Article Text

Download PDFPDF
Biomarkers and atrial fibrillation: is it prime time yet?
  1. Rajiv Mahajan,
  2. Dennis H Lau,
  3. Prashanthan Sanders
  1. Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, South Australia, Australia
  1. Correspondence to Dr Rajiv Mahajan, Department of Cardiology, Centre for Heart Rhythm Disorders (CHRD), Royal Adelaide Hospital, Adelaide, SA 5000, Australia; raj.mahajan{at}adelaide.edu.au

Statistics from Altmetric.com

Atrial fibrillation (AF) is a global epidemic with increasing burden on healthcare systems.1 AF is associated with increased risk of thromboembolic stroke, heart failure, cognitive dysfunction and mortality. In improving prognosis, the focus of management revolves around stroke prevention with clinical scores developed to identify people with increased stroke risk. The CHADS2 and CHA2DS2-VASc scores are the most commonly used scores, with the latter being better able to discriminate low-risk subjects.2 However, both the risk scores have a modest predictive value for identifying high-risk subjects for stroke with C statistics ranging from 0.60 to 0.80 (median 0.683) for CHADS2 and 0.64–0.79 (median 0.673) for CHA2DS2-VASc suggesting further scope for improvement.3 The C statistics of 1 means perfect discrimination and 0.5 means random chance. C statistics from 0.7 to 0.8 are considered to be of intermediate predictive value and those from 0.8 to 0.9 are considered to be of excellent predictive value.

More recently, attention has been drawn to ways that can improve the predictive value of these clinical stroke risk scores. Renal impairment, although associated with increased risk of AF and stroke, does not significantly improve the predictive value.4 This can be explained by the increased association of renal impairment with conditions that already constitute these clinical scores. Echocardiographic parameters, for example, systolic dysfunction on transthoracic echocardiogram5 and spontaneous echo contrast and left atrial appendage velocity on …

View Full Text

Footnotes

  • Contributors RM, DHL and PS were involved in generating the focus of the manuscript. RM drafted the manuscript. All authors reviewed and agreed to the manuscript as written.

  • Competing interests The University of Adelaide received fees for PS's services on the advisory board of Biosense-Webster, Medtronic, St Jude Medical, Sanofi-Aventis and Merck, Sharpe and Dohme. The University of Adelaide received fees for lectures provided by PS for Biosense-Webster, Medtronic, St Jude Medical, Boston Scientific, Merck, Sharpe and Dohme, Biotronik and Sanofi-Aventis. The University of Adelaide has received research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik and Sorin to support PS's research. RM is supported by the Leo J Mahar Lectureship from the University of Adelaide, Adelaide, Australia. DHL is supported by a Postdoctoral Fellowship from the National Health and Medical Research Council of Australia. PS is supported by a Practitioner Fellowship from the National Health and Medical Research Council of Australia and by the National Heart Foundation of Australia.

  • Provenance and peer review Commissioned; internally peer reviewed.

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Linked Articles