Cardiac Electrical Remodeling in a Rat Model of Severe Pulmonary Arterial Hypertension and Right Heart Failure
Bibliographic record
Abstract
Abstract Background: Pulmonary arterial hypertension (PAH) is a progressive incurable disease with unclear etiology. Primary cause of death in PAH patients is right heart failure, occurring as a direct consequence of increased right ventricular (RV) afterload. Importantly, around 25% of deaths have been linked to cardiac arrhythmias. However, mechanisms underlying arrhythmia susceptibility in patients with elevated RV pressure remains unclear. In this study, we investigated electrophysiological remodeling of the heart during progressive PAH using the monocrotaline (MCT) rat model. Methods: Male Fischer CDF rats were treated with MCT (60 mg/kg, s.c.) or vehicle. Catheterization and echocardiography were performed at experimental endpoint (4 and 5 weeks post-MCT injection) to assess disease progression. Electrocardiogram was recorded in anesthetized rats after echocardiography to study electrical abnormality. At 4 and 5 weeks, hearts were excised, Langendorff-perfused, and action potentials (AP) were measured by optical mapping. Results: MCT treatment led to a progressive increase in RV systolic pressure at 4- and 5-week time-points, compared to controls. At 4-week post-MCT, we observed RV hypertrophy with preserved RV fractional shortening, cardiac index and RV internal diameter, indicating adaptive RV remodeling. Conversely, mal-adaptive RV remodeling was observed at 5-weeks post-MCT, as indicated by a decrease in RV fractional shortening and cardiac index, together with a marked increase in RV internal diameter. While no significant changes in AP duration or electrocardiogram parameters were observed at the 4-week time-point, repolarization was delayed after 5 weeks, which prolonged AP duration and the QT interval on the electrocardiogram. Conclusion: Transition from adaptive to mal-adaptive RV remodeling in PAH is associated with altered electrophysiology of the RV. These changes may contribute to increased susceptibility to arrhythmias and sudden death in PAH.
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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 | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| 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) | 0.002 | 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".