In summary, we have characterized an age-associated accumulation of senescent myofibroblasts in the aged infarcted rabbit heart, and our findings suggest that these senescent cells remodel the electrophysiology of IBZ myocytes at least via direct myocyte-fibroblast coupling mediated by Cx43, which would increase risk of cardiac arrhythmias. The gene discussed is GJA1; the disease is cardiac arrhythmia.