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. Author manuscript; available in PMC: 2016 Jun 22.
Published in final edited form as: Circ Cardiovasc Genet. 2014 Jan 8;7(1):33–42. doi: 10.1161/CIRCGENETICS.113.000315

Figure 6.

Figure 6

Kcne2 deletion causes fasting-dependent ischemia and AV block during ischemia. A. Representative ECGs recorded from overnight-fasted 7m-old female Kcne2+/+ and Kcne2−/− mice (n = 7). Scale bar, 500 ms. B. Mean electrocardiographic parameters measured from traces recorded from overnight-fasted mice as in panel A (n = 7). *p < 0.05; NS, no significant difference. C. Mean heart mass (absolute and normalized to tibia length) for mice as in panel B. NS, no significant difference. D. Mean post-reperfusion serum [K+] for fasted 7m-old female Kcne2+/+ and Kcne2−/− mice (n = 7). *p < 0.05. Values for fed mice (dashed lines) from Figure 4 A are shown for comparison (n = 23-40). E. Representative ECGs recorded during coronary artery ligation of overnight fasted 7m-old female Kcne2+/+ and Kcne2−/− mice (n = 7). AV block, atrioventricular block. Scale bar, 500 ms. F. Mean ST heights from traces as in panel e, *p < 0.05 between genotypes by repeated measures ANOVA (n = 7). G. Left, western blots of ventricular pERK and tERK from mice as in panel B, isolated from control (C, non-operated) mice or after ischemia/reperfusion (post-reperfusion); right, pERK/tERK protein band density in post-reperfusion mouse ventricles measured from blots on left (n = 3-4). NS, no significant difference. H. Cardiac arrhythmia incidence and mortality during ischemia and post-ischemia reperfusion in 7m-old female Kcne2+/+ and Kcne2−/− mice as in panel f (n = 7). Sinus, remained in sinus rhythm; AVB, atrioventricular block; VT, ventricular tachycardia then recovery to sinus; SCD, sudden cardiac death after AVB. Numbers of animals per category are indicated in parentheses. *p < 0.05. I. Mean AV block:QRS ratio plotted versus duration of runs of AV block for the three Kcne2−/− mice summarized in panel H that exhibited AV block. Each shade indicates a different mouse; one mouse (open squares) exhibited 4 distinct runs of AV block. J. (i) Existing model for the mechanism of monogenic predisposition to SCD. (ii) Multifactorial etiology of Kcne2-associated arrhythmogenesis and SCD supported by the findings herein. EADs, early after-depolarizations; DADs, delayed after-depolarizations; TdP, torsades de pointe.