Evidence map›Paper›PMID 34583686›Full record

ArticleCardiovascular diabetology2021

Diabetes status-related differences in risk factors and mediators of heart failure in the general population: results from the MORGAM/BiomarCaRE consortium.

Matti A Vuori, Jaakko Reinikainen, Stefan Söderberg, Ellinor Bergdahl, Pekka Jousilahti, Hugh Tunstall-Pedoe, Tanja Zeller, Dirk Westermann, Susana Sans, Allan Linneberg and 6 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Cardiovascular diabetology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact, top 81% 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

7 citing papers in PubMed, 0 citations in OpenAlex.

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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

16 authors at 9 institutions in 7 countries.

Matti A VuoriDivision of Medicine, University of Turku and Turku University Hospital, Kiinanmyllynkatu 2, 20521, Turku, Finland. makvuo@utu.fi.ORCID 0000-0003-2529-3332
Jaakko ReinikainenDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
Stefan SöderbergDepartment of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Ellinor BergdahlDepartment of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Pekka JousilahtiDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
Hugh Tunstall-PedoeCardiovascular Epidemiology Unit, Institute of Cardiovascular Research, University of Dundee, Dundee, UK.
Tanja ZellerUniversity Heart Center Hamburg, Hamburg, Germany.
Dirk WestermannUniversity Heart Center Hamburg, Hamburg, Germany.
Susana SansCatalan Department of Health, Barcelona, Spain.
Allan LinnebergCenter for Clinical Research and Prevention, Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark.
Licia IacovielloDepartment of Epidemiology and Prevention, IRCCS Neuromed, Pozzilli, Italy.
Simona CostanzoDepartment of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Veikko SalomaaDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
Stefan BlankenbergUniversity Heart Center Hamburg, Hamburg, Germany.
Kari KuulasmaaDepartment of Public Health and Welfare, Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
Teemu J NiiranenDivision of Medicine, University of Turku and Turku University Hospital, Kiinanmyllynkatu 2, 20521, Turku, Finland.
Finnish Institute for Health and Welfare · FIUniversität Hamburg · DEUmeå University · SEUniversity of Copenhagen · DKCatalan Society of Family and Community Medicine · ESTurku University Hospital · FIUniversity of Dundee · GBUniversity of Insubria · ITUniversity of Turku · FI

Funding

Medical Research Council G0601463Terveyden Tutkimuksen Toimikunta 321351
6 · The paper itself

Abstract

backgroundThe risk of heart failure among diabetic individuals is high, even under tight glycemic control. The correlates and mediators of heart failure risk in individuals with diabetes need more elucidation in large population-based cohorts with long follow-up times and a wide panel of biologically relevant biomarkers.

methodsIn a population-based sample of 3834 diabetic and 90,177 non-diabetic individuals, proportional hazards models and mediation analysis were used to assess the relation of conventional heart failure risk factors and biomarkers with incident heart failure.

resultsOver a median follow-up of 13.8 years, a total of 652 (17.0%) and 5524 (6.1%) cases of incident heart failure were observed in participants with and without diabetes, respectively. 51.4% were women and the mean age at baseline was 48.7 (standard deviation [SD] 12.5) years. The multivariable-adjusted hazard ratio (HR) for heart failure among diabetic individuals was 2.70 (95% confidence interval, 2.49-2.93) compared to non-diabetic participants. In the multivariable-adjusted Cox models, conventional cardiovascular disease risk factors, such as smoking (diabetes: HR 2.07 [1.59-2.69]; non-diabetes: HR 1.85 [1.68-2.02]), BMI (diabetes: HR 1.30 [1.18-1.42]; non-diabetes: HR 1.40 [1.35-1.47]), baseline myocardial infarction (diabetes: HR 2.06 [1.55-2.75]; non-diabetes: HR 2.86 [2.50-3.28]), and baseline atrial fibrillation (diabetes: HR 1.51 [0.82-2.80]; non-diabetes: HR 2.97 [2.21-4.00]) had the strongest associations with incident heart failure. In addition, biomarkers for cardiac strain (represented by nT-proBNP, diabetes: HR 1.26 [1.19-1.34]; non-diabetes: HR 1.43 [1.39-1.47]), myocardial injury (hs-TnI, diabetes: HR 1.10 [1.04-1.16]; non-diabetes: HR 1.13 [1.10-1.16]), and inflammation (hs-CRP, diabetes: HR 1.13 [1.03-1.24]; non-diabetes: HR 1.29 [1.25-1.34]) were also associated with incident heart failure. In general, all these associations were equally strong in non-diabetic and diabetic individuals. However, the strongest mediators of heart failure in diabetes were the direct effect of diabetes status itself (relative effect share 43.1% [33.9-52.3] and indirect effects (effect share 56.9% [47.7-66.1]) mediated by obesity (BMI, 13.2% [10.3-16.2]), cardiac strain/volume overload (nT-proBNP, 8.4% [-0.7-17.4]), and hyperglycemia (glucose, 12.0% [4.2-19.9]).

conclusionsThe findings suggest that the main mediators of heart failure in diabetes are obesity, hyperglycemia, and cardiac strain/volume overload. Conventional cardiovascular risk factors are strongly related to incident heart failure, but these associations are not stronger in diabetic than in non-diabetic individuals. Active measurement of relevant biomarkers could potentially be used to improve prevention and prediction of heart failure in high-risk diabetic patients.

Indexed as

AdultBiomarkersBlood GlucoseC-Reactive ProteinDiabetes MellitusEuropeFemaleHealth StatusHeart Disease Risk FactorsHeart FailureHumansIncidenceInflammation MediatorsMaleMiddle AgedNatriuretic Peptide, BrainBiomarkersBlood GlucoseC-Reactive ProteinInflammation MediatorsNatriuretic Peptide, BrainPeptide Fragmentspro-brain natriuretic peptide (1-76)Troponin IBiomarkerCardiovascular diseaseDiabetesHazardHeart failureMediationRisk

Identifiers

PMID34583686
PMCPMC8479921
OpenAlexW3204395795

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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.