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. 2006 May 3;103(20):7906–7910. doi: 10.1073/pnas.0602133103

Fig. 1.

Fig. 1.

Calstabin-2 deficiency causes pacing-induced bidirectional VT and MAP alternans, which are prevented by JTV519. (A) Representative lead I and II ECG tracings and simultaneous left ventricular epicardial MAP recording from a placebo-treated calstabin-2+/− mouse during overdrive pacing at CL 30 ms as documented by PES trace. Pacing triggered sustained bidirectional VT, as evidenced by simultaneous ECG and MAP recordings shown at higher resolution in B. Pacing stimuli (arrows) induced MAP alternans that continued after cessation of pacing in placebo-treated calstabin-2+/− mice (CL 32 ms). (C) Bar graphs summarizing simultaneous occurrence of bidirectional MAP alternans (Left) and sustained VT (sVT) (Center) or nonsustained VT (nsVT) (Right) arrhythmias in placebo-treated (J−) or JTV519-treated (J+) calstabin-2+/− (open bars) or calstabin-2−/− (filled bars) mice during ISO stimulation (0.5 mg·kg−1 body weight). Mouse numbers and dimensions are as indicated. sVT, >10 beats (Center); nsVT, 3–10 arrhythmogenic beats (Right). GT, genotype.