Probably, there is an explanation for this finding that this polymorphic variant of AMPD1 C34T could weaken the AMPD activity, and promote the elevated circulating levels of adenosine, a crucial protective agent, which was in part the consequence of the attenuation of myocardial fibrosis and ventricular remodeling, and thus contributing to less severe CVD [13, 30]. This evidence concerns the gene AMPD1 and Myocardial fibrosis.