Treat or Not Treat COVID-19 with Combined Renin–Angiotensin System and Neprilysin Inhibition: Have We Found a Solution?
Bibliographic record
Abstract
Since 2019, coronavirus disease 2019 (COVID-19) has affected millions of individuals worldwide, leading to multiple deaths and numerous long-term multiorgan sequelae.In patients with COVID-19, cardiovascular diseases, including heart failure (HF), are common and associated with an increased risk for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections 1 and high mortality rates. 2 Epidemiological data revealed that prevalent HF was an independent predictor of increased in-hospital mortality 2 : in an Italian cohort, nearly 42% of patients with known HF who had been hospitalized with COVID-19 died during hospitalization.2 Although SARS-CoV-2 infection affects primarily the respiratory system, infected individuals can develop multiple de-novo cardiovascular complications, including HF, 3 arrhythmia, acute coronary syndrome or (peri-) myocarditis.4 Persistent cardiac injury, defined as long-term high-sensitivity cardiac troponin T (hs-cTnT) elevation or persistent abnormalities in cardiac magnetic resonance 3 -even after the primary SARS-CoV-2 infection was cured-has been described.3 Proposed underlying mechanisms include activation of inflammatory and thrombotic cascades, 1 direct viral infiltration or emerging/worsening of underlying baseline myocardial structural or atherosclerotic abnormalities. 1 In a detailed review of the European Society of Cardiology task force for the management of COVID-19, 5,6 the dysregulation of angiotensin-converting enzyme (ACE)/ACE2 system due to direct SARS-CoV-2 interaction is highlighted as one of the central pathways.7 In brief, SARS-CoV-2 binds to the ACE2 receptor-located among others on myocytes-to mediate cellular internalization (Figure 1).7,8 Thus, viral infiltration can lead to inflammation, cardiac fibrosis and direct cardiac damage by microvascular and macrovascular dysfunction (e.g.myocarditis with consequent arrhythmias or HF). 5 In combination with immune over-reactivity or 'cytokine storm', these processes can destabilize atherosclerotic plaques resulting in acute coronary syndrome.
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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 | 0.004 | 0.008 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.003 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.002 | 0.003 |
| Open science | 0.002 | 0.001 |
| Research integrity | 0.004 | 0.006 |
| Insufficient payload (model declined to judge) | 0.007 | 0.003 |
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".