During bradycardia, particularly in pathological conditions, such as myocardial infarction, heart failure, and ventricular hypertrophy, the pathological upregulation of Nav1.8-mediated INa,L significantly elevates the risk of arrhythmias at slow heart rates, with this effect being most prominent in M cells and Purkinje fibers. This evidence concerns the gene SCN10A and Ventricular hypertrophy.