Figure 7. IL‐6‐induced PR‐interval prolongation: proposed mechanism of action.
Systemic inflammatory activation, by increasing circulating IL‐6 levels could promote PR‐interval prolongation by affecting the electric properties of different cells in the atrioventricular (AV) node. The results of the present study suggest that these changes may consist, at least in part, in a down‐regulation of the gap‐junctions containing connexin43 (Cx43), which couple adjacent myocytes, as well as myocytes and macrophages, at the AV node.