Background:Supraventricular tachycardia (SVT) is very common in daily clinical
practice, especially in the emergency department, with rapid onset and urgent management. The
review highlights the recent genetic predispositions and mechanisms in SVT.Methods:Through analysis of epidemiology, familial clustering, and gene mutations of the relevant
literature,the review elucidates the genetic properties and potential pathophysiology of
SVT.Results:There are many pathophysiological mechanisms related to atrioventricular node reentrant
tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Currently, there
is relatively little research on inappropriate sinus tachycardia (IST), atrial tachycardia (AT), and
congenital junctional ectopic tachycardia (CJET). It seems that every type of SVT has gene mutations
in ion channels, with three types of SVT having gene mutations in signaling pathways,
and others including gene mutations in beta-adrenergic-receptor autoantibodies, autonomic
nervous system, and AV node structure.Conclusion:SVT has certain genetic characteristics and is often associated with other heart
diseases. From the analysis of mutated genes in SVT, it appears to be a type of cardiac ion
channel disease. Unlike common ion channel diseases, it is more insidious and more susceptible
to external factors. The confirmation of the genetic basis of SVT provides direction for future
hazard stratification assessment and gene targeted therapy drug research.