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Long-Term Survival and Apolipoprotein A1 Level in Chronic Heart Failure: Interaction With Tumor Necrosis Factor α

Tímea Gombos1, Zsolt Förhécz1, Zoltán Pozsonyi1

  • 1IIIrd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.

Journal of Cardiac Failure
|June 19, 2016
PubMed

Insights

Low Apolipoprotein A1 (ApoA1) levels predict mortality in chronic heart failure (CHF) patients, particularly those with TNFα -308 GG genotype. This highlights the interplay of inflammation and malnutrition in CHF progression.

Area of Science:

  • Cardiology
  • Biochemistry
  • Genetics

Background:

  • Apolipoprotein A1 (ApoA1), a key component of high-density lipoprotein (HDL), possesses anti-inflammatory and antioxidative properties and is a prognostic marker in chronic heart failure (CHF).
  • Tumor necrosis factor alpha (TNFα) elevation is linked to poorer outcomes in heart failure (HF), but its association with the TNFα -308 promoter polymorphism is unclear.

Purpose of the Study:

  • To investigate the association between ApoA1 and TNFα levels and mortality in CHF patients.
  • To evaluate the potential interaction between ApoA1, TNFα levels, and the TNFα -308 polymorphism regarding mortality risk.

Main Methods:

  • A cohort of 195 CHF patients was followed for 5 years.
  • Measurements included ApoA1 levels, TNFα levels, and TNFα -308 polymorphism status.

Main Results:

  • Low ApoA1 and high TNFα levels correlated with more severe disease.
  • TNFα -308 A allele carriers exhibited higher ApoA1 levels than GG genotype patients (P = .007).
  • Decreased ApoA1 levels independently predicted 5-year mortality (adjusted HR = 1.10, P = .011).
  • An interaction was observed: low ApoA1 levels had a more pronounced adverse effect on survival in patients with the TNFα -308 GG genotype.

Conclusions:

  • Lower ApoA1 levels are strongly linked to adverse outcomes in CHF patients, modulated by TNFα -308 polymorphism.
  • These findings suggest a complex role for malnutrition and inflammation in the pathogenesis of CHF.
Abstract

Keywords:
Apolipoprotein A1 (ApoA1)TNFα −308 G/A promoter polymorphismsTumor necrosis factor alpha (TNFα)cholesterol paradoxchronic heart failure (CHF)

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