Figure 2.

Electrical remodelling in patients with an abnormal PTFV₁. (A) Original Western blot for the analysis of CaMKII activity, assessed by a specific HDAC4 (Histone Deacetylase 4) pull‐down assay in atrial homogenates of CABG patients with a normal and an abnormal PTFV₁. (B) Densiometric analysis revealed a significantly increased CaMKII activity (CaMKII‐HDAC4 binding normalized to CaMKII expression) in patients with an abnormal PTFV₁ (n = 9 vs. 11). (C) Moreover, linear regression analysis showed a significant positive correlation between PTFV₁ and CaMKII activity (n = 20). (D) Representative original recordings of electrically stimulated trabeculae (stimulated contractions indicated by red vertical lines) for a patient with a normal PTFV₁ and a patient with an abnormal PTFV₁ before and after wash‐in of the CaMKII inhibitor KN93. (E) Intriguingly, the mean severity of premature atrial contractions (PACs) was significantly increased in patients with an abnormal PTFV₁ (n = 14 vs. 16) but could be significantly reduced by CaMKII inhibition with KN93 (n = 11). Moreover, the inactive analogue KN92 did not show any anti‐arrhythmic effect. (F) Additionally, we observed a significant positive correlation between PTFV₁ and the severity of PACs (n = 30). Interestingly, this correlation was completely abolished upon CaMKII inhibition with KN93 (n = 23). *P < 0.05 vs. normal PTFV₁, ^# P < 0.05 vs. ISO + Ca, Mann–Whitney test, two‐way ANOVA post hoc corrected by Holm–Sidak, and linear regression analysis, as appropriate.