| Autor: |
Frencken JF; Department of Epidemiology, Julius Center for Health Sciences and Primary Care.; Department of Intensive Care Medicine, and., van Smeden M; Department of Epidemiology, Julius Center for Health Sciences and Primary Care., van de Groep K; Department of Epidemiology, Julius Center for Health Sciences and Primary Care.; Department of Intensive Care Medicine, and., Ong DSY; Department of Intensive Care Medicine, and.; Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, the Netherlands., Klein Klouwenberg PMC; Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, the Netherlands., Juffermans N; Department of Intensive Care., Bonten MJM; Department of Epidemiology, Julius Center for Health Sciences and Primary Care.; Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, the Netherlands., van der Poll T; Center for Experimental and Molecular Medicine, and.; Division of Infectious Diseases, Amsterdam University Medical Centers, Academic Medical Center, Amsterdam, the Netherlands., Cremer OL; Department of Intensive Care Medicine, and. |
| Jazyk: |
angličtina |
| Zdroj: |
Annals of the American Thoracic Society [Ann Am Thorac Soc] 2022 May; Vol. 19 (5), pp. 773-780. |
| DOI: |
10.1513/AnnalsATS.202106-689OC |
| Abstrakt: |
Rationale: Myocardial injury occurs frequently during sepsis and is independently associated with mortality. However, its etiology remains largely unknown. Objectives: To assess the relative contributions of hyperinflammation, activated coagulation, and endothelial dysfunction to myocardial injury in critically ill patients with sepsis. Methods: We included consecutive patients with sepsis presenting to two tertiary intensive care units in the Netherlands between 2011 and 2013. High-sensitivity cardiac troponin I as well as a wide range of plasma biomarkers related to inflammation, coagulation, and endothelial function were measured. Structural equation modeling was used to construct latent variables representing each of these pathophysiological constructs and to subsequently study their associations with troponin elevation while adjusting for confounders. Results: We analyzed 908 (88%) of 1,037 eligible patients, 553 (61%) of whom had raised high-sensitivity cardiac troponin I levels upon intensive care unit admission. The latent variables included interleukin (IL)-6, IL-8, and IL-1β for inflammation; platelet count, prothrombin time, and protein C for coagulation; and soluble E-selectin, intercellular adhesion molecule-1, and angiopoietin-2 for endothelial function. After adjustment for age and cardiovascular comorbidities, structural equation modeling analysis showed that activated coagulation was independently associated with elevated troponin during sepsis (standardized regression coefficient, 0.551; 95% confidence interval [CI], 0.257-0.845; P < 0.001) whereas hyperinflammation and endothelial dysfunction were not (standardized regression coefficient, -0.161; 95% CI, -0.418 to 0.096 and -0.054; 95% CI, -0.168 to 0.060, respectively). Conclusions: Our findings suggest that myocardial injury during sepsis is mediated by systemic activation of coagulation rather than by circulating inflammatory mediators or activation of the endothelium. These findings may guide evaluation of strategies to protect the myocardium during sepsis. Clinical trial registered with clinicaltrials.gov (NCT01905033). |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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