Evidence map›Paper›PMID 26302064›Full record

ArticleNutrition & diabetes2015

Obesity and carotid artery remodeling.

M Kozakova, C Palombo, C Morizzo, K Højlund, M Hatunic, B Balkau, P M Nilsson, E Ferrannini

Open access · goldAbstract read
In one paragraph

Article in Nutrition & diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Gut REG3γ-AssociatedFrontiers in immunology · 2017
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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

8 authors at 5 institutions in 5 countries.

M KozakovaDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
C PalomboDepartment of Surgical, Medical, Molecular Pathology and Critical Care, University of Pisa, Pisa, Italy.
C MorizzoDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
K HøjlundDepartment of Endocrinology, Odense University Hospital, Odense, Denmark.
M HatunicMater Misericordiae University Hospital, Dublin, Ireland.
B BalkauINSERM, CESP, Center for Research in Epidemiology and Population Health, U1018, University Paris Sud, Villejuif, France.
P M NilssonDepartment of Clinical Science, Lund University, Skåne University Hospital, Malmö, Sweden.
E FerranniniDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
University of Pisa · ITCentre de recherche en Epidémiologie et Santé des Populations · FRLund University · SEMater Misericordiae University Hospital · IEOdense University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectiveThe present study tested the hypothesis that obesity-related changes in carotid intima-media thickness (IMT) might represent not only preclinical atherosclerosis but an adaptive remodeling meant to preserve circumferential wall stress (CWS) in altered hemodynamic conditions characterized by body size-dependent increase in stroke volume (SV) and blood pressure (BP). SUBJECTS/

methodsCommon carotid artery (CCA) luminal diameter (LD), IMT and CWS were measured in three different populations in order to study: (A) cross-sectional associations between SV, BP, anthropometric parameters and CCA LD (266 healthy subjects with wide range of body weight (24-159 kg)); (B) longitudinal associations between CCA LD and 3-year IMT progression rate (ΔIMT; 571 healthy non-obese subjects without increased cardiovascular (CV) risk); (C) the impact of obesity on CCA geometry and CWS (88 obese subjects without CV complications and 88 non-obese subjects matched for gender and age).

resultsCCA LD was independently associated with SV that was determined by body size. In the longitudinal study, baseline LD was an independent determinant of ΔIMT, and ΔIMT of subjects in the highest LD quartile was significantly higher (28±3 μm) as compared with those in the lower quartiles (8±3, 16±4 and 16±3 μm, P=0.001, P<0.05 and P=0.01, respectively). In addition, CCA CWS decreased during the observational period in the highest LD quartile (from 54.2±8.6 to 51.6±7.4 kPa, P<0.0001). As compared with gender- and age-matched lean individuals, obese subjects had highly increased CCA LD and BP (P<0.0001 for both), but only slightly higher CWS (P=0.05) due to a significant increase in IMT (P=0.005 after adjustment for confounders).

conclusionsOur findings suggest that in obese subjects, the CCA wall thickens to compensate the luminal enlargement caused by body size-induced increase in SV, and therefore, to normalize the wall stress. CCA diameter in obesity could represent an additional biomarker, depicting the impact of altered hemodynamics on arterial wall.

Identifiers

PMID26302064
PMCPMC4558557
OpenAlexW1947997395

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.