Short-Term Oral Anticoagulation Versus Antiplatelet Therapy Following Transcatheter Left Atrial Appendage Closure.


Journal

Circulation. Cardiovascular interventions
ISSN: 1941-7632
Titre abrégé: Circ Cardiovasc Interv
Pays: United States
ID NLM: 101499602

Informations de publication

Date de publication:
08 2020
Historique:
entrez: 11 8 2020
pubmed: 11 8 2020
medline: 22 6 2021
Statut: ppublish

Résumé

The impact of antithrombotic therapy on coagulation system activation after left atrial appendage closure (LAAC) remains unknown. This study sought to compare changes in coagulation markers associated with short-term oral anticoagulation (OAC) versus antiplatelet therapy (APT) following LAAC. Prospective study including 78 atrial fibrillation patients undergoing LAAC with the Watchman device. F1+2 (prothrombin fragment 1+2) and TAT (thrombin-antithrombin III) were assessed immediately before the procedure, and at 7, 30, and 180 days after LAAC. Forty-eight patients were discharged on APT (dual: 31, single: 17) and 30 on OAC (direct anticoagulants: 26, vitamin K antagonists: 4), with no differences in baseline-procedural characteristics between groups except for higher spontaneous echocardiography contrast in the OAC group. OAC significantly reduced coagulation activation within 7 days post-LAAC compared with APT (23% [95% CI, 5%-41%] versus 82% [95% CI, 54%-111%] increase for F1+2, OAC (versus APT) was associated with a significant attenuation of coagulation system activation post-LAAC. Spontaneous echocardiography contrast pre-LAAC associated with enhanced coagulation activation post-LAAC, which in turn increased the risk of device thrombosis. These results highlight the urgent need for randomized trials comparing OAC versus APT post-LAAC.

Sections du résumé

BACKGROUND
The impact of antithrombotic therapy on coagulation system activation after left atrial appendage closure (LAAC) remains unknown. This study sought to compare changes in coagulation markers associated with short-term oral anticoagulation (OAC) versus antiplatelet therapy (APT) following LAAC.
METHODS
Prospective study including 78 atrial fibrillation patients undergoing LAAC with the Watchman device. F1+2 (prothrombin fragment 1+2) and TAT (thrombin-antithrombin III) were assessed immediately before the procedure, and at 7, 30, and 180 days after LAAC.
RESULTS
Forty-eight patients were discharged on APT (dual: 31, single: 17) and 30 on OAC (direct anticoagulants: 26, vitamin K antagonists: 4), with no differences in baseline-procedural characteristics between groups except for higher spontaneous echocardiography contrast in the OAC group. OAC significantly reduced coagulation activation within 7 days post-LAAC compared with APT (23% [95% CI, 5%-41%] versus 82% [95% CI, 54%-111%] increase for F1+2,
CONCLUSIONS
OAC (versus APT) was associated with a significant attenuation of coagulation system activation post-LAAC. Spontaneous echocardiography contrast pre-LAAC associated with enhanced coagulation activation post-LAAC, which in turn increased the risk of device thrombosis. These results highlight the urgent need for randomized trials comparing OAC versus APT post-LAAC.

Identifiants

pubmed: 32772571
doi: 10.1161/CIRCINTERVENTIONS.120.009039
doi:

Substances chimiques

Anticoagulants 0
Biomarkers 0
Fibrinolytic Agents 0
Peptide Fragments 0
Platelet Aggregation Inhibitors 0
antithrombin III-protease complex 0
prothrombin fragment 1.2 0
Antithrombin III 9000-94-6
Prothrombin 9001-26-7
Peptide Hydrolases EC 3.4.-

Types de publication

Comparative Study Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

e009039

Auteurs

Lluis Asmarats (L)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Gilles O'Hara (G)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Jean Champagne (J)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Jean-Michel Paradis (JM)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Mathieu Bernier (M)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Kim O'Connor (K)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Jonathan Beaudoin (J)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Lucia Junquera (L)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

David Del Val (D)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Guillem Muntané-Carol (G)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Mélanie Côté (M)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

Josep Rodés-Cabau (J)

Department of Cardiology, Quebec Heart and Lung Institute, Laval University, Quebec City, Canada.

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