Key result
Scn5a+/- mice exhibited ventricular arrhythmias, ST elevation, and conduction disorders including increased QT dispersion, establishing them as a suitable model for Brugada syndrome.
Why the study?
Does administration of flecainide and quinidine alter ECG properties in Scn5a+/- mice modeling Brugada syndrome?
Does administration of flecainide and quinidine alter ECG properties in Scn5a+/- mice modeling Brugada syndrome?
The Scn5a+/- mouse serves as a suitable in vivo model for Brugada syndrome, demonstrating that altered QT dispersion may indicate increased transmural repolarization gradients useful for risk stratification.
Answers are grounded in this paper and cite their sources.
Should not yet change Brugada practice; extends preclinical modeling but leaves QT dispersion utility open.
OBJECTIVES: We investigate the extent to which the electrocardiographic (ECG) properties of intact Scn5a+/- mice reproduce the corresponding clinical Brugada syndrome phenotype and use this model to investigate the role of conduction and repolarization abnormalities in the arrhythmogenic mechanism. METHODS AND RESULTS: The ECGs were obtained from anesthetized wild-type and Scn5a+/- mice, before and after administration of the known pro- and antiarrhythmic agents flecainide and quinidine. The ECG intervals were measured and their dispersions calculated. Scn5a+/- hearts showed ventricular arrhythmias, ST elevation, and conduction disorders including increased QT dispersion, accentuated by flecainide. Quinidine did not cause ventricular arrhythmias but exerted variable effects on ST segments and worsened conduction abnormalities. CONCLUSIONS: The ECG features in an Scn5a+/- mouse establish it as a suitable model for Brugada syndrome and demonstrate abnormal conduction and repolarization phenomena. Altered QT dispersion, taken to indicate increased transmural repolarization gradients, may be useful in clinical risk stratification.
No takes yet. Share an insight, caveat, or question.
Martin et al. (2010) studied Brugada syndrome. Scn5a+/- genotype vs. Wild-type genotype was evaluated on ECG intervals, dispersions, ventricular arrhythmias, and ST elevation. Scn5a+/- mice exhibited ventricular arrhythmias, ST elevation, and conduction disorders including increased QT dispersion, establishing them as a suitable model for Brugada syndrome.
Synapse has enriched 10 related papers. Consider them for comparative context: