ArticleJACC. Clinical electrophysiology2020
Evidence of Superior and Inferior Sinoatrial Nodes in the Mammalian Heart.
Article in JACC. Clinical electrophysiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Publication guidelines for human heart rate and heart rate variability studies in psychophysiology-Part 1: Physiological underpinnings and foundations of measurement.Psychophysiology · 2024Guideline
- Sinoatrial Node Impulses Emerge From Unique Synchronization Processing Solutions of Partially Stochastic Local Calcium Signals.JACC. Clinical electrophysiology · 2026Article
- Localization and electrophysiological characterization of the dominant pacemaker in the adult chicken sinoatrial junction.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2026Article
- Regulation of Pacemaker Current in the Sinoatrial Node by Zonula Occludens-1.bioRxiv : the preprint server for biology · 2026Article
- Beat-locked ATP microdomains in the sinoatrial node map a Ca2+-timed energetic hierarchy and regional pacemaker roles.The Journal of general physiology · 2026Article
- Cardiac Pacemaker Cells Harness Stochastic Resonance to Ensure Fail-Safe Operation at Low Rates Bordering on Sinus Arrest.bioRxiv : the preprint server for biology · 2026Article
- Pacemaking in the heart: a redundant and robust system of mutually entrained oscillators driving cardiac automaticity.The Journal of physiology · 2026Review
- Stress-induced pacemaker desynchronization in the sinoatrial node.Frontiers in cardiovascular medicine · 2026Article
- Microvascular Rarefaction in the Sinoatrial Node: A Potential Mechanism for Pacemaker Dysfunction in Early HFpEF.JACC. Clinical electrophysiology · 2025Article
- Aging and sinus node dysfunction: mechanisms and future directions.Clinical science (London, England : 1979) · 2025Review
- Phasic effects of cardiac-synchronized vagus nerve stimulation on spatiotemporal behavior of the sinoatrial node in swine.Heart rhythm O2 · 2025Article
- Glucagon-like peptide-1 increases heart rate by a direct action on the sinus node.Cardiovascular research · 2024Article
- Pacemaker Channels and the Chronotropic Response in Health and Disease.Circulation research · 2024Review
- Sinoatrial node heterogeneity and fibroblasts increase atrial driving capability in a two-dimensional human computational model.Frontiers in physiology · 2024Article
- The mechano-electric feedback mediates the dual effect of stretch in mouse sinoatrial tissue.Journal of molecular and cellular cardiology plus · 2023Article
- What makes the sinoatrial node tick? A question not for the faint of heart.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Local tissue mechanics control cardiac pacemaker cell embryonic patterning.Life science alliance · 2023Article
- Emergent activity, heterogeneity, and robustness in a calcium feedback model of the sinoatrial node.Biophysical journal · 2023Article
- Synergy between Membrane Currents Prevents Severe Bradycardia in Mouse Sinoatrial Node Tissue.International journal of molecular sciences · 2023Article
- Sinus node dysfunction: current understanding and future directions.American journal of physiology. Heart and circulatory physiology · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesThis study sought to investigate the shift of leading pacemaker locations in healthy and failing mammalian hearts over the entire range of physiological heart rates (HRs), and to molecularly characterize spatial regions of spontaneous activity.
backgroundA normal heartbeat originates as an action potential in a group of pacemaker cells known as the sinoatrial node (SAN), located near the superior vena cava. HRs and the anatomical site of origin of pacemaker activity in the adult heart are known to dynamically change in response to various physiological inputs, yet the mechanism of this pacemaker shift is not well understood.
methodsOptical mapping was applied to ex vivo rat and human isolated right atrial tissues, and HRs were modulated with acetylcholine and isoproterenol. RNA sequencing was performed on tissue areas that elicited spontaneous activity, and comparisons were made to neighboring myocardial tissues.
resultsFunctional and molecular evidence identified and confirmed the presence of 2 competing right atrial pacemakers localized near the superior vena cava and the inferior vena cava-the superior SAN (sSAN) and inferior SAN (iSAN), respectively-which preferentially control the fast and slow HRs. Both of these regions were evident in non-failing rat and human hearts and maintained spontaneous activity in the rat heart when physically separated from one another. Molecular analysis of these 2 pacemaker regions revealed unique but similar transcriptional profiles, suggesting iSAN dominance when the sSAN is silent.
conclusionsThe presence of 2 spatially distinct dominant pacemakers, sSAN and iSAN, in the mammalian heart clarifies previous identification of migrating pacemakers and corresponding changes in P-wave morphology in mammalian species.
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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 Socratic graph.