Left ventricular dysfunction: causes, natural history, and hopes for reversal
Bibliographic record
Abstract
Left ventricular dysfunction (LVD) with subsequent congestive heart failure (CHF) constitutes the final common pathway for a host of cardiac disorders. Coronary artery narrowing or ischaemic heart disease is the dominant cause of heart failure and is often associated with acute or prior myocardial infarction. The remaining aetiologies include cardiomyopathy, hypertension, and a variety of other factors such as valve disease or myocarditis. Heart failure is an enormous problem. Data from the Framingham heart study shows that it develops in approximately 16% of men and 18% of women who have diabetes; 12% of men and 8% of women who have hypertension; and 30% of both sexes who have myocardial infarction.1 Interestingly, over the second half of the 20th century there has been a striking increase in the frequency of coronary artery disease and diabetes as aetiological factors for CHF, whereas the impact of hypertension and rheumatic valve disease has declined. LVD produces many changes in the structure and function of the heart through a variety of mechanisms. The muscle of the heart is encased in a collagen weave. There are interstitial spaces that are associated with a variety of elements, a number of which can contribute to the development of CHF. The extracellular matrix has a scaffolding function, which supports myocytes and blood vessels. It also provides lateral connections between the cells and muscular bundles that govern not only the architecture of the heart, but also its ability to contract. Moreover, the extracellular matrix contributes to the heart's tensile strength and resilience, which helps resist deformation, maintaining the elliptical shape of the heart and its thickness. Once left ventricular dysfunction occurs a series of compensatory mechanisms are triggered which lead to a host of …
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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 | 0.001 | 0.003 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.002 | 0.003 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.002 | 0.002 |
| Insufficient payload (model declined to judge) | 0.004 | 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".