Currently, the most widely recognized mechanism is that HCN channels expression is abnormally increased in the ventricles during ventricular dilatation, myocardial infarction, and HF, and the enhancement of If current causes increased ventricular autorhythmicity, which leads to the occurrence of ventricular tachyarrhythmia (39). This evidence concerns the gene MALAT1 and Ventriculomegaly.