↓ Skip to main content

Distinct Myocardial Targets for Diabetes Therapy in Heart Failure With Preserved or Reduced Ejection Fraction

Overview of attention for article published in JACC: Heart Failure, January 2018
Altmetric Badge

About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (95th percentile)
  • Good Attention Score compared to outputs of the same age and source (77th percentile)

Mentioned by

twitter
79 X users
facebook
2 Facebook pages

Citations

dimensions_citation
95 Dimensions

Readers on

mendeley
111 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Distinct Myocardial Targets for Diabetes Therapy in Heart Failure With Preserved or Reduced Ejection Fraction
Published in
JACC: Heart Failure, January 2018
DOI 10.1016/j.jchf.2017.07.012
Pubmed ID
Authors

Walter J. Paulus, Elisa Dal Canto

Abstract

Noncardiac comorbidities such as diabetes mellitus (DM) have different outcomes in heart failure with preserved ejection fraction (HFpEF) compared with heart failure with reduced ejection fraction (HFrEF). These different outcomes are the result of distinct myocardial effects of DM on HFpEF and HFrEF, which relate to different mechanisms driving myocardial remodeling in each heart failure phenotype. Myocardial remodeling is driven by microvascular endothelial inflammation in HFpEF and by cardiomyocyte cell death in HFrEF. Evidence consists of: different biomarker profiles, in which inflammatory markers are prominent in HFpEF and markers of myocardial injury or wall stress are prominent in HFrEF; reduced coronary flow reserve with microvascular rarefaction in HFpEF; and upregulation of free radical-producing enzymes in endothelial cells in HFpEF and in cardiomyocytes in HFrEF. As biopsies from patients with diabetic cardiomyopathy reveal, DM affects failing myocardium by phenotype-specific mechanisms. In HFpEF, DM mainly increases cardiomyocyte hypertrophy and stiffness, probably because of hyperinsulinemia and microvascular endothelial inflammation. In HFrEF, DM augments replacement fibrosis because of cardiomyocyte cell death induced by lipotoxicity or advanced glycation end products. Because DM exerts distinct effects on myocardial remodeling in HFpEF and HFrEF, the heart failure phenotype is important for DM therapy.

X Demographics

X Demographics

The data shown below were collected from the profiles of 79 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 111 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 111 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 21 19%
Researcher 14 13%
Student > Bachelor 12 11%
Student > Doctoral Student 9 8%
Other 8 7%
Other 17 15%
Unknown 30 27%
Readers by discipline Count As %
Medicine and Dentistry 45 41%
Biochemistry, Genetics and Molecular Biology 16 14%
Agricultural and Biological Sciences 7 6%
Nursing and Health Professions 4 4%
Pharmacology, Toxicology and Pharmaceutical Science 3 3%
Other 5 5%
Unknown 31 28%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 45. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 January 2018.
All research outputs
#945,279
of 25,806,763 outputs
Outputs from JACC: Heart Failure
#300
of 1,627 outputs
Outputs of similar age
#21,330
of 452,385 outputs
Outputs of similar age from JACC: Heart Failure
#10
of 45 outputs
Altmetric has tracked 25,806,763 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 96th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,627 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 30.4. This one has done well, scoring higher than 81% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 452,385 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 95% of its contemporaries.
We're also able to compare this research output to 45 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 77% of its contemporaries.