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A common variant of the AMPD1 gene predicts improved survival in patients with ischemic left ventricular dysfunction

Yoshikazu Yazaki1, Joseph B Muhlestein, John F Carlquist

  • 1Cardiovascular Department, LDS Hospital, Salt Lake City, Utah 84143, USA.

Journal of Cardiac Failure
|August 17, 2004
PubMed

Insights

The adenosine monophosphate deaminase (AMPD)-1 gene variant C34T improves survival in heart failure patients with ischemic left ventricular dysfunction. This genetic factor offers a survival benefit specifically in those with ischemic heart conditions.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Cardiology
  • Heart Failure Pathophysiology

Background:

  • A prior study indicated the adenosine monophosphate deaminase (AMPD)-1 C34T gene variant may predict heart failure outcomes.
  • This variant's potential role in ischemic preconditioning via increased tissue adenosine was proposed.

Purpose of the Study:

  • To investigate if the survival advantage associated with the AMPD-1 C34T variant is specific to patients with ischemic left ventricular dysfunction.
  • To determine the prognostic value of the AMPD-1 C34T polymorphism in heart failure.

Main Methods:

  • A cohort of 390 heart failure patients with left ventricular ejection fraction <40% was analyzed.
  • Multivariate analysis was employed to identify independent predictors of transplant-free cardiovascular survival.
  • Patients were stratified into ischemic and non-ischemic subgroups.

Main Results:

  • In the ischemic subgroup (n=210), AMPD-1 T allele carriage was an independent predictor of improved transplant-free cardiovascular survival (HR=0.43, CI=0.20-0.94, P=.035).
  • No significant survival benefit was observed in the non-ischemic group, though statistical power was limited.

Conclusions:

  • The AMPD-1 C34T polymorphism significantly impacts transplant-free cardiovascular survival.
  • This genetic influence is particularly relevant in the context of ischemic left ventricular dysfunction.
Abstract

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