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

Walter J Paulus1, Elisa Dal Canto1

  • 1Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands.

JACC. Heart Failure
|December 30, 2017
PubMed

Insights

Diabetes mellitus (DM) impacts heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF) differently. DM causes microvascular inflammation in HFpEF and cardiomyocyte death in HFrEF, affecting myocardial remodeling uniquely.

Area of Science:

  • Cardiology
  • Endocrinology
  • Pathology

Background:

  • Noncardiac comorbidities like diabetes mellitus (DM) present distinct clinical outcomes in heart failure with preserved ejection fraction (HFpEF) versus heart failure with reduced ejection fraction (HFrEF).
  • These divergent outcomes stem from DM's differential impact on myocardial remodeling mechanisms specific to each heart failure phenotype.

Purpose of the Study:

  • To elucidate the phenotype-specific mechanisms through which diabetes mellitus influences myocardial remodeling in HFpEF and HFrEF.
  • To correlate these distinct mechanisms with observed clinical outcomes and guide therapeutic strategies.

Main Methods:

  • Analysis of biomarker profiles, focusing on inflammatory markers in HFpEF and myocardial injury/wall stress markers in HFrEF.
  • Assessment of coronary flow reserve and microvascular rarefaction in HFpEF.
  • Examination of myocardial biopsies from patients with diabetic cardiomyopathy to identify DM-induced cellular and molecular changes.

Main Results:

  • Myocardial remodeling in HFpEF is characterized by microvascular endothelial inflammation, leading to increased cardiomyocyte hypertrophy and stiffness, potentially driven by hyperinsulinemia.
  • In HFrEF, myocardial remodeling is driven by cardiomyocyte cell death, resulting in augmented replacement fibrosis due to lipotoxicity and advanced glycation end products.
  • Biomarker profiles and microvascular function assessments support these distinct pathogenic pathways.

Conclusions:

  • Diabetes mellitus exerts distinct, phenotype-specific effects on myocardial remodeling in HFpEF and HFrEF.
  • Understanding these differences is crucial for tailoring diabetes mellitus therapies to optimize outcomes in patients with different heart failure phenotypes.

Keywords:
diabetes mellitusheart failuremyocardium

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