Evidence map›Paper›PMID 40037794›Full record

ArticleSleep2025

Polysomnographic sleep architectural disruption associated with atrial fibrillation development.

Catherine M Heinzinger, Nicolas R Thompson, Alex Milinovich, Matheus Araujo, Cinthya Pena Orbea, Nancy Foldvary-Schaefer, Michael Faulx, David R Van Wagoner, Mina K Chung, Reena Mehra

Abstract read
In one paragraph

Article in Sleep, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Influence of sleep architectural disruptions on the evolution of atrial fibrillation.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Catherine M HeinzingerSleep Disorders Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0002-5407-0296
Nicolas R ThompsonDepartment of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA.
Alex MilinovichDepartment of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA.
Matheus AraujoSleep Disorders Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0003-0979-3417
Cinthya Pena OrbeaSleep Disorders Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.
Nancy Foldvary-SchaeferSleep Disorders Center, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0001-8900-3280
Michael FaulxHeart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA.
David R Van WagonerLerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0001-8250-9828
Mina K ChungLerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Reena MehraDepartment of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, WA, USA.

Funding

Project 3 Genes to Omics-Informed Drugs: Drug Repositioning and Testing to Prevent AF ProgressionsP01HL158502 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI Robert Alden Koeth · 2022 to 2026
$16.9M
NHLBI NIH HHS P01 HL158502
6 · The paper itself

Abstract

STUDY

objectivesTo examine the unclear, inconsistent role of sleep architectural disruption in atrial fibrillation (AF) development.

methodsPatients (age ≥ 18 years) who underwent in-laboratory sleep studies at Cleveland Clinic 2000-2015 were examined (follow-up: 7.8 ± 3.5 years). Primary predictors were arousal index and total sleep time. Secondary predictors included sleep efficiency, wakefulness after sleep onset, sleep and REM latency, and percentage of each sleep stage. Predictors were fit to Cox proportional hazard models predicting time from sleep study to AF by diagnosis code. Covariates included demographics, anthropometrics, tobacco use, sleepiness, apnea-hypopnea index, sleep apnea-specific hypoxic impact, cardiovascular risk factors and disease, mood disorders, medications, and positive airway pressure.

resultsIn our cohort (n = 27 232, age: 49.4 ± 14.5 years, 43.7% male, 73.9% white), 2077 (7.6%) developed incident AF. Arousal index was not associated with AF incidence. For every hour of decreased total sleep time, AF incidence increased 8% (HR = 1.08, 95% CI = 1.04 to 1.11). For every 10-unit decrease in sleep efficiency, AF incidence increased 6% (HR = 1.06, 95% CI = 1.04 to 1.09). For every hour of increased wakefulness after sleep onset, AF incidence increased 11% (HR = 1.11, 95% CI = 1.05 to 1.16). For every 10-unit increase in percent N1, AF incidence increased 6% (HR = 1.06, 95% CI = 1.01 to 1.10).

conclusionsLess sleep time and greater sleep disruption were associated with increased incident AF in this large clinical cohort. These results suggest that sleep macro-architecture can influence AF development. Mechanistic and prospective studies are needed to verify whether sleep disruption is a novel target for AF prevention.

Indexed as

Atrial FibrillationPolysomnographySleep Wake DisordersAdultArousalCohort StudiesFemaleHumansIncidenceMaleMiddle AgedRisk FactorsSleepatrial fibrillationsleep durationsleep stages

Identifiers

PMID40037794
PMCPMC13032129

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.