Ca²⁺/calmodulin-dependent protein kinase II regulates cardiac Na⁺ channels
J. Clin. Invest. Stefan Wagner, et al. 116:3127 doi:10.1172/JCI26620 [Go to this article.]

Figure 8
Arrhythmias in CaMKIIδ_C-Tg mice. (A) Original ECG traces during programmed electrical stimulation in vivo. In WT mice, 2 consecutive premature beats (S2-S3, coupling interval 38 ms) did not induce arrhythmias (top). In contrast, in 2 different Tg mice, the same protocol induced monomorphic (middle) or polymorphic VT (bottom). (B) Representative ECG traces before and after isoproterenol (Iso) administration. P-waves (indicated by asterisks) were apparent during normal rhythms (WT with or without isoproterenol) but were absent in Tg mice after isoproterenol administration. This apparent AV dissociation indicates arrhythmia. (C) Frequency of arrhythmia induction was significant in Tg but not WT mice for both programmed electrical stimulation (left) and isoproterenol administration (right). (D) Resting ECG parameters (RR interval, corrected QT [QT_c] interval, QRS duration, and PR interval). (E) Right-ventricular MAPs from hearts paced at basic cycle lengths (BCLs) of 100 (top) and 150 ms (bottom) for WT mouse hearts (left), Tg mouse hearts (middle), and Tg mouse hearts during infusion with KN93 (right). (F) Mean MAP durations at 90% repolarization (APD90). At slower heart rates (BCL, 150 ms), APD90 was significantly prolonged in Tg versus WT mice (but could not be reduced by KN93). At higher heart rates, there was no significant prolongation of APD90 in Tg versus WT.