Key result
Mice lacking Connexin40 (Cx40-/-) exhibited increased susceptibility to atrial tachyarrhythmias (50% vs 0%) and a 30% reduction in atrial conduction velocity compared to wild-type mice.
Why the study?
Does the lack of gap junction protein Connexin40 alter cardiac conduction and arrhythmia susceptibility in mice?
Population
Mice lacking the gap junction protein connexin40, wild type, and heterozygous mice
Comparison
Genetic knockout of Connexin40 (Cx40-/-) vs Wild type mice and heterozygous mice
Design
Preclinical
Authors
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Cx40 loss promotes atrial arrhythmogenesis in mice; leaves open its role and therapeutic targeting in human AF.
Does the lack of gap junction protein Connexin40 alter cardiac conduction and arrhythmia susceptibility in mice?
Absolute Event Rate: 50% vs 0%
Connexin40 is a critical determinant of atrial and AV conduction, and its absence increases susceptibility to atrial tachyarrhythmias in a murine model.
Verheule et al. (1999) studied Cardiac conduction abnormalities (n=19). Connexin40 knockout (Cx40-/-) vs. Wild type (Cx40+/+) and heterozygous (Cx40+/-) mice was evaluated on Atrial tachyarrhythmias induced by atrial burst pacing. Mice lacking Connexin40 (Cx40-/-) exhibited increased susceptibility to atrial tachyarrhythmias (50% vs 0%) and a 30% reduction in atrial conduction velocity compared to wild-type mice.
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