New insights into the molecular basis of atrial fibrillation: mechanistic and therapeutic implications
Bibliographic record
Abstract
This editorial refers to a collection of nine reviews and nine original articles that are part of this special issue on atrial fibrillation, guest edited by Dobromir Dobrev and Stanley Nattel. Atrial fibrillation (AF), the most common sustained arrhythmia, is associated with substantial cardiovascular morbidity and mortality, with stroke being the most critical complication.1 Present drugs used for AF therapy have major limitations, including incomplete efficacy and risks of life-threatening proarrhythmic events and bleeding complications.1,2 Non-pharmacological ablation procedures are efficient and relatively safe, but the very large size of the patient population allows ablation treatment of only a small number of patients. Therefore, drug therapy remains the mainstay of AF treatment. Maintenance of sinus rhythm (rhythm control) appears preferable, but studies to date have failed to demonstrate tangible advantages of rhythm control. The failure to show benefits in mortality and stroke incidence motivates attempts to identify new therapeutic targets relating to basic mechanisms underlying arrhythmia susceptibility. A better mechanistic understanding of the molecular basis of AF may allow for the development of safer and more effective treatment approaches. The mechanisms underlying AF susceptibility are multiple and incompletely understood. The two major determinants of AF maintenance are reentry and ectopic impulse formation (ectopic activity).3 Reentry induction requires an appropriate arrhythmogenic substrate and a trigger that initiates reentry within the substrate. The likelihood of reentry is determined by the tissue properties of conduction and refractoriness, with slow conduction and short refractoriness making persistence of reentry more likely. Ectopic activity is governed by factors controlling the occurrence of afterdepolarizations, primarily Ca2+ handling abnormalities that can cause early and delayed afterdepolarizations. The changes in atrial structure and function that result from heart disease, and indeed AF itself, constitute atrial remodelling and are key elements of the …
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.002 | 0.002 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.002 |
| Bibliometrics | 0.000 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".