Serum markers of angiogenesis and myocardial ultrasonic tissue characterization in patients with dilated cardiomyopathy

Eur J Heart Fail. 2005 Jun;7(4):689-95. doi: 10.1016/j.ejheart.2004.09.011.

Abstract

Background and aims: It has been proven that a disturbance in angiogenesis contributes to the progression of myocardial interstitial fibrosis in idiopathic dilated cardiomyopathy (DCM). This study was designed to evaluate the relationship between serum activity of angiogenic factors and myocardial ultrasonic tissue characterization in patients with DCM.

Methods and results: We studied 30 patients with DCM and 15 healthy control subjects. Serum levels of vascular endothelial growth factor (VEGF), interleukin (IL)-4 and IL-13 were measured using enzyme-linked immunosorbent assay. We determined calibrated myocardial integrated backscatter (IB) as the value of myocardial interstitial fibrosis using ultrasonic tissue characterization and also quantified the magnitude of cyclic variations in IB (CV-IB). Serum levels of VEGF and IL-13 were significantly higher in patients with DCM than in control subjects (both P<0.05). Calibrated IB was significantly higher and CV-IB was markedly lower in patients with DCM than in control subjects (both P<0.01). In patients with DCM, the levels of IL-13 significantly correlated with calibrated IB (r=0.520, P=0.018). In addition, there was a significant negative correlation between levels of VEGF and CV-IB (r=-0.611, P=0.007).

Conclusion: The increase in serum VEGF and IL-13 may be closely related to alterations in myocardial texture in DCM.

MeSH terms

  • Adult
  • Aged
  • Cardiomyopathy, Dilated / blood*
  • Cardiomyopathy, Dilated / diagnostic imaging*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Humans
  • Interleukin-13 / blood*
  • Interleukin-4 / blood*
  • Male
  • Middle Aged
  • Neovascularization, Physiologic / physiology
  • Ultrasonography
  • Vascular Endothelial Growth Factor A / blood*

Substances

  • Interleukin-13
  • Vascular Endothelial Growth Factor A
  • Interleukin-4