title: Assessment of the markers of platelet and coagulation activation following transcatheter closure of atrial septal defects.
abstract: BACKGROUND
  Aspirin has been routinely prescribed following transcatheter closure of secundum atrial septal defects (ASDs) but its rationale has not been clinically or biologically evaluated; and despite aspirin, thrombotic complications occur following transcatheter ASD closure. We therefore evaluated the presence, degree and timing of the activation of the coagulation and platelet systems following transcatheter closure of ASDs.
  
  
  RESULTS
  Fourteen consecutive patients (9 females, mean age 41+/-22 years) who underwent successful transcatheter closure of an ASD defect with the Amplatzer septal occluder were prospectively studied. Measurements of the prothrombin fragment 1+2 (F1+2) levels and the percentage of activated platelets (determined by P-selectin expression detected by flow cytometry) were taken at baseline just before the procedure, and at 1, 7, 30 and 90 days following device implantation. F1+2 levels increased from 0.85+/-0.29 nmol/l at baseline to a maximal value of 1.20+/-0.52 nmol/l at 7 days, gradually returning to the baseline levels at 90 days (0.79+/-0.54 nmol/l) (p<0.001). F1+2 levels at 7 days were also significantly higher than those obtained in a control group of 20 healthy subjects (p=0.016). A greater increase in coagulation activation was observed in cases of residual shunt following ASD closure (r=0.53, p=0.050). No significant variations in the percentage of platelets expressing P-selectin were detected at any time.
  
  
  CONCLUSIONS
  Transcatheter closure of ASDs with the Amplatzer septal occluder was associated with a significant increase in F1+2 levels during the first week after device implantation, but there was no detectable effect on platelet system activation. These findings raise the question whether the optimal prophylactic approach following transcatheter ASD closure should be anticoagulant instead of antiplatelet therapy.
authors.affiliation: Department of Cardiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain. joseprodes@hotmail.com
authors.forename: Josep
authors.initials: J
authors.lastname: Rodés-Cabau
authors.forename: Andrés
authors.initials: A
authors.lastname: Palacios
authors.forename: Carles
authors.initials: C
authors.lastname: Palacio
authors.forename: Josep
authors.initials: J
authors.lastname: Girona
authors.forename: Enrique
authors.initials: E
authors.lastname: Galve
authors.forename: Arturo
authors.initials: A
authors.lastname: Evangelista
authors.forename: Jaume
authors.initials: J
authors.lastname: Casaldáliga
authors.forename: Dipma
authors.initials: D
authors.lastname: Albert
authors.forename: Marta
authors.initials: M
authors.lastname: Picó
authors.forename: Jordi
authors.initials: J
authors.lastname: Soler-Soler
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D006328:Cardiac Catheterization; D004621:Embolization, Therapeutic / Q000295:instrumentation; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006344:Heart Septal Defects, Atrial / Q000097:blood* / Q000601:surgery*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation; D011446:Prospective Studies; D012107:Research Design; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers