Editorial
CPAP initiation in persistent atrial fibrillation: Have we overslept the alarm clock?

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Conflict of interest

The authors report no relationships that could be construed as a conflict of interest.

Cited by (3)

  • Screening for Obstructive Sleep Apnea in an Atrial Fibrillation Population: What's the Best Test?

    2021, CJC Open
    Citation Excerpt :

    Because of the high OSA prevalence in the AF population, the absence of typical signs and symptoms of OSA, and the inadequacy of screening questionnaires (SBQ, NoSAS), objective evaluation with an HSAT should be considered for patients with AF, as supported by the review by Desteghe et al.6 We also agree with these author’s suggestion of an integrated cardiology clinic-based model linked to a sleep centre or clinic, with a target population of symptomatic AF patients who require drug therapy, direct cardioversion, or pulmonary vein isolation. Management strategies would also include lifestyle modifications, which are essential for the comprehensive management of AF.31 Limitations of our work include the recruitment of patients from a single centre and the use of level III testing rather than PSG for the diagnosis of OSA.

  • Previously Undetected Obstructive Sleep Apnea in Patients With New-Onset Atrial Fibrillation

    2021, American Journal of Cardiology
    Citation Excerpt :

    Such negative impact of OSA appears to be proportional to its severity degree, although it also accounts for mild and moderate OSA-AF patients.3,4,20 The use of CPAP not always encompasses a more favorable arrhythmia control outcome: although a 40% reduction in the arrhythmia burden and a lesser progression from paroxysmal to more persistent AF forms driven by CPAP have been described, several meta-analyses and randomized-control studies have not confirmed a univocal “antiarrhythmic” effect of this therapy.7–9,11,22 Sleep apnea participates to the pathophysiological process of AF's atrial remodeling by means of direct (release of inflammatory precursors, a number of hemodynamic phenomena, recurrent hypoxia/hypercapnia to the atrial tissue, autonomic dysfunction) and indirect (it augments the AF burden itself) mechanisms.

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