Therefore, the purpose of this study was to examine: (i) whether miR-1 and Cx43 dysfunctions underlie the onset of VT associated to cardiac hypertrophy in a rat model of pressure overload; (ii) whether miR-1 directly modulates Cx43 expression and activity in hypertrophic myocytes in vitro and in vivo; (iii) to assess whether the treatment of pathologic LVH by AT1R blockade could normalize miR-1 levels, limit the adverse electrical remodeling of Cx43 and reduce the induction of life-threatening VT. The gene discussed is GJA1; the disease is cardiac hypertrophy.