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Impaired glucose tolerance and insulin resistance in heart failure: underrecognized and undertreated?

Mamas A Mamas1, Christi Deaton, Martin K Rutter

  • 1Manchester Royal Infirmary, Biomedical Research Centre, Manchester, UK. mamasmamas1@yahoo.co.uk

Journal of Cardiac Failure
|August 28, 2010
PubMed

Insights

Abnormal glucose regulation and insulin resistance are common in heart failure patients without diabetes, predicting worse outcomes. Targeting myocardial metabolic pathways may offer new therapeutic strategies for this high-risk group.

Area of Science:

  • Cardiology
  • Endocrinology
  • Metabolic Syndrome

Background:

  • Heart failure (HF) and diabetes mellitus (DM) share a long-recognized association.
  • Abnormal glucose regulation (AGR) and insulin resistance (IR) are prevalent in HF patients even without DM, often underrecognized.
  • These metabolic abnormalities predict each other and are linked to HF development and progression.

Purpose of the Study:

  • To review the prevalence and prognostic significance of AGR and IR in HF patients without DM.
  • To explore the pathophysiological mechanisms linking AGR/IR with HF.
  • To discuss potential therapeutic strategies targeting myocardial metabolism.

Main Methods:

  • Literature review focusing on epidemiological studies and pathophysiological mechanisms.
  • Analysis of the correlation between glucose intolerance severity and HF severity.
  • Examination of metabolic shifts in cardiac tissue.

Main Results:

  • AGR and IR are significantly underdiagnosed in HF patients without DM.
  • The severity of glucose intolerance in HF patients correlates with HF severity.
  • Glucose intolerance in HF is an independent predictor of adverse outcomes.

Conclusions:

  • Cardiac metabolic alterations, including a shift towards fatty acid metabolism, may contribute to HF pathophysiology in patients with AGR/IR.
  • Pharmacological targeting of myocardial metabolic pathways presents a novel therapeutic avenue for at-risk HF patients with AGR/IR.
Abstract

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