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. Author manuscript; available in PMC: 2014 Jul 18.
Published in final edited form as: Biochem Pharmacol. 2013 Sep 23;86(11):1576–1583. doi: 10.1016/j.bcp.2013.09.012

Table 1.

Arrhythmia prevalence in bortezomib-treated CASQ2 mutant mice.

Genotype N (mice) Sinus rate (beats/min, mean ± SD) Rest
PVC
Rest
VT
Stress
PVC
Stress
VT
Epi
PVC
Epi
VT
KO Baseline 4 448 ± 3 4 4 4 4 4 4
KO Bortezomib 4 507 ± 31 4 4 4 4 4 4
D307H Baseline 4 495 ± 144 4 3 4 4 4 4
D307H Bortezomib 4 557 ± 51 1 0* 4 1* 4 4

Mutant mice (D307H and KO) were treated with 4 injections of bortezomib [1 μg/g] IV for 11 days. Then, Mice were subjected to telemetric heart rhythm monitoring and provocation testing on day 11, 1 h after the last injection (see Section 2). Results were compared to arrhythmia incidence in the same mice subjected to the same provocation testing prior to bortezomib therapy. A decrease in arrhythmia incidence was observed in D307H mice following bortezomib treatment. However, there was no protection of bortezomib against arrhythmia after epinephrine [0.5 μg/g] stimulation. There was no effect on arrhythmia in the KO group.

Numbers represent number of mice having a given type of arrhythmia. Abbreviations: Epi: epinephrine; PVC: premature ventricular contraction, VT, ventricular tachycardia; D307H, CASQ2D307H/D307H; CASQ2Δ/Δ, KO; wild type, WT. p <0.05 *