Actigraphy-based sleep disruption and diurnal biomarkers of autonomic function in paroxysmal atrial fibrillation

TL;DR

This study finds that sleep disruption in people with paroxysmal atrial fibrillation is linked to changes in autonomic function, with effects varying between sleep and wakefulness.

Contribution

The study reveals diurnal patterns of autonomic dysfunction associated with sleep disruption in paroxysmal atrial fibrillation patients.

Findings

Longer sleep latency is linked to reduced parasympathetic activity during wakefulness.

Higher sleep efficiency is associated with increased heart rate variability and parasympathetic modulation.

Sleep fragmentation increases sympathetic activation and alters autonomic balance during sleep.

Abstract

Sleep architectural disruption is associated with atrial fibrillation (AF); however, associated autonomic influences remain unclear and it is unknown if this detriment persists during wakefulness. We hypothesize sleep disruption and autonomic dysfunction have diurnal patterning in patients with paroxysmal AF.

We analyzed data from the Sleep Apnea and Atrial Fibrillation Biomarkers and Electrophysiologic Atrial Triggers (SAFEBEAT) study designed to examine paroxysmal AF and sleep apnea, including simultaneous collection of continuous electrocardiogram monitoring (Heartrak Telemetry®) and actigraphy (Actiwatch GTX) for 7–21 days. Heart rate variability (HRV) measures in time-domain (standard deviation of normal-to-normal (NN) intervals (SDNN), coefficient of variation (CV)) and frequency-domain (low frequency power (LFP), high frequency power (HFP)) were used as surrogates of autonomic function and averaged per sleep/wake per day. A linear mixed-effects model assuming compound symmetry correlation structure was used to assess the relationship of HRV with actigraphy-derived sleep data.

The analytic sample (age 60.1 ± 12.0 years, body mass index 32.6 ± 6.7 kg/m2, 36% female, 75% White) included 100 participants with paroxysmal AF. Longer sleep latency was associated with lower HFP during wakefulness (coefficient − 0.0501, p = 0.031). Higher sleep efficiency was associated with increased SDNN (coefficient 0.0007, p = 0.014) and CV (coefficient 0.0167, p = 0.047). Higher arousal index was associated with increased CV (coefficient 0.0166, p = 0.007) and LFP (coefficient 0.0232, p = 0.003). During sleep, longer average awakenings duration was associated with increased LFP/HFP ratio (coefficient 0.1977, p < 0.001) and reduced HFP (coefficient − 0.1338, p < 0.001). Significant sleep-wake interactions were observed for sleep latency with HFP (p = 0.024), sleep efficiency with SDNN and CV (both p < 0.01), WASO with SDNN, CV, and LFP (all p < 0.05), and frequency of awakenings with CV and LFP (both p < 0.05).

Actigraphy-based measures of sleep disruption were associated with autonomic function alterations exhibiting diurnal variability in paroxysmal AF. Greater overall HRV and parasympathetic modulation were related to better sleep quality. Increased sympathetic activation was associated with sleep fragmentation. Results provide insights into differential autonomic dysfunction related to sleep disruption that may contribute to atrial arrhythmogenesis.

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