Background: A debate about the scientific quality of COVID-19 themed research has emerged. We explored whether the quality of evidence of COVID-19 publications is lower when compared to nonCOVID-19 publications in the three highest ranked scientific medical journals.Methods: We searched the PubMed Database from March 12 to April 12, 2020 and identified 559 publications in the New England Journal of Medicine, the Journal of the American Medical Association, and The Lancet which were divided into COVID-19 (cases, n = 204) and nonCOVID-19 (controls, n = 355) associated content. After exclusion of secondary, unauthored, response letters and non-matching article types, 155 COVID-19 publications (including 13 original articles) and 130 nonCOVID-19 publications (including 52 original articles) were included in the comparative analysis. The hierarchical level of evidence was determined for each publication included and compared between cases and controls as the main outcome. A quantitative scoring of quality was carried out for the subgroup of original articles. The numbers of authors and citation rates were also compared between groups.Results: The 130 nonCOVID-19 publications were associated with higher levels of evidence on the level of evidence pyramid, with a strong association measure (Cramer’s V: 0.452, P <0.001). The 155 COVID-19 publications were 186-fold more likely to be of lower evidence (95% confidence interval [CI] for odds ratio, 7.0–47; P <0.001). The quantitative quality score (maximum possible score, 28) was significantly different in favor of nonCOVID-19 (mean difference, 11.1; 95% CI, 8.5–13.7; P <0.001). There was a significant difference in the early citation rate of the original articles that favored the COVID-19 original articles (median [interquartile range], 45 [30–244] vs. 2 [1–4] citations; P <0.001).Conclusions: We conclude that the quality of COVID-19 publications in the three highest ranked scientific medical journals is below the quality average of these journals. These findings need to be verified at a later stage of the pandemic.

Summary: Pulmonary aspiration of gastric content is a significant cause of anaesthesia‐related morbidity and mortality. High‐quality prospective randomised evidence to support prevention strategies, such as rapid sequence intubation, is difficult to generate due to well‐described practical, ethical and methodological barriers. We aimed to generate an understanding of worldwide practice through surveying clinically practicing anaesthetists and airway experts. Our survey was designed to assess the influence of: departmental standards; patient factors; socio‐economic factors; training; and supervision. We surveyed 10,003 anaesthetists who responded to an invitation to participate on LinkedIn. We then surveyed 16 international airway experts on the same content. When asked about a hypothetical patient with intestinal obstruction, respondents expressed preferences for [OR (95% CI )]: the head‐up or ‐down position 4.26 (3.98–4.55), p < 0.001; nasogastric tube insertion 29.5 (26.9–32.3), p < 0.001; and the use of cricoid force 2.80 (2.62–3.00), p < 0.001, as compared with a hypothetical patient without intestinal obstruction also requiring rapid sequence intubation. Respondents from lower income countries were more likely to prefer [OR (95% CI ]: the supine position 2.33 (2.00–2.63), p < 0.001; nasogastric tube insertion 1.29 (1.09–1.51), p = 0.002; and cricoid force application 2.54 (2.09–3.09), p < 0.001 as compared with respondents from higher income countries for a hypothetical patient with intestinal obstruction. This survey, which we believe is the largest of its kind, demonstrates that preferences for positioning, nasogastric tube use and cricoid force application during rapid sequence intubation vary substantially. Achieving agreed consensus may yield better training in the principles of rapid sequence intubation.

Since its introduction, the number of heart surgeries has risen continuously. It is a high-risk procedure, usually involving cardiopulmonary bypass, which is associated with an inflammatory reaction that can lead to perioperative and postoperative organ dysfunction. The extent of complications following cardiac surgery has been the focus of interest for several years because of their impact on patient outcomes. Recently, numerous scientific efforts have been made to uncover the complex mechanisms of interaction between inflammation, oxidative stress, and endothelial dysfunction that occur after cardiac surgery. Numerous factors, such as surgical and anesthetic techniques, hypervolemia and hypovolemia, hypothermia, and various drugs used during cardiac surgery trigger the development of systemic inflammatory response and the release of oxidative species. They affect the endothelium, especially endothelial glycocalyx (EG), a thin surface endothelial layer responsible for vascular hemostasis, its permeability and the interaction between leukocytes and endothelium. This review highlights the current knowledge of the molecular mechanisms involved in endothelial dysfunction, particularly in the degradation of EG. In addition, the major inflammatory events and oxidative stress responses that occur in cardiac surgery, their interaction with EG, and the clinical implications of these events have been summarized and discussed in detail. A better understanding of the complex molecular mechanisms underlying cardiac surgery, leading to endothelial dysfunction, is needed to improve patient management during and after surgery and to develop effective strategies to prevent adverse outcomes that complicate recovery.

Cardiac surgery is one of the highest-risk procedures, usually involving cardiopulmonary bypass and commonly inducing endothelial injury that contributes to the development of perioperative and postoperative organ dysfunction. Substantial scientific efforts are being made to unravel the complex interaction of biomolecules involved in endothelial dysfunction to find new therapeutic targets and biomarkers and to develop therapeutic strategies to protect and restore the endothelium. This review highlights the current state-of-the-art knowledge on the structure and function of the endothelial glycocalyx and mechanisms of endothelial glycocalyx shedding in cardiac surgery. Particular emphasis is placed on potential strategies to protect and restore the endothelial glycocalyx in cardiac surgery. In addition, we have summarized and elaborated the latest evidence on conventional and potential biomarkers of endothelial dysfunction to provide a comprehensive synthesis of crucial mechanisms of endothelial dysfunction in patients undergoing cardiac surgery, and to highlight their clinical implications.

Surgical myocardial revascularization, regardless of the technique used, causes ischemia–reperfusion injury (IRI) in the myocardium mediated by inflammation and degradation of the endothelial glycocalyx (EG). We investigated the difference between on-pump and off-pump techniques in terms of the concentration of proinflammatory interleukin (IL)-18 and the EG degradation products syndecan-1 and hyaluronic acid measured by ELISA in the peripheral and cardiac circulation during open heart surgery and in the early postoperative period. The concentration of IL-18, C-reactive protein (CRP), and cardiac troponin T (cTnT) and the leukocyte count increased statistically significantly in revascularized patients at 24 and 72 h after revascularization compared to the beginning of the procedure and was always statistically significantly higher in on-pump patients. Syndecan-1 and hyaluronic acid only increased in on-pump patients 24 and 72 h after revascularization. IL-18 correlated positively with syndecan-1 and CRP only in the pump setting and with the number of leukocytes in both revascularization regimens 24 and 72 h after the surgery. cTnT and hyaluronic acid did not correlate with IL-18. Our results suggest that IL-18 plays an important role in the early inflammatory response in patients during open heart surgery and in the early postoperative period, leading to additional damage to the EG, while it is probably not responsible for myocardial necrosis. It could serve as a biomarker to identify high-risk patients and as a therapeutic target to reduce inflammation and EG degradation. In addition, measurement of IL-18 could help improve the treatment, recovery, and outcomes of patients after heart surgery.