What is the clinical evidence from this study?

Study design: Cohort. Population: Atrial fibrillation (n=62927). Intervention: Circadian rest-activity rhythm (CRAR) abnormalities (low amplitude) vs. Normal CRAR (high amplitude). Primary outcome: Incidence of atrial fibrillation (HR 1.41, 95% CI 1.25-1.58).

What does this research mean for the field?

Low amplitude of circadian rest-activity rhythm is associated with a 41% higher risk of incident atrial fibrillation compared to high amplitude in the general population. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

March 4, 2023Open Access

Association of accelerometer-derived circadian abnormalities and genetic risk with incidence of atrial fibrillation

LYLulu YangHenan Psychiatric Hospital HFHongliang FengGuangzhou Psychiatric Hospital SASizhi AiFirst Affiliated Hospital of Guangzhou Medical University

Key Result

Low amplitude of circadian rest-activity rhythm was associated with a 41% higher risk of incident atrial fibrillation (HR 1.41) compared to high amplitude in the general population.

Study Design

Type

Cohort (n=62,927)

Multicenter

Yes

Structured PICO

Do accelerometer-derived circadian abnormalities and high genetic risk increase the incidence of atrial fibrillation in a general population without prior AF?

Population

62,927 white British participants of the UK Biobank without atrial fibrillation at baseline, mean age 62.48 years, 56.13% female.

Intervention

Accelerometer-measured circadian rest-activity rhythm (CRAR) abnormalities (characterized by low amplitude, delayed acrophase, and low mesor) and high genetic risk (assessed via polygenic risk scores).

Comparator

Normal circadian rest-activity rhythm characteristics and low genetic risk.

Outcome

Incidence of atrial fibrillation or atrial flutter ascertained through hospital inpatient and death records at a median follow-up of 6.16 years.hard clinical

Accelerometer-measured circadian rhythm abnormalities, particularly when combined with high genetic risk, are significantly associated with an increased risk of incident atrial fibrillation in the general population.

Main Result

Effect estimate: HR 1.41 (95% CI 1.25-1.58)

Limitations

UK Biobank is not representative of the general population due to a 'healthy volunteer' bias.
Some covariates such as lifestyle were collected a median of 5.7 years prior to accelerometer wear.
Residual or unmeasured confounding, such as sleep medication use, could not be ruled out.
Incident AF cases were ascertained through hospital and death records only, likely missing some cases.
CRAR is susceptible to masking effects from imposed social schedules and may be less stable than other circadian markers.
The 7-day accelerometer monitoring duration may not fully represent long-term behavior.
The study was restricted to individuals of European descent, limiting generalizability to other populations.

Abstract

Evidence suggests potential links between circadian rhythm and atrial fibrillation (AF). However, whether circadian disruption can predict the onset of AF in the general population remains largely unknown. We aim to investigate the association of accelerometer-measured circadian rest-activity rhythm (CRAR, the most prominent circadian rhythm in humans) with the risk of AF, and examine joint associations and potential interactions of CRAR and genetic susceptibility with AF incidence. We include 62,927 white British participants of UK Biobank without AF at baseline. CRAR characteristics, including amplitude (strength), acrophase (timing of peak activity), pseudo-F (robustness), and mesor (height), are derived by applying an extended cosine model. Genetic risk is assessed with polygenic risk scores. The outcome is the incidence of AF. During a median follow-up of 6.16 years, 1920 participants developed AF. Low amplitude hazard ratio (HR): 1.41, 95% confidence interval (CI): 1.25-1.58, delayed acrophase (HR: 1.24, 95% CI: 1.10-1.39), and low mesor (HR: 1.36, 95% CI: 1.21-1.52), but not low pseudo-F, are significantly associated with a higher risk of AF. No significant interactions between CRAR characteristics and genetic risk are observed. Joint association analyses reveal that participants with unfavourable CRAR characteristics and high genetic risk yield the highest risk of incident AF. These associations are robust after controlling for multiple testing and in a series of sensitivity analyses. Accelerometer-measured CRAR abnormalities, characterized by decreased strength and height, and later timing of peak activity of circadian rhythm, are associated with a higher risk of AF in the general population.

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