ArticlemedRxiv : the preprint server for health sciences2026
Shared Neurocardiac Pathways Linking Atrial Fibrillation and Depression: A UK Biobank Analysis.
Article in medRxiv : the preprint server for health sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundAtrial fibrillation (AF) and major depressive disorder (MDD) frequently co-occur and are each associated with adverse cardiovascular outcomes, yet the biological pathways linking these conditions remain poorly defined. Using the UK Biobank, we evaluated shared neurocardiac, inflammatory, and cardiovascular correlates underlying the AF-MDD association.
objectivesTo assess bidirectional associations between AF and MDD and determine whether shared inflammatory, cardiovascular, autonomic, and neuroimaging correlates characterize their comorbidity.
methodsWe analyzed individuals with AF (N≥1,716), MDD (N≥4,550), comorbid AF-MDD (N≥243), and healthy comparators (HCs; N≥33,041). Bidirectional associations were examined using cross-sectional and Cox proportional hazard models. Mediation analyses evaluated contributions of inflammatory markers and cardiovascular risk. Central autonomic network structure and function was assessed using MRI-derived morphometry and resting-state connectivity.
resultsAF and MDD demonstrated bidirectional associations: AF was associated with a 44% higher risk of incident MDD, and MDD with a 26% higher risk of incident AF. Inflammatory biomarkers and cardiovascular risk partially mediated these associations (6.85% and 32.01%, respectively). AF was associated with greater gray matter volume in ventromedial prefrontal and insular cortices and increased central autonomic network connectivity, whereas MDD showed opposite structural and functional patterns. The comorbid AF-MDD group exhibited distinct, non-additive neural profiles.
conclusionsAF and MDD demonstrate bidirectional associations characterized by shared inflammatory, cardiovascular, and neural correlates, alongside distinct and non-additive alterations within central autonomic network circuits. These findings support a systems-level neurocardiac framework linking cardiac and psychiatric disease and highlight the importance of integrated approaches to risk assessment and multidisciplinary management in patients with AF-MDD comorbidity.
Identifiers
What OpenQuestion holds
Registered trials
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.