Enhanced thrombogenesis but not platelet activation is associated with transcatheter closure of patent foramen ovale in patients with cryptogenic stroke.
OBJECTIVE
No studies have yet determined whether antiplatelet or anticoagulant therapy is the more appropriate treatment after transcatheter closure of patent foramen ovale (PFO) in patients with cryptogenic stroke. The objective of this study was to prospectively evaluate the presence, degree, and timing of activation of the platelet and coagulation systems after transcatheter closure of PFO in patients with cryptogenic stroke.


METHODS
Twenty-four consecutive patients (mean age, 44+/-10 years; 11 men) with previous cryptogenic stroke who had undergone successful transcatheter closure of PFO were included in the study. Prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin III (TAT) were used as markers of coagulation activation, and soluble P-selectin and soluble CD40 ligand were used as markers of platelet activation. Measurements of all hemostatic markers were taken at baseline just before the procedure and at 7, 30, and 90 days after device implantation.


RESULTS
F1+2 and TAT levels increased from 0.41+/-0.16 nmol/L and 2.34+/-1.81 ng/mL, respectively, at baseline to a maximal value of 0.61+/-0.16 nmol/L and 4.34+/-1.83 ng/mL, respectively, at 7 days, gradually returning to baseline levels at 90 days (P<0.001 for both markers). F1+2 and TAT levels at 7 days after PFO closure were higher than those obtained in a group of 25 healthy controls (P<0.001 for both markers). Levels of soluble P-selectin and soluble CD40 ligand did not change at any time after PFO closure.


CONCLUSIONS
Transcatheter closure of PFO is associated with significant activation of the coagulation system, with no increase in platelet activation markers. These findings raise the question of whether optimal antithrombotic treatment after PFO closure should be short-term anticoagulant rather than antiplatelet therapy.
Bédard
Elisabeth
E
Institut de Cardiologie de Québec-Hôpital Laval, 2725, chemin Sainte-Foy, G1V 4G5 Québec, Canada.
Rodés-Cabau
Josep
J
Houde
Christine
C
Mackey
Ariane
A
Rivest
Donald
D
Cloutier
Stéphanie
S
Noël
Martin
M
Marrero
Alier
A
Côté
Jean-Marc
JM
Chetaille
Philippe
P
Delisle
George
G
Leblanc
Marie-Helene
MH
Bertrand
Olivier F
OF
D000328:Adult; D000925:Anticoagulants / Q000627:therapeutic use; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000187:drug effects / Q000502:physiology*; D023201:CD40 Ligand / Q000097:blood; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D005260:Female; D006344:Heart Septal Defects, Atrial / Q000150:complications* / Q000503:physiopathology / Q000601:surgery*; D006801:Humans; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D015539:Platelet Activation / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011446:Prospective Studies; D011498:Protein Precursors / Q000097:blood; D011516:Prothrombin; D020521:Stroke / Q000209:etiology* / Q000503:physiopathology; D013927:Thrombosis / Q000209:etiology* / Q000503:physiopathology; D013997:Time Factors
D000925:Anticoagulants; D015415:Biomarkers; D019007:P-Selectin; D010446:Peptide Fragments; D010975:Platelet Aggregation Inhibitors; D011498:Protein Precursors; C046193:antithrombin III-protease complex; D023201:CD40 Ligand; C029733:prothrombin fragment 1; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases