Relationship between circulating endothelial progenitor cells and insulin resistance in non-diabetic patients with

Alexander E Berezin1, Alexander A Kremzer2

  • 1State Medical University, Internal Medicine Department, Zaporozhye, Ukraine.

Insights

Insulin resistance (IR) is linked to lower circulating endothelial progenitor cells (EPCs) in heart failure patients. This suggests IR may worsen heart function by reducing proangiogenic EPCs.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Metabolic Syndrome

Background:

  • Chronic heart failure (CHF) is a complex condition often associated with metabolic disturbances.
  • Endothelial progenitor cells (EPCs) play a crucial role in vascular repair and angiogenesis.
  • Insulin resistance (IR) is a common comorbidity in patients with cardiovascular diseases.

Purpose of the Study:

  • To investigate the association between insulin resistance (IR) and the counts of specific circulating endothelial progenitor cell (EPC) phenotypes in patients with ischemic chronic heart failure (CHF).
  • To identify potential predictors for the depletion of EPCs in CHF patients with IR.

Main Methods:

  • The study included 300 patients diagnosed with CHF and coronary artery disease or myocardial infarction.
  • Insulin resistance was quantified using the homeostasis model assessment for insulin resistance (HOMA-IR).
  • Circulating EPC populations (CD45(-)CD34(+), CD14(+)CD309(+), and CD14(+)CD309(+)Tie2(+)) were analyzed via flow cytometry.

Main Results:

  • Patients with IR exhibited significantly lower counts of circulating EPCs compared to those without IR.
  • Key predictors for EPC depletion included NT-pro-brain natriuretic peptide (BNP), left ventricular ejection fraction, and NYHA class.
  • High-sensitivity C-reactive protein also emerged as a predictor for the depletion of CD14(+)CD309(+) and CD14(+)CD309(+)Tie2(+) EPCs.

Conclusions:

  • Insulin resistance may be an independent factor contributing to the reduced levels of proangiogenic EPCs in non-diabetic CHF patients.
  • These findings highlight a potential mechanism linking metabolic dysfunction to impaired vascular repair in heart failure.
  • Further research could explore therapeutic strategies targeting IR to improve EPC levels and cardiovascular outcomes.
Abstract

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