Evidence map›Paper›PMID 28178970›Full record

ArticleCardiovascular diabetology2017

Obesity and type 2 diabetes have additive effects on left ventricular remodelling in normotensive patients-a cross sectional study.

Kirstie A De Jong, Juliane K Czeczor, Smithamol Sithara, Kevin McEwen, Gary D Lopaschuk, Alan Appelbe, Kimberly Cukier, Mark Kotowicz, Sean L McGee

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

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  9. Role of inflammation in diabetic cardiomyopathy.Therapeutic advances in endocrinology and metabolism · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Kirstie A De JongMetabolic Research Unit, Metabolic Reprogramming Laboratory, School of Medicine, Deakin University, Waurn Ponds, VIC, Australia. kgraham@deakin.edu.au.ORCID 0000-0003-3249-1628
Juliane K CzeczorMetabolic Research Unit, Metabolic Reprogramming Laboratory, School of Medicine, Deakin University, Waurn Ponds, VIC, Australia.
Smithamol SitharaMetabolic Research Unit, Metabolic Reprogramming Laboratory, School of Medicine, Deakin University, Waurn Ponds, VIC, Australia.
Kevin McEwenMetabolic Research Unit, Metabolic Reprogramming Laboratory, School of Medicine, Deakin University, Waurn Ponds, VIC, Australia.
Gary D LopaschukDepartment of Pediatrics, University of Alberta, Edmonton, AB, T6G 2H7, Canada.
Alan AppelbeCardiology Department, Barwon Health, University Hospital Geelong, Victoria, Australia.
Kimberly CukierGeelong Endocrinology and Diabetes Centre, Geelong, VIC, Australia.
Mark KotowiczEndocrinology Department, Barwon Health, University Hospital, Geelong, VIC, Australia.
Sean L McGeeMetabolic Research Unit, Metabolic Reprogramming Laboratory, School of Medicine, Deakin University, Waurn Ponds, VIC, Australia.
Deakin University · AUBarwon Health · AUUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIt is unclear whether obesity and type 2 diabetes (T2D), either alone or in combination, induce left ventricular hypertrophy (LVH) independent of hypertension. In the current study, we provide clarity on this issue by rigorously analysing patient left ventricular (LV) structure via clinical indices and via LV geometric patterns (more commonly used in research settings). Importantly, our sample consisted of hypertensive patients that are routinely screened for LVH via echocardiography and normotensive patients that would normally be deemed low risk with no further action required.

methodsThis cross sectional study comprised a total of 353 Caucasian patients, grouped based on diagnosis of obesity, T2D and hypertension, with normotensive obese patients further separated based on metabolic health. Basic metabolic parameters were collected and LV structure and function were assessed via transthoracic echocardiography. Multivariable logistic and linear regression analyses were used to identify predictors of LVH and diastolic dysfunction.

resultsMetabolically healthy normotensive obese patients exhibited relatively low risk of LVH. However, normotensive metabolically non-healthy obese, T2D and obese/T2D patients all presented with reduced normal LV geometry that coincided with increased LV concentric remodelling. Furthermore, normotensive patients presenting with both obesity and T2D had a higher incidence of concentric hypertrophy and grade 3 diastolic dysfunction than normotensive patients with either condition alone, indicating an additive effect of obesity and T2D. Alarmingly these alterations were at a comparable prevalence to that observed in hypertensive patients. Interestingly, assessment of LVPWd, a traditional index of LVH, underestimated the presence of LV concentric remodelling. The implications for which were demonstrated by concentric remodelling and concentric hypertrophy strongly associating with grade 1 and 3 diastolic dysfunction respectively, independent of sex, age and BMI. Finally, pulse pressure was identified as a strong predictor of LV remodelling within normotensive patients.

conclusionsThese findings show that metabolically non-healthy obese, T2D and obese/T2D patients can develop LVH independent of hypertension. Furthermore, that LVPWd may underestimate LV remodelling in these patient groups and that pulse pressure can be used as convenient predictor of hypertrophy status.

Indexed as

Ventricular Function, LeftVentricular RemodelingAgedBlood PressureChi-Square DistributionComorbidityCross-Sectional StudiesDiabetes Mellitus, Type 2Echocardiography, DopplerFemaleHumansHypertensionHypertrophy, Left VentricularIncidenceLinear ModelsLogistic ModelsEchocardiographyLeft ventricular diastolic dysfunctionLeft ventricular hypertrophyObesityType 2 diabetes

Identifiers

PMID28178970
PMCPMC5299776
OpenAlexW2587673510

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.