Association of endothelial activation assessed through endothelin-I precursor peptide measurement with mortality in COVID-19 patients: an observational analysis

Respiratory Research

Luca Bernasconi¹  Angelika Hammerer-Lercher¹  Alexander Kutz²  Daniel Koch²  Selina Wolfisberg²  Claudia Gregoriano²  Dominik Damm²  Sebastian Haubitz³  Christoph A. Fux³  Beat Mueller⁴  Philipp Schuetz⁴  Anna Conen⁵ 

[1] Institute of Laboratory Medicine, Kantonsspital Aarau, Aarau, Switzerland;Medical University Department of Medicine, Kantonsspital Aarau, Tellstrasse, CH-5001, Aarau, Switzerland;Medical University Department of Medicine, Kantonsspital Aarau, Tellstrasse, CH-5001, Aarau, Switzerland;Department of Infectious Diseases and Hospital Hygiene, Kantonsspital Aarau, Switzerland;Medical University Department of Medicine, Kantonsspital Aarau, Tellstrasse, CH-5001, Aarau, Switzerland;University of Basel, Basel, Switzerland;University of Basel, Basel, Switzerland;Department of Infectious Diseases and Hospital Hygiene, Kantonsspital Aarau, Switzerland;

关键词: COVID-19;    Endothelin-1;    All-cause 30-day mortality;    ProET-1;    Prognostic marker;    Risk assessment;    SARS-CoV-2;   

DOI  :  10.1186/s12931-021-01742-8

来源: Springer

【 摘 要 】

BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) has been linked to thrombotic complications and endothelial dysfunction. We assessed the prognostic implications of endothelial activation through measurement of endothelin-I precursor peptide (proET-1), the stable precursor protein of Endothelin-1, in a well-defined cohort of patients hospitalized with COVID-19.MethodsWe measured proET-1 in 74 consecutively admitted adult patients with confirmed COVID-19 and compared its prognostic accuracy to that of patients with community-acquired pneumonia (n = 876) and viral bronchitis (n = 371) from a previous study by means of logistic regression analysis. The primary endpoint was all-cause 30-day mortality.ResultsOverall, median admission proET-1 levels were lower in COVID-19 patients compared to those with pneumonia and exacerbated bronchitis, respectively (57.0 pmol/l vs. 113.0 pmol/l vs. 96.0 pmol/l, p < 0.01). Although COVID-19 non-survivors had 1.5-fold higher admission proET-1 levels compared to survivors (81.8 pmol/l [IQR: 76 to 118] vs. 53.6 [IQR: 37 to 69]), no significant association of proET-1 levels and mortality was found in a regression model adjusted for age, gender, creatinine level, diastolic blood pressure as well as cancer and coronary artery disease (adjusted OR 0.1, 95% CI 0.0009 to 14.7). In patients with pneumonia (adjusted OR 25.4, 95% CI 5.1 to 127.4) and exacerbated bronchitis (adjusted OR 120.1, 95% CI 1.9 to 7499) we found significant associations of proET-1 and mortality.ConclusionsCompared to other types of pulmonary infection, COVID-19 shows only a mild activation of the endothelium as assessed through measurement of proET-1. Therefore, the high mortality associated with COVID-19 may not be attributed to endothelial dysfunction by the surrogate marker proET-1.

【 授权许可】

CC BY