ReviewTrends in cardiovascular medicine2014
Sinus node dysfunction in catecholaminergic polymorphic ventricular tachycardia: risk factor and potential therapeutic target?
Review in Trends in cardiovascular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Atropine-induced sinus tachycardia protects against exercise-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2020Trial
- Clinical and genetic analysis of pediatric catecholaminergic polymorphic ventricular tachycardia: focus on sinus bradycardia and neurodevelopmental disorders.Frontiers in pediatrics · 2026Article
- Familial risk of sinus node dysfunction indicating pacemaker implantation: a nationwide cohort study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Article
- Profiling Reduced Expression of Contractile and Mitochondrial mRNAs in the Human Sinoatrial Node vs. Right Atrium and Predicting Their Suppressed Expression by Transcription Factors and/or microRNAs.International journal of molecular sciences · 2024Article
- Catecholaminergic Polymorphic Ventricular Tachycardia: Clinical Characteristics, Diagnostic Evaluation and Therapeutic Strategies.Journal of clinical medicine · 2024Review
- Clinical characteristics and follow-up of complex arrhythmias associated withFrontiers in genetics · 2024Article
- Age-dependent contribution of intrinsic mechanisms to sinoatrial node function in humans.Scientific reports · 2023Article
- Human Sinoatrial Node Pacemaker Activity: Role of the Slow Component of the Delayed Rectifier KInternational journal of molecular sciences · 2023Article
- Molecular and tissue mechanisms of catecholaminergic polymorphic ventricular tachycardia.The Journal of physiology · 2020Review
- Chronotropic incompetence as a risk predictor in children and young adults with catecholaminergic polymorphic ventricular tachycardia.Journal of cardiovascular electrophysiology · 2019Article
- Gene Therapy for Catecholaminergic Polymorphic Ventricular Tachycardia by Inhibition of CaCirculation · 2019Article
- SK4 KEMBO molecular medicine · 2017Article
- Tachycardia-bradycardia syndrome: Electrophysiological mechanisms and future therapeutic approaches (Review).International journal of molecular medicine · 2017Review
- Atrial arrhythmias in inherited arrhythmogenic disorders.Journal of arrhythmia · 2016Review
- STIM1-Ca2+ signaling modulates automaticity of the mouse sinoatrial node.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A case of catecholaminergic polymorphic ventricular tachycardia masquerading as an intractable seizure.Annals of pediatric cardiologyArticle
- Catecholaminergic polymorphic ventricular tachycardia: An exciting new era.Annals of pediatric cardiologyReview
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 at 2 institutions in 3 countries.
Funding
Abstract
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited heart rhythm disorder characterized by the occurrence of potentially life-threatening polymorphic ventricular tachyarrhythmias in conditions of physical or emotional stress. The underlying cause is a dysregulation in intracellular Ca handling due to mutations in the sarcoplasmic reticulum Ca release unit. Recent experimental work suggests that sinus bradycardia, which is sometimes observed in CPVT patients, may be another primary defect caused by CPVT mutations. Herein, we review the pathophysiology of CPVT and discuss the role of sinus node dysfunction as a modulator of arrhythmia risk and potential therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.