Therefore, we hypothesized that the intronic SNP rs4822489 could affect the expression of ADORA2A by influencing the alternative splicing of its mRNA, leading to alteration of the number and function of ADORA2A, which might in turn weaken or eliminate the cardioprotective effects of that receptor, including expanding the coronary artery and increasing cardiac contractility and output, to ultimately aggravate any heart damage and accelerate the progression of heart failure. This evidence concerns the gene ADORA2A and heart failure.