Evidence map›Paper›PMID 25339298›Full record

ReviewJournal of human hypertension2015

Pathogenesis of obstructive sleep apnoea in hypertensive patients: role of fluid retention and nocturnal rostral fluid shift.

L H White, T D Bradley, A G Logan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of human hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

16 citing papers in PubMed, 47 citations in OpenAlex.

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  9. Review
  10. Sitting Less and Moving More: Implications for Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018
    Review
  11. Impact of concomitant medications on obstructive sleep apnoea.British journal of clinical pharmacology · 2017
    Review
  12. Review
  13. Article
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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

3 authors at 3 institutions in 1 country.

L H White1] Sleep Research Laboratory, Toronto Rehabilitation Institute, Toronto, Ontario, Canada [2] Centre for Sleep Medicine and Circadian Biology of the University of Toronto, Toronto, Ontario, Canada.
T D Bradley1] Sleep Research Laboratory, Toronto Rehabilitation Institute, Toronto, Ontario, Canada [2] Centre for Sleep Medicine and Circadian Biology of the University of Toronto, Toronto, Ontario, Canada [3] Department of Medicine of the University Health Network, Toronto General Hospital, Toronto, Ontario, Canada [4] Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
A G Logan1] Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada [2] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Lunenfeld-Tanenbaum Research Institute · CAToronto Rehabilitation Institute · CAToronto Sleep Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obstructive sleep apnoea (OSA) is highly prevalent in hypertensive patients, particularly those with drug resistance. Evidence from animal experiments, epidemiologic studies and clinical trials strongly suggest a causal link. Mechanistic studies argue for increased sympathetic neural activity and endothelial dysfunction. However, disturbances in fluid volume regulation and distribution may also be involved in the pathogenesis of these two conditions. Several studies have shown a high prevalence of OSA in fluid-retaining states including hypertension, a direct relationship between the severity of OSA and the volume of fluid displaced from the legs to the neck during sleep, and a decrease in upper airway cross-sectional area in response to graded lower body positive pressure. Treatments targeting fluid retention and redistribution, including diuretics, mineralocorticoid antagonists, exercise, and possibly renal denervation lower blood pressure and reduce the apnoea-hypopnoea index, a measure of OSA severity. From these observations, it has been postulated that during the daytime, excess fluid collects in the lower extremities due to gravity, and on lying down overnight is redistributed rostrally to the neck, where it may narrow the upper airway and increase its collapsibility, predisposing to OSA when pharyngeal dilator muscle activity decreases during sleep. This article discusses the associations between OSA and hypertension and reviews the evidence for fluid accumulation and its nocturnal rostral redistribution in the pathogenesis of OSA in hypertensive patients.

Indexed as

Fluid ShiftsContinuous Positive Airway PressureDenervationExerciseExtracellular FluidHeart FailureHumansHypertensionKidneySleep Apnea, Obstructive

Identifiers

PMID25339298
OpenAlexW2095298753

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.