We thank O’Hare et al.1 for the interest and overview they have provided of the REVERSE-AF (PREVEntion and regReSsive Effect of weight-loss and risk factor modification on Atrial Fibrillation) study. This study highlights the impact of dedicated risk factor modification and targeted weight loss on the natural course of atrial fibrillation (AF) and its ability to reverse the type of AF.2

It is stated that one of the limitations of quantifying AF burden was the use of 7-day Holter monitoring, ECG, or implantable devices. Although this may be a limitation, it is one that is familiar for many of the large studies to date which report AF burden in the same manner. It is worth noting that the same monitoring was used in all groups thereby reducing the risks of selection or reporting biases. Importantly, these findings are not isolated to our observational series,3–5 but was also seen in our randomized controlled study.6

Although the ideal scenario may be to use implantable devices in all patients to therefore maximize the ability to capture episodes of AF, this method is both costly and invasive, therefore restricting the use of these devices. These devices are not without some inherent limitations. The algorithm used by these devices is based primarily on the R-R interval regularity for AF detection. This can result in under sensing of beats, oversensing of irregular atrial and ventricular premature beats and due to the memory can be filled electrograms may be deleted and not retrievable.7 With improvement over time in technology these limitations may be reduced.

Additionally, one of the key purposes for AF management is that of symptom control. As seen in the ARREST-AF cohort study, risk factor management and weight loss not only reduced symptoms but also the requirement for undertaking AF ablation.4

Finally, it is with anticipation that we also await the results of further studies in which long-term ambulatory and invasive monitoring is being used (ACTRN12613000444785). This will further our understanding and provide the ability to corroborate the patient symptoms to the burden and rule out asymptomatic AF. Additionally, the ability to undertake mapping of the atria to characterize substrate changes will also provide insight in the role of reversal of the AF substrate.

Funding

Postgraduate Scholarship from the National Health and Medical Research Council of Australia and the Robert J. Craig Scholarship from the University of Adelaide to M.E.M.; Postdoctoral Fellowship from the National Health and Medical Research Council of Australia to R.K.P.; Robert J. Craig Lectureship from the University of Adelaide to D.H.L.; Practitioner Fellowships from the National Health and Medical Research Council of Australia and by the National Heart Foundation of Australia to P.S.

Conflict of interest: P.S. reports having served on the advisory board of Biosense-Webster, Medtronic, and St Jude Medical. He reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Biosense-Webster, Medtronic, and St Jude Medical. He reports that the University of Adelaide has received on his behalf research funding from Medtronic, St Jude Medical, Boston Scientific, Biotronik and Sorin. All other authors have no disclosures.

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