Great debate: device-detected subclinical atrial fibrillation should be treated like clinical atrial fibrillation

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2024

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Sanders, P.
Svennberg, E.
Diederichsen, S.Z.
Crijns, H.J.G.M.
Lambiase, P.D.
Boriani, G.
Van Gelder, I.C.

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European Heart Journal, 2024; 45(29):2594-2603

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Prashanthan Sanders, Emma Svennberg, Søren Z. Diederichsen, Harry J. G. M. Crijns, Pier D. Lambiase, Giuseppe Boriani, and Isabelle C. Van Gelder

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Abstract

Automated continuous rhythm monitoring has been made possible with the extensive use of cardiac implantable electronic devices (CIEDs). A highly prevalent finding in devices with atrial sensing capabilities is atrial high-rate episodes (AHREs). These events have had variable definitions in the literature but are commonly referred to as atrial tachyarrhythmias with a rate of >175 b.p.m. and a duration of >5 min.1–3 False positives are fairly common—contributed by artefacts, noise, and far-field R-waves.4 Subclinical atrial fibrillation (SCAF) describes mostly asymptomatic device-detected AHREs confirmed to be AF, atrial flutter, or atrial tachycardia after a visual review of CIED tracings. In contrast, clinical AF is defined as symptomatic or asymptomatic AF of at least 30 s and documented by surface electrocardiogram (ECG).5 A recent meta-analysis of 54 studies reported a pooled prevalence of SCAF of 28.1% and found SCAF to be more frequent in older patients with multiple comorbidities and higher thromboembolic risks.6 At present, there is a knowledge gap regarding the clinical significance of short episodes of SCAF and the optimal management approach especially surrounding oral anticoagulation (OAC) therapy. Currently, available evidence shows mixed results delineating the association between SCAF and its risk of stroke. TRENDS and MOST studies showed an increased risk of stroke, along with cardiovascular and all-cause mortality in patients with SCAF, and their findings were supported by other large trials.1–3,7 An important randomized trial, the STROKESTOP study, highlighted the benefit of treating asymptomatic AF towards reducing the primary combined endpoint of ischaemic stroke, systemic embolism, death from any cause, haemorrhagic stroke, or hospitalization for bleeding.8 However, previous studies have shown that, although stroke risk for patients with SCAF is higher than those without, it is lower than for patients with clinical AF.9–12 The LOOP study also had negative results with no significant reduction in the primary endpoint despite higher detection of AF from loop recorders with subsequent increase in the initiation of OAC.13 It has been postulated that the risk of stroke is related to the duration and burden of SCAF. Longer duration of SCAF episodes between 12 and 23 h is independently associated with the risk of clinical AF.14 Device-detected AF and higher CHA2DS2-VASc scores at baseline also predict the subsequent development of clinical AF.15 These factors possibly contributed to the higher risk of stroke with SCAF episodes lasting >24 h as reported in the ASSERT study.9 The heterogeneity of SCAF definition and differences in previously analysed patient populations add to the complexity of determining the optimal burden and duration of SCAF that could benefit from OAC therapy. The risk of bleeding is also a major concern, as studies of novel OAC have demonstrated a risk of bleeding from 3% to 5%.16–20 Two large randomized controlled trials, NOAH-AFNET 6 and ARTESIA, have recently added to our understanding of the role of nonvitamin K antagonist OAC in this group of patients.21,22 Although providing further information, the management of device-detected silent AF should be focused on offering a personalized, patient-centred approach; balancing the risks and benefits of OAC initiation; as well as identifying and reducing the factors driving AF progression to improve overall clinical outcomes. Although providing the clinician with greater granularity of rhythm monitoring, several important questions remain. Here, we present the debate on the equipoise related to device-detected SCAF and how the clinician should manage these patients (Graphical Abstract).

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© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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