AI Article Synopsis
- The SCN5A gene is crucial for heart function, and mutations can lead to serious heart rhythm issues.
- In a study using transgenic mice that overexpress SCN5A, key cardiac metrics like heart rate and QRS duration did not change compared to normal mice.
- However, TG-WT mice showed a shorter P wave and PR interval on ECGs, indicating irregularities in heart electrical activity, along with more frequent premature atrial contractions.
Article Abstract
The Cardiac sodium channel gene SCN5A plays a critical role in cardiac electrophysiology and its mutations, either gain- or loss-of-functions, are associated with lethal arrhythmias. In this study, we investigated the effect of overexpression of SCN5A on the cardiac phenotype in a transgenic mouse model (TG-WT L10). Compared to NTG mice, heart rate, QRS duration, and QT intervals remained unchanged in TG-WT mice. Moreover, no spontaneous ventricular arrhythmias were detected in TG-WT hearts. Despite these results, a mild, irregular cardiac phenotype was observed in TG-WT mice. The P wave and PR interval were significantly shorter in TG-WT compared with NTG mice (P, 8.8+/-0.8 ms vs. 12.6+/-0.9 ms; PR, 12.5+/-2 ms vs. 33.5+/-0.7 ms). Furthermore, spontaneous premature atrial contractions were often detected in TG-WT mice. These results suggest that the expression level of the SCN5A gene is a determinant for the length of the P wave duration and PR interval on electrocardiograms (ECG).
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885482 | PMC |
| http://dx.doi.org/10.1016/j.bbrc.2007.01.170 | DOI Listing |
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