Evidence mapPaperPMID 30605420Full record

ReviewCirculation research2019

Heart Failure in Type 2 Diabetes Mellitus.

Helena C Kenny, E Dale Abel

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 344 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
344citing papers in PubMed, 11 pooled it
50.6field-weighted citation impact, top 1% 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

344 citing papers in PubMed, 11 syntheses or guidelines pooled it, 652 citations in OpenAlex.

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284 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Helena C KennyFrom the Fraternal Order of Eagles Diabetes Research Center, and Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City.
E Dale AbelFrom the Fraternal Order of Eagles Diabetes Research Center, and Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City.
Fraternal Order of Eagles · US

Funding

Insulin resistance and cardiac dysfunction in obesityR01HL073167 · UNIVERSITY OF UTAH · 2003 to 2005
$1.3M
Insulin Signaling and the Heart in DiabetesR01HL070070 · UNIVERSITY OF UTAH · 2004 to 2005
$774k
Targeting Antioxidant Therapy to Cardiac MitochondriaR21DK073590 · UNIVERSITY OF UTAH · 2005 to 2005
$187k
NHLBI NIH HHS R01 HL070070NHLBI NIH HHS R01 HL073167NHLBI NIH HHS R01 HL108379NHLBI NIH HHS R01 HL112413NHLBI NIH HHS R01 HL127764NHLBI NIH HHS R61 HL141783NHLBI NIH HHS U01 HL087947NIDDK NIH HHS R01 DK092065NIDDK NIH HHS R21 DK073590
6 · The paper itself

Abstract

Patients with diabetes mellitus have >2× the risk for developing heart failure (HF; HF with reduced ejection fraction and HF with preserved ejection fraction). Cardiovascular outcomes, hospitalization, and prognosis are worse for patients with diabetes mellitus relative to those without. Beyond the structural and functional changes that characterize diabetic cardiomyopathy, a complex underlying, and interrelated pathophysiology exists. Despite the success of many commonly used antihyperglycemic therapies to lower hyperglycemia in type 2 diabetes mellitus the high prevalence of HF persists. This, therefore, raises the possibility that additional factors beyond glycemia might contribute to the increased HF risk in diabetes mellitus. This review summarizes the state of knowledge about the impact of existing antihyperglycemic therapies on HF and discusses potential mechanisms for beneficial or deleterious effects. Second, we review currently approved pharmacological therapies for HF and review evidence that addresses their efficacy in the context of diabetes mellitus. Dysregulation of many cellular mechanisms in multiple models of diabetic cardiomyopathy and in human hearts have been described. These include oxidative stress, inflammation, endoplasmic reticulum stress, aberrant insulin signaling, accumulation of advanced glycated end-products, altered autophagy, changes in myocardial substrate metabolism and mitochondrial bioenergetics, lipotoxicity, and altered signal transduction such as GRK (g-protein receptor kinase) signaling, renin angiotensin aldosterone signaling and β-2 adrenergic receptor signaling. These pathophysiological pathways might be amenable to pharmacological therapy to reduce the risk of HF in the context of type 2 diabetes mellitus. Successful targeting of these pathways could alter the prognosis and risk of HF beyond what is currently achieved using existing antihyperglycemic and HF therapeutics.

Indexed as

AnimalsBiomarkersBlood GlucoseDiabetes Mellitus, Type 2Diabetic CardiomyopathiesHeart FailureHumansHypoglycemic AgentsMyocytes, CardiacRisk AssessmentRisk FactorsSignal TransductionTreatment OutcomeVentricular FunctionBiomarkersBlood GlucoseHypoglycemic Agentsdiabetes mellitusdiabetic cardiomyopathyheart failurehyperglycemiaprognosis

Identifiers

PMID30605420
PMCPMC6447311
OpenAlexW2917743074

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.