Athletic Status and Arrhythmogenic Right Ventricular Dysplasia/ Cardiomyopathy: From Physiological Observations to Pathological Explanation
Bibliographic record
Abstract
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a heritable condition characterized by replacement of cardiomyocytes, primarily in the right ventricle, by fibrofatty tissue. A number of genetic studies have identified mutations in various components of cardiac desmosomes that appear to precede fibrofatty replacement. The resulting disruption of normal myocardial architecture in ARVD/C results in right ventricular (RV) dysfunction, life-threatening arrhythmias and sudden cardiac death. There is a striking incidence of athletic individuals affected by this disease. Currently there is no explanation for the association between athletic activity and development of ARVD/C. The goal of this paper is to suggest that increased levels of nitric oxide (NO) and reactive oxygen species, secondary to endurance exercise, initiates a cascade of reactions leading to fibrofatty changes in the RV and thus ARVD/C. This involves increased expression of adipogenic and fibrogenic genes as one of the steps in pathogenesis. According to the hypothesis, arrhythmias can happen in the presence or absence of pathological changes secondary to NO effects on remodeling and ion channels, respectively. Furthermore, the different effects of prolonged exercise on the RV and left ventricle (LV) could help explain the incidence of ARVD/C as a primarily RV disease. Verification of this hypothesis would have prognostic and management implications. Drugs inhibiting NO production might benefit patients with ARVD/C. A better understanding of exercise physiology in terms of NO production would help to redefine the management scheme in terms of exercise in patients with ARVD/C. A redirection of research towards identification of special physiological markers would be appropriate, and may reveal additional steps leading from tissue exposure to NO, to pathological changes.
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) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.002 |
| 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 | 0.000 |
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 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".