Key result
RGS2 knockout mice were significantly more susceptible to electrically induced atrial tachycardia/fibrillation compared to wild-type mice (50% vs 4%, P<0.05).
Why the study?
Does RGS2 deficiency increase susceptibility to atrial arrhythmia in a mouse model?
Population
One-month-old male RGS2(-/-) and C57BL/6 wild-type (WT) mice (n=47)
Comparison
Knockout of RGS2 (RGS2(-/-)) vs C57BL/6 wild-type (WT) mice
Design
Preclinical
Authors
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RGS2 may regulate atrial arrhythmogenesis in mice; hypothesis-generating and should not yet influence clinical practice or human trials.
Does RGS2 deficiency increase susceptibility to atrial arrhythmia in a mouse model?
Absolute Event Rate: 50% vs 4%
p-value: p=<0.05
RGS2 deficiency in mice enhances susceptibility to atrial tachycardia/fibrillation via increased M3 muscarinic receptor activity, suggesting RGS2 is an important cholinergic regulator in the atrium.
Tuomi et al. (2009) studied Atrial fibrillation susceptibility (n=47). RGS2 knockout (RGS2(-/-)) vs. C57BL/6 wild-type (WT) mice was evaluated on Susceptibility to atrial tachycardia/fibrillation (AT/F) induction (p=<0.05). RGS2 knockout mice were significantly more susceptible to electrically induced atrial tachycardia/fibrillation compared to wild-type mice (50% vs 4%, P<0.05).
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