TY - JOUR
T1 - Association between sympathoadrenal activation, fibrinolysis, and endothelial damage in septic patients
T2 - a prospective study
AU - Johansson, Pär I
AU - Haase, Nicolai
AU - Perner, Anders
AU - Ostrowski, Sisse R
N1 - Copyright © 2014 Elsevier Inc. All rights reserved.
PY - 2014/6
Y1 - 2014/6
N2 - Purpose: The purpose of this study is to investigate potential associations between sympathoadrenal activation and/or vasopressor/inotropic therapy and endothelial activation, damage, and coagulopathy in septic patients. Materials and methods: Septic patients included in the Scandinavian Starch for Severe Sepsis/Septic Shock trial who were expected not to receive catecholamines at screening preintervention (baseline) and had baseline blood sampled. Clinical, outcome data, and measurements of plasma concentration (p-) biomarkers reflecting sympathoadrenal activation, endothelial activation and damage, natural anticoagulation, fibrinolysis, cell damage, and platelet activation. Results: Sixty-seven patients were included, of whom 14 turned out to receive noradrenaline infusion at blood sampling. These 14 patients had p-noradrenaline 5-fold higher than patients not receiving catecholamines (n = 53), whereas no other baseline preintervention biomarkers differed. In the 53 patients not receiving catecholamines at blood sampling, endogenous p-noradrenaline correlated positively with adrenaline, syndecan 1, soluble vascular endothelial growth factor receptor 1, soluble CD40 ligand, tissue-type plasminogen activator, and plasminogen activator inhibitor 1 (PAI-1) and negatively with PAI-1/tissue-type plasminogen activator ratio (all P <. .05) and was independently associated with syndecan 1, soluble vascular endothelial growth factor receptor 1, and PAI-1 (all P <. .05), and 28- and 90-day mortality (. P <. .05). Conclusions: In septic patients, endogenous noradrenaline was independently associated with biomarkers of endothelial activation, damage, fibrinolysis and mortality, comparable with findings in trauma and myocardial infarction patients. The catecholamine surge in critical illness may contribute to balance endothelial damage and procoagulation with hypocoagulability and hyperfibrinolysis in the circulating blood.
AB - Purpose: The purpose of this study is to investigate potential associations between sympathoadrenal activation and/or vasopressor/inotropic therapy and endothelial activation, damage, and coagulopathy in septic patients. Materials and methods: Septic patients included in the Scandinavian Starch for Severe Sepsis/Septic Shock trial who were expected not to receive catecholamines at screening preintervention (baseline) and had baseline blood sampled. Clinical, outcome data, and measurements of plasma concentration (p-) biomarkers reflecting sympathoadrenal activation, endothelial activation and damage, natural anticoagulation, fibrinolysis, cell damage, and platelet activation. Results: Sixty-seven patients were included, of whom 14 turned out to receive noradrenaline infusion at blood sampling. These 14 patients had p-noradrenaline 5-fold higher than patients not receiving catecholamines (n = 53), whereas no other baseline preintervention biomarkers differed. In the 53 patients not receiving catecholamines at blood sampling, endogenous p-noradrenaline correlated positively with adrenaline, syndecan 1, soluble vascular endothelial growth factor receptor 1, soluble CD40 ligand, tissue-type plasminogen activator, and plasminogen activator inhibitor 1 (PAI-1) and negatively with PAI-1/tissue-type plasminogen activator ratio (all P <. .05) and was independently associated with syndecan 1, soluble vascular endothelial growth factor receptor 1, and PAI-1 (all P <. .05), and 28- and 90-day mortality (. P <. .05). Conclusions: In septic patients, endogenous noradrenaline was independently associated with biomarkers of endothelial activation, damage, fibrinolysis and mortality, comparable with findings in trauma and myocardial infarction patients. The catecholamine surge in critical illness may contribute to balance endothelial damage and procoagulation with hypocoagulability and hyperfibrinolysis in the circulating blood.
KW - Aged
KW - Biological Markers
KW - Blood Coagulation
KW - Blood Coagulation Disorders
KW - CD40 Ligand
KW - Catecholamines
KW - Endothelium, Vascular
KW - Fibrinolysis
KW - Humans
KW - Male
KW - Middle Aged
KW - Norepinephrine
KW - Plasminogen Activator Inhibitor 1
KW - Prospective Studies
KW - Sepsis
KW - Shock
KW - Syndecans
KW - Tissue Plasminogen Activator
KW - Vascular Endothelial Growth Factor A
KW - Vascular Endothelial Growth Factor Receptor-1
U2 - 10.1016/j.jcrc.2013.10.028
DO - 10.1016/j.jcrc.2013.10.028
M3 - Journal article
C2 - 24581948
SN - 0883-9441
VL - 29
SP - 327
EP - 333
JO - Journal of Critical Care
JF - Journal of Critical Care
IS - 3
ER -