Concerning the diagnosis of obstructive sleep apnea (OSA) and central sleep related breathing disorders and their prevalence in patients with atrial fibrillation, the authors themselves emphasize their study’s limitation—namely, that it was cardiorespiratory polygraphy that was undertaken and not an analysis of the sleep architecture. As a possible consequence, the recording period of this examination may be longer than the actual sleeping period itself, with an apnea-hypopnea index (AHI) that is set too low.
However, it is clearly more important that not performing an EEG and not analyzing sleep stages mean that no conclusions can be drawn about whether the known OSA and central SA induced psychophysiological insomnia parameters, such as microarousal, sleep fragmentation, REM or deep sleep deficits via the hypothalamic-pituitary-adrenal axis—that is, stressors that can be captured primarily by polysomnography—have an arrhythmic effect. We have observed an association between the periodic limb movements in sleep (PLMS) with atrial fibrillation that seems too frequent to be just down to chance. The pathophysiological hypotheses concerning pressure stress and diastolic dysfunctions as a monocausal association seem less plausible to me.
References
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