Chronic antiplatelet therapy is not associated with alterations in the presentation, outcome, or host response biomarkers during sepsis: a propensity-matched analysis
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Sepsis is a major health burden worldwide. Preclinical investigations in animals and retrospective studies in patients have suggested that inhibition of platelets may improve the outcome of sepsis. In this study we investigated whether chronic antiplatelet therapy impacts on the presentation and outcome of sepsis, and the host response.
We performed a prospective observational study in 972 patients admitted with sepsis to the mixed intensive care units (ICUs) of two hospitals in the Netherlands between January 2011 and July 2013. Of them, 267 patients (27.5 %) were on antiplatelet therapy (95.9 % acetylsalicylic acid) before admission. To account for differential likelihoods of receiving antiplatelet therapy, a propensity score was constructed, including variables associated with use of antiplatelet therapy. Cox proportional hazards regression was used to estimate the association of antiplatelet therapy with mortality.
Antiplatelet therapy was not associated with sepsis severity at presentation, the primary source of infection, causative pathogens, the development of organ failure or shock during ICU stay, or mortality up to 90 days after admission, in either unmatched or propensity-matched analyses. Antiplatelet therapy did not modify the values of 19 biomarkers providing insight into hallmark host responses to sepsis, including activation of the coagulation system, the vascular endothelium, the cytokine network, and renal function, during the first 4 days after ICU admission.
Pre-existing antiplatelet therapy is not associated with alterations in the presentation or outcome of sepsis, or the host response.
KeywordsSepsis Antiplatelet Mortality Intensive care unit
The authors acknowledge Rolf H. H. Groenwold, MD, PhD (Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands) for statistical advice and the following members of the MARS consortium for participation in data collection: Friso M. de Beer, MD, Lieuwe D. J. Bos, PhD, Gerie J. Glas, MD, Roosmarijn T. M. van Hooijdonk, MD (Department of Intensive Care, Academic Medical Center, University of Amsterdam), Mischa A. Huson, MD (Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam), David S. Y. Ong, MD, PharmD (Department of Intensive Care Medicine, Department of Medical Microbiology and Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands), Laura R. A. Schouten, MD (Department of Intensive Care, Academic Medical Center, University of Amsterdam), Brendon P. Scicluna, PhD (Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam), Marleen Straat, MD, Esther Witteveen, MD, and Luuk Wieske, MD, PhD (Department of Intensive Care, Academic Medical Center, University of Amsterdam).
This research was performed within the framework of CTMM, the Center for Translational Molecular Medicine (www.ctmm.nl), project MARS (Grant 04I-201). The sponsor CTMM was not involved in the design and conduction of the study; nor was the sponsor involved in collection, management, analysis, and interpretation of the data or preparation, review, or approval of the manuscript. Decision to submit the manuscript was not dependent on the sponsor.
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Conflicts of interest
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