Context The left atrial appendage (LAA) has been suggested to be the dominant location of thrombus in atrial fibrillation (AF) and has led to the development of LAA occlusion as a therapeutic modality to reduce stroke risk. However, the patient populations that would benefit most from this therapy are not well defined.
Objective A systematic review was performed to better define subgroups amenable to appendage closure.
Data sources The English scientific literature was searched using Pubmed through to March 1, 2011. Reference lists of relevant and review articles were screened to retrieve additional articles.
Study selection Studies were only included if they described the location of thrombus in left atrium. Case reports and case series describing less than 10 thrombi were excluded.
Data extraction Two reviewers independently extracted data and assessed quality of each study.
Results A total of 34 studies reporting on the location of atrial thrombus in patients with AF were included: 17 in valvular AF, 10 non-valvular AF and 8 in mixed valvular and non-valvular AF. Atrial thrombi were located outside the LAA in 56% (95% CI 53, 60) of valvular AF, 22% (95% CI 19, 25) in mixed cohorts and 11% (95% CI 6, 15) non-valvular AF. In non valvular AF, the studies with higher proportion of thrombi in the left atrial cavity had non-anticoagulated patients and a greater proportion of ventricular dysfunction and history of stroke.
Conclusion The location of atrial thrombus in patients with AF is dependent on the underlying substrate. In valvular AF, more than half the thrombi are located in the left atrial cavity. In the non-valvular AF group, a smaller proportion of thrombi were located outside the appendage. However, in certain subgroups (ie. non anti-coagulated, left ventricular dysfunction or prior stroke) the chances of left atrial cavity thrombus are higher.
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This study was presented at the Annual Scientific Sessions of the Heart Rhythm Society, May 2011, San Francisco, USA and published in abstract form (Heart Rhythm 2011;8:S29).
Funding RM and HSA are supported by the Australian Postgraduate Award from the University of Adelaide. RM is supported by the Leo J Mahar Electrophysiology Scholarships from the University of Adelaide. AGB, KCR-T and PS are funded by the National Heart Foundation of Australia. HSL and MA are supported by a Postgraduate Medical Scholarship from the National Health and Medical Research Council of Australia. ANG is supported by the Michel Mirowski Fellowship from the Heart Rhythm Society. SN is supported by the Robert J Craig Electrophysiology Scholarship from the University of Adelaide. DHL is supported by a Postdoctoral Fellowship from the National Health and Medical Research Council of Australia.
Competing interests KCR-T reports having served on the advisory board of St Jude Medical. PS reports having served on the advisory board of St Jude Medical, Bard Electrophysiology, Biosense-Webster, Medtronic, Sanofi-Aventis, and Merck, lecture fees from St Jude Medical, Bard Electrophysiology, Biosense-Webster, Medtronic and Merck and research funding from St Jude Medical, Bard Electrophysiology, Biosense-Webster and Medtronic.
Provenance and peer review Not commissioned; internally peer reviewed.
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