ArticleExpert review of cardiovascular therapy2010
Novel insights into the cellular basis of atrial fibrillation.
Article in Expert review of cardiovascular therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
5 citing papers in PubMed, 5 citations in OpenAlex.
- Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?Cells · 2022Article
- Misinterpretation of the mouse ECG: 'musing the waves of Mus musculus'.The Journal of physiology · 2014Review
- Isolating primary melanocyte-like cells from the mouse heart.Journal of visualized experiments : JoVE · 2014Article
- Atrial fibrillation in the elderly: the potential contribution of reactive oxygen species.Journal of geriatric cardiology : JGC · 2012Article
- New Biparietal Bipolar Catheter Prototype for Hybrid Atrial Fibrillation Ablation.Innovations (Philadelphia, Pa.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Atrial fibrillation is the most common clinical cardiac arrhythmia. It is often initiated by ectopic beats arising from the pulmonary veins and atria. While pulmonary vein myocytes most likely contribute to atrial ectopic beats initiating atrial fibrillation, emerging evidence suggests the existence of other cell populations that may also contribute to atrial arrhythmias. In addition to sinus node-like and intestinal Cajal-like cells, we recently characterized a novel, melanocyte-like cell population in murine and human hearts that may contribute to atrial arrhythmogenic triggers in mice. Murine cardiac melanocyte-like cells are electrically excitable, and express adrenergic and muscarinic receptors. Adult mice lacking the gene encoding dopachrome tautomerase (Dct) are susceptible to atrial arrhythmias, and Dct is expressed by both murine and human cardiac melanocytes. While Dct-expressing cells are present in human hearts in regions from which atrial arrhythmias often arise, the contribution of these cells to clinical atrial arrhythmias remains to be determined.
Indexed as
Identifiers
What OpenQuestion holds
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.