Arrhythmogenic consequences of Na+ channel mutations in the transmurally heterogeneous mammalian left ventricle: Analysis of the I1768V SCN5A mutation

Our findings suggest that an increase in sustained inward Na+ current arising from the I1768V SCN5A mutation leads to clinically relevant arrhythmias in the transmurally heterogeneous canine left ventricular myocardium. This novel approach for simulating transmural heterogeneity provides new insight into the development of rhythm disturbances in the mammalian left ventricle.