ReviewCurrent cardiology reviews2025
A New Mechanism of Supraventricular Tachycardia: Gene Mutation.
Review in Current cardiology reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Environmental Exposures and Epigenetic Remodeling in Supraventricular Tachycardias: What Atrial Fibrillation Can and Cannot Tell Us.Life (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
backgroundSupraventricular 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.
methodsThrough analysis of epidemiology, familial clustering, and gene mutations of the relevant literature, the review elucidates the genetic properties and potential pathophysiology of SVT.
resultsThere 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.
conclusionSVT 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.
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