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

Yang, Lulu (författare)
Feng, Hongliang (författare)
Ai, Sizhi (författare)
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Liu, Yue (författare)
Lei, Binbin (författare)
Chen, Jie (författare)
Tan, Xiao (författare)
Karolinska Institutet,Uppsala universitet,Lung- allergi- och sömnforskning,Department of Big Data in Health Science, Zhejiang University School of Public Health; Department of Psychiatry, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
Benedict, Christian, Docent, 1976- (författare)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap
Wang, Ningjian (författare)
Wing, Yun Kwok (författare)
Qi, Lu (författare)
Zhang, Jihui (författare)
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 (creator_code:org_t)
2023-03-04
2023
Engelska.
Ingår i: npj Digital Medicine. - : Springer Nature. - 2398-6352. ; 6:1
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kardiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)

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