Abstract
Background: Previous studies have shown that the adenosine monophosphate deaminase 1(AMPD1)C34T polymorphism is associated with a longer transplant free survival in patients with congestive heart failure. It has been postulated that increased regional and circulating adenosine may contribute to vasodilatation and after-load reduction. However, this polymorphism is also associated with a skeletal myopathy. It is unclear whether this polymorphism has beneficial impact, through enhanced endogenous after load reduction, or detrimental impact, through impaired skeletal muscle metabolism, on the exercise capacity of patients with heart failure.
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