SARS-CoV-2 targets endothelial cells through the angiotensin-converting enzyme 2 receptor. The resulting endothelial injury induces widespread thrombosis and microangiopathy. Nevertheless, early specific markers of endothelial dysfunction and vascular redox status in COVID-19 patients are currently missing. Observational study including ICU and non-ICU adult COVID-19 patients admitted in hospital for acute respiratory failure, compared with control subjects matched for cardiovascular risk factors similar to ICU COVID-19 patients, and ICU septic shock patients unrelated to COVID-19. Early SARS-CoV-2 infection was associated with an imbalance between an exacerbated oxidative stress (plasma peroxides levels in ICU patients vs. controls: 1456.0 ± 400.2 vs 436 ± 272.1 mmol/L; P < 0.05) and a reduced nitric oxide bioavailability proportional to disease severity (5-α-nitrosyl-hemoglobin, HbNO in ICU patients vs. controls: 116.1 ± 62.1 vs. 163.3 ± 46.7 nmol/L; P < 0.05). HbNO levels correlated with oxygenation parameters (PaO₂/FiO₂ ratio) in COVID-19 patients (R² = 0.13; P < 0.05). Plasma levels of angiotensin II, aldosterone, renin or serum level of TREM-1 ruled out any hyper-activation of the renin-angiotensin-aldosterone system or leucocyte respiratory burst in ICU COVID-19 patients, contrary to septic patients. Endothelial oxidative stress with ensuing decreased NO bioavailability appears as a likely pathogenic factor of endothelial dysfunction in ICU COVID-19 patients. A correlation between NO bioavailability and oxygenation parameters is observed in hospitalized COVID-19 patients. These results highlight an urgent need for oriented research leading to a better understanding of the specific endothelial oxidative stress that occurs during SARS-CoV-2. Stated in the acknowledgments section.

Purpose of review: To highlight the importance of frailty assessment in thoracic surgery patients. Recent findings: Frailty results from an accelerated loss of functional reserve associated with ageing and leads to increased vulnerability following surgery. It is a complex and multidimensional syndrome involving physiological and psychosocial systems. Frailty is a separate entity from comorbidities and disabilities. Frailty is associated with an increased risk of complications and a higher mortality rate after thoracic surgery. Patients can easily be screened for frailty and frail patients can benefit from further assessment of all areas of frailty secondarily. Prehabilitation and rehabilitation can help limit frailty-related complications after thoracic surgery. Summary: Frailty should be part of the routine preoperative evaluation for thoracic surgery. Frailty must be considered in assessing eligibility for surgery and in planning prehabilitation and rehabilitation if necessary.

Background: Neutrophil extracellular traps’ (NETs’) formation is a mechanism of defense that neutrophils deploy as an alternative to phagocytosis, to constrain the spread of microorganisms. Aim: The aim was to evaluate biomarkers of NETs’ formation in a patient cohort admitted to intensive care unit (ICU) due to infection. Methods: Forty-six septic shock patients, 22 critical COVID-19 patients and 48 matched control subjects were recruited. Intact nucleosomes containing histone 3.1 (Nu.H3.1), or citrullinated histone H3R8 (Nu.Cit-H3R8), free citrullinated histone (Cit-H3), neutrophil elastase (NE) and myeloperoxidase (MPO) were measured. Results: Significant differences in Nu.H3.1 and NE levels were observed between septic shock and critical COVID-19 subjects as well as with controls (p-values < 0.05). The normalization of nucleosome levels according to the neutrophil count improved the discrimination between septic shock and critical COVID-19 patients. The ratio of Nu.Cit-H3R8 to Nu.H3.1 allowed the determination of nucleosome citrullination degree, presumably by PAD4. Conclusions: H3.1 and Cit-H3R8 nucleosomes appear to be interesting markers of global cell death and neutrophil activation when combined. Nu.H3.1 permits the evaluation of disease severity and differs between septic shock and critical COVID-19 patients, reflecting two distinct potential pathological processes in these conditions.

Severe forms of coronavirus 2019 (COVID-19) disease are caused by an exaggerated systemic inflammatory response and subsequent inflammation-related coagulopathy. Anti-inflammatory treatment with low dose dexamethasone has been shown to reduce mortality in COVID-19 patients requiring oxygen therapy. However, the mechanisms of action of corticosteroids have not been extensively studied in critically ill patients in the context of COVID-19. Plasma biomarkers of inflammatory and immune responses, endothelial and platelet activation, neutrophil extracellular trap formation, and coagulopathy were compared between patients treated or not by systemic dexamethasone for severe forms of COVID-19. Dexamethasone treatment significantly reduced the inflammatory and lymphoid immune response in critical COVID-19 patients but had little effect on the myeloid immune response and no effect on endothelial activation, platelet activation, neutrophil extracellular trap formation, and coagulopathy. The benefits of low dose dexamethasone on outcome in critical COVID-19 can be partially explained by a modulation of the inflammatory response but not by reduction of coagulopathy. Future studies should explore the impact of combining dexamethasone with other immunomodulatory or anticoagulant drugs in severe COVID-19.

Background: The triage of patients presenting with chest pain on admission to the emergency department uses scales based on patient clinical presentation or an electrocardiogram (ECG). These scales have different sensitivity and specificity. Although a good sensitivity allows for the prompt identification of high-risk patients, specificity prevent ED overcrowding. Moreover, ECG at triage avoids missing ST elevation myocardial infarction, which requires urgent revascularization. Our study therefore aimed to investigate whether a scale combining ECG and cardiovascular risk factors (CVRF) improves the diagnostic performance of ED chest pain triage scale. Methods and results: In this prospective single-center observational study involving 505 patients, the standard ECG-based FRENCH scale was compared to a scale combining the ECG-based FRENCH scale and the patients CVRF. The new scale was called the “modified” FRENCH. The accuracy of patient CVRF collection was evaluated by comparing the results of triage nurses and ED physicians. Compared with the standard FRENCH scale, the modified FRENCH scale had an increased sensitivity (61% versus 75%) but a decrease in specificity (76% versus 64%) resulting in a similar diagnostic performance. Using CVRF collected by the ED physicians, the modified FRENCH scale had a sensitivity of 87% and a specificity of 56% with a significant improvement in his diagnostic performance compared with standard FRENCH scales. This improvement can be explained by an accurate collection of the CVRF by physicians compared with nurses, as suggested by the weak to moderate correlation between their respective data collection. Conclusion: In conclusion, combining ECG and accurately collected cardiovascular risks factor improves the diagnostic performance of the ECG based chest pain triage in the ED. Trial registration: Trial registration number: NCT03913767.