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Since the beginning of the COVID-19 pandemic, SARS-CoV-2 has caused a global burden for health care systems due to high morbidity and mortality rates, leading to caseloads that episodically surpass hospital resources. Due to different disease manifestations, the triage of patients at high risk for a poor outcome continues to be a major challenge for clinicians. The AIFELL score was developed as a simple decision instrument for emergency rooms to distinguish COVID-19 patients in severe disease stages from less severe COVID-19 and non-COVID-19 cases. In the present study, we aimed to evaluate the AIFELL score as a prediction tool for clinical deterioration and disease severity in hospitalized COVID-19 patients. During the second wave of the COVID-19 pandemic in Switzerland, we analyzed consecutively hospitalized patients at the Triemli Hospital Zurich from the end of November 2020 until mid-February 2021. Statistical analyses were performed for group comparisons and to evaluate significance. AIFELL scores of patients developing severe COVID-19 stages IIb and III during hospitalization were significantly higher upon admission compared to those patients not surpassing stages I and IIa. Group comparisons indicated significantly different AIFELL scores between each stage. In conclusion, the AIFELL score at admission was useful to predict the disease severity and progression in hospitalized COVID-19 patients.

© 2015 Elsevier Ltd. All rights reserved. Excessive proliferation of human pulmonary artery smooth muscle cells (HPASMC) is one of the major factors that trigger vascular remodeling in hypoxia induced pulmonary hypertension. Several studies have implicated that hypoxia inhibits the tumor suppressor p21 (CDKN1A). However the precise mechanism is unknown. The mouse model of hypoxia induced PH and in vitro experiments were used to assess the impact of microRNAs (miRNAs) on the expression of CDKN1A. In these experiments the miRNA family miR 130 was identified to regulate the expression of CDKN1A. Transfection of HPASMC with miR 130 decreased the expression of CDKN1A and in turn significantly increased smooth muscle proliferation. Conversely inhibition of miR 130 by anti miRs and seed blockers increased the expression of CDKN1A. Reporter gene analysis proved a direct miR 130 CDKN1A target interaction. Exposure of HPASMC to hypoxia was found to induce the expression of miR 130 with concomitant decrease of CDKN1A. These findings were confirmed in the mouse model of hypoxia induced pulmonary hypertension showing that the use of seed blockers against miR 130 restored the expression of CDKN1A. These data suggest that miRNA family miR 130 plays an important role in the repression of CDKN1A by hypoxia. miR 130 enhances hypoxia induced smooth muscle proliferation and might be involved in the development of right ventricular hypertrophy and vascular remodeling in pulmonary hypertension.

Background: Registries are important for real-life epidemiology on different pulmonary hypertension (PH) groups. Objective: To provide long-term data of the Swiss PH registry of 1998-2012. Methods: PH patients have been classified into 5 groups and registered upon written informed consent at 5 university and 8 associated hospitals since 1998. New York Heart Association (NYHA) class, 6-min walk distance, hemodynamics and therapy were registered at baseline. Patients were regularly followed, and therapy and events (death, transplantation, endarterectomy or loss to follow-up) registered. The data were stratified according to the time of diagnosis into prevalent before 2000 and incident during 2000-2004, 2005-2008 and 2009-2012. Results: From 996 (53% female) PH patients, 549 had pulmonary arterial hypertension (PAH), 36 PH due to left heart disease, 127 due to lung disease, 249 to chronic thromboembolic PH (CTEPH) and 35 to miscellaneous PH. Age and BMI significantly increased over time, whereas hemodynamic severity decreased. Overall, event-free survival was 84, 72, 64 and 58% for the years 1-4 and similar for time periods since 2000, but better during the more recent periods for PAH and CTEPH. Of all PAH cases, 89% had target medical therapy and 43% combination therapy. Of CTEPH patients, 14 and 2% underwent pulmonary endarterectomy or transplantation, respectively; 87% were treated with PAH target therapy. Conclusion: Since 2000, the incident Swiss PH patients registered were older, hemodynamically better and mostly treated with PAH target therapies. Survival has been better for PAH and CTEPH diagnosed since 2008 compared with earlier diagnosis or other classifications.

Pulmonary hypertension is defined as an increase of the mean pulmonary arterial pressure above 25 mm Hg and as such the diagnosis requires invasive haemo­ dynamic measurement by right heart catheterisation. More than just a single disease pulmonary hyperten­ sion is an umbrella term that includes many different disorders and pathophysiological entities. However most forms of pulmonary hypertension share a final common pathway in particular the trias of vasocon­ striction microthrombosis and vascular remodelling. The classification of pulmonary hypertension has been subjected to many changes within the last decade. At the same time major achievements in our understand­ ing of the complex pathobiology have been made. Here these developments are discussed in the light of the re­ cently published report from the fifth World Sympo­ sium on pulmonary hypertension.

Levels of microRNAs (miRNAs) are increasingly assessed in biological fluids, for example, in samples obtained by bronchoalveolar lavage (BAL). "Post-collection kinetics" of miRNA expression levels, however, have not been investigated to date. In these experiments, we analyzed the dynamic expression profile of 5 different miRNAs (miR-17, miR-19b, miR-20b, miR-125a, and miR-223-3p) in BAL within the first 24 h following collection by routine bronchoscopy. miRNAs were quantified 0, 1, 4, 8, and 24 h after collection in samples that were kept at 4 °C or at room temperature. The expression of all five miRNAs was found to remain stable between the first 8 h after collection. 24 h after collection miRNAs faced substantial alterations in their expression profile. These data emphasize that BAL samples intended for further miRNA analysis can be handled at room temperature within the first 8 h after bronchoscopy.

The role of differential cytology patterns in peripheral blood and bronchoalveolar lavage samples is increasingly investigated as a potential adjunct to diagnose acute and chronic allograft dysfunction after lung transplantation. While these profiles might facilitate the diagnosis of acute cellular rejection, low sensitivity and specificity of these patterns limit direct translation in a clinical setting. In this context, the identification of other biomarkers is needed. This review article gives an overview of cytokine profiles of plasma and bronchoalveolar lavage samples during acute cellular rejection. The value of these cytokines in supporting the diagnosis of acute cellular rejection is discussed. Current findings on the topic are highlighted and experimental settings for future research projects are identified.

Diagnosis of acute lung allograft rejection is currently based on transbronchial lung biopsies. Additional methods to detect acute allograft dysfunction derived from plasma and bronchoalveolar lavage samples might facilitate diagnosis and ultimately improve allograft survival. This review article gives an overview of the cell profiles of bronchoalveolar lavage and plasma samples during acute lung allograft rejection. The value of these cells and changes within the pattern of differential cytology to support the diagnosis of acute lung allograft rejection is discussed. Current findings on the topic are highlighted and trends for future research are identified.

Pulmonary hypertension is an " umbrella term" used for a spectrum of entities resulting in an elevation of the pulmonary arterial pressure. Clinical symptoms include dyspnea and fatigue which in the absence of adequate therapeutic intervention may lead to progressive right heart failure and death. The pathogenesis of pulmonary hypertension is characterized by three major processes including vasoconstriction vascular remodeling and microthrombotic events. In addition accumulating evidence point to a cytokine driven inflammatory process as a major contributor to the development of pulmonary hypertension.This review summarizes the latest clinical and experimental developments in inflammation associated with pulmonary hypertension with special focus on Interleukin 6 and its role in vascular remodeling in pulmonary hypertension. © 2014 Groth et al.; licensee BioMed Central Ltd.