In a previous study, we demonstrated that the angiotensinogen (AGT) promoter polymorphism G-6A is highly associated with susceptibility to acquired SSS.[8] Based on functional studies, including electrophoretic mobility shift assay (EMSA) and luciferase assay results, we confirmed that nucleotide G at position -6 of the AGT gene modulates binding affinity with nuclear factors and yields lower transcriptional activity than nucleotide A. The G-6A AGT promoter polymorphism modulates AGT expression and therefore associated with acquired SSS. This evidence concerns the gene AGT and sick sinus syndrome.