to provide insight into preventing postprocedural embolism. Hypothesis: We hypothesis that the activation status of coagulation and the platelet would be changed after the closure of ASD. Methods: Forty consecutive patients who underwent transcatheter closure of ASD with the Lifetech ASD occluder (Lifetech Scientific, Shenzhen, China) were included in this prospective study. The serum level of prothrombin fragment 1 + 2 (F1 + 2) and expressions of P-selectin (CD62P) and platelet glycoprotein IIb/IIIa receptor (CD41a) on the surface of platelets were evaluated at baseline and at 1 day, 1 month, and 3 months after the closure. Results: The median F1 + 2 level was 0.96 nmol/L. This increased to a maximal value of 1.43 nmol/L at 1 day after closure, but gradually returned to the baseline level at 1 month after closure and remained there at 3 months after closure (medianswere 0.98 nmol/L and 1.08 nmol/L, respectively). Platelet surface expression of CD62P and CD41a decreased at 1 day, 1 month, and 3 months after closure. For CD62P, average expressions were 8.21%±2.11%, 6.28%±1.72%, 5.29%±1.52%, and 4.41%±1.11%, respectively, for baseline and 1 day, 1 month, and 3 months after closure. For CD41a, average expressionswere 79.37%±14.14%, 71.98%±13.77, 56.69%±13.05%, and 54.88%±11.62%, respectively. Conclusions: Transcatheter closure of ASD with the Lifetech ASD occluder was associated with significantly increased coagulation activation and decreased platelet activation. No evidence supporting the use of aspirin to prevent thrombus formation after closure was found. © 2010 Wiley Periodicals, Inc.
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CITATION STYLE
Zeng, X. C., Wu, W. F., Huang, K., Guo, S. L., & Liu, T. W. (2010). Enhanced prothrombin formation and platelet activation in Chinese patients after transcatheter closure of atrial septal defect. Clinical Cardiology, 33(7). https://doi.org/10.1002/clc.20752
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