Author + information
- Jacqueline Saw, MDa,∗ (, )
- Jens Erik Nielsen-Kudsk, MDb,
- Martin Bergmann, MD, PhDc,
- Matthew J. Daniels, MD, PhDd,e,f,g,
- Apostolos Tzikas, MD, PhDh,
- Mark Reisman, MDi and
- Bushra S. Rana, MDj
- aDivision of Cardiology, Vancouver General Hospital, Vancouver, British Columbia, Canada
- bDepartment of Cardiology, Aarhus University Hospital, Skejby, Denmark
- cCardiologicum Hamburg, Hamburg, Germany
- dDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom
- eBHF Centre of Research Excellence, University of Oxford, Oxford, United Kingdom
- fDepartment of Cardiology, Oxford University NHS Hospitals Trust, Oxford, United Kingdom
- gDepartment of Biotechnology, Graduate School of Engineering, Osaka University, Suita, Osaka, Japan
- hAHEPA University Hospital, Interbalkan European Medical Center, Thessaloniki, Greece
- iDivision of Cardiology, University of Washington Medical Center, Seattle, Washington
- jPapworth Hospital NHS Foundation Trust, Cambridge, United Kingdom
- ↵∗Address for correspondence:
Dr. Jacqueline Saw, University of British Columbia, Vancouver General Hospital, 2775 Laurel Street, 9th Floor, Vancouver, British Columbia V5Z 1M9, Canada.
Objectives The aim of this study is to review the evidence on the use of antithrombotic therapy and risk of device-related thrombosis after left atrial appendage closure.
Background Left atrial appendage closure (LAAC) is increasingly performed for stroke prevention in patients with nonvalvular atrial fibrillation, especially those who cannot tolerate or are ineligible for oral anticoagulation.
Methods After device implantation for LAAC, different antithrombotic regimens with varying duration of therapy are currently used. Such selection depends on patients’ risk for bleeding and physicians’ choice.
Results Device-related thrombosis remains an Achilles’ heel of LAAC, and the etiology remains incompletely understood. Dual-antiplatelet therapy, and direct oral anticoagulation may have similar safety and device-related thrombosis occurrence in real-world LAAC registries compared with warfarin and aspirin. Device imaging surveillance should be routinely performed to assess for device-related thrombosis, which if diagnosed should be treated aggressively, as it is associated with higher thromboembolic risks.
Conclusions Given the uncertainties and therapeutic dilemma, the authors provide an in-depth discussion of the options and rationale for antithrombotic therapy post-LAAC.
Dr. Saw has received unrestricted research grant support from the Canadian Institutes of Health Research, the Heart & Stroke Foundation of Canada, the National Institutes of Health, the University of British Columbia Division of Cardiology, AstraZeneca, Abbott Vascular, Boston Scientific, and Servier; speaking honoraria from AstraZeneca, St. Jude Medical, Boston Scientific, and Sunovion; consultancy and advisory board honoraria from AstraZeneca and Abbott Vascular; and proctorship honoraria from Abbott Vascular and Boston Scientific. Dr. Nielsen-Kudsk is a proctor and consultant for and has received grant support from Abbott Vascular. Dr. Bergmann has received speaking honoraria from Abbott Vascular, St. Jude Medical, Boston Scientific, Bayer, Boehringer Ingelheim, Daiichi Sankyo, and Pfizer. Dr. Daniels is supported by the Wellcome Trust (grant WT098519MA). Dr. Tzikas is a proctor and consultant for Abbott Vascular. Dr. Rana has received honoraria for teaching materials and lectures from Abbott Vascular, Boston Scientific, and Occlutech. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 14, 2018.
- Revision received October 29, 2018.
- Accepted November 6, 2018.
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