Mitral Valve Remodeling in Response to Atrial and Ventricular Changes: Mechanisms and Clinical Implications for Functional Mitral Regurgitation
Bibliographic record
Abstract
Mitral regurgitation (MR) is a frequent and heterogeneous disease associated with significant morbidity and mortality. Normal mitral valve closure requires a complex interplay between left ventricular shape and dynamics, papillary muscles, mitral annulus, and both mitral leaflets. Anomalies of the left ventricle or the left atrium can therefore cause functional mitral regurgitation (FMR), which can be improved by related therapeutic interventions. However, heart failure therapies (revascularization, resynchronization, and pharmacological treatment) are incomplete treatments for FMR, which remains frequent. Another key component in FMR is the valve itself, as the leaflets undergo significant changes in the process. Those changes can be beneficial and prevent FMR, or detrimental and contribute to valve dysfunction. Mitral valve remodeling starts with biological changes occurring at the cellular level and is ultimately reflected macroscopically by leaflet enlargement and/or thickening. This remodeling also modifies the biomechanical properties of the valve, critical for adequate coaptation. Some conditions result in adequate valve enlargement, which remains proportional with the annulus and ventricular sizes, preventing FMR despite significant myocardial disease. Other conditions, ischemic heart disease in particular, are associated with maladaptive valve changes with excessive thickening and fibrotic remodeling. This adverse evolution is associated with the presence of transforming growth factor beta in the leaflets, which can be influenced pharmacologically. Clinical observational studies and experimental works are suggesting potential therapeutic targets to prevent FMR by influencing the valve biology. While those interventions still require clinical validation, they could represent an entirely new strategy for this common and morbid disease.
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 machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 0.001 |
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 source (direct Gemma or distilled Codex), 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".