Baseline L-ascorbic acid levels in OVATION65
CCCF ePoster library. Viens I. 11/12/19; 285177; EP62
Isabelle Viens
Isabelle Viens
Login now to access Regular content available to all registered users.

You may also access this content "anytime, anywhere" with the Free MULTILEARNING App for iOS and Android
Abstract
Rate & Comment (0)
ePoster
Topic: Other

 Viens, Isabelle1,2, St-Arnaud, Charles1, Battista, Marie-Claude 1,2, Haroune, Lounes 1,2, Masse, Marie-Hélène 1,2, D'Aragon, Frédérick 1,2,  Marsault, Éric1,2, Boumahni, Dounia 3,  Porteus, Rebecca K.5,  Quiroz Martinez, Hector1, Chassé, Michaël 3,4, Marchand, Joannie 2,  Garant, Marie-Pierre2, Pinto, Ruxandra 6 , Charbonney, Emmanuel 3,4 ,Wilcox, Elizabeth7, Adhikari, Neill 6,7 & Lamontagne, François1,2.

 

1 Université de Sherbrooke, Sherbrooke, Canada

2 Centre de recherche du CHU de Sherbrooke, Sherbrooke, Canada

3 Centre hospitalier universitaire de Montréal, Montréal, Canada

4 Université de Montréal, Montréal, Canada

5 Ottawa Hospital Research Institute, Ottawa, Canada

6 Sunnybrook Health Sciences Centre, Toronto, Canada

7 University of Toronto, Toronto, Canada

 


Introduction: Some evidence suggests that pharmacologic norepinephrine increases oxidative stress [1, 2] and low plasma ascorbic acid (AA) levels have been associated with higher C-reactive protein [3]. In OVATION65, patients with vasodilatory hypotension are randomized to permissive hypotension vs. usual care. Our overall goal is to determine whether lower norepinephrine exposure via permissive hypotension reduces organ injury to a greater extent in patients with low baseline AA. Our first step was to measure baseline plasma AA levels in OVATION65 participants and healthy volunteers.

Objectives: Describe baseline plasma L-AA in 1) OVATION65 participants and 2) healthy volunteers; 3) determine associations between baseline L-AA and prespecified baseline and outcome variables in OVATION65 participants.

Methods: This analysis includes 65 OVATION65 participants from 7 Canadian hospitals. Patients were 65 years old with vasodilatory hypotension, ≤12 hours since vasopressor initiation and anticipated to remain on vasopressors for ≥6 more hours. Exclusion criteria included acute spinal cord or brain injury; acute hemorrhage, ventricular failure or post-cardiopulmonary bypass vasoplegia; <1 year since solid organ transplantation; extracorporeal life support at baseline; lacking commitment to life-sustaining therapies; previous enrollment in OVATION65; and lack of physician equipoise. Patients were randomized to permissive hypotension (mean arterial pressure [MAP] target 60-65 mmHg) or usual care. We determined the association between baseline AA, measured immediately after randomization, and APACHE II score, duration of ICU stay, and the worst (lowest) MAP/vasopressor (VP) index during the first 24 hours following randomization (MAP and VP doses were measured hourly). AA was also measured in 11 healthy volunteers. All blood samples were collected in K2-EDTA vacutainers, packaged on ice, centrifuged within 1 hour and stored at -80C. AA levels were measured using liquid chromatography with tandem mass spectrometry (LC-MS/MS). Analyses were blinded to group allocation.

Results: The mean age of OVATION65 participants was 75 years (standard deviation [SD] 7), and 24 (37%) were women. The mean APACHE II and clinical frailty scale scores were 24 (SD 6) and 4 (SD 1), respectively. Median (interquartile range [IQR]) duration of ICU stay was 6 (3-11) days. Median worst MAP/VP index was 465 (150-835) mmHg/g/kg/min. Median (IQR) baseline AA level was 0.88 (0-0.95) mol/L; 26/65 (40%) had a level below the detectable threshold (0.25 mol/L). We found no association between AA and the 3 prespecified variables. In healthy volunteers, median (IQR) L-AA was 36 (29-43) mol/L.

Conclusion: Using LC-MS/MS, AA levels in volunteers were comparable to those reported in other studies using high performance LC (HPLC), but levels were lower in OVATION65 participants compared to other cohorts of critically ill patients [3]. Current results preclude the evaluation of associations between baseline AA levels and outcomes. Further analyses of AA stability at different stages of sample processing are required to determine if and how samples may have been compromised.

Acknowledgement: This project was funded by the Lotte & John Hecht Memorial Foundation.


1. Deo, S.H., et al., Norepinephrine increases NADPH oxidase-derived superoxide in human peripheral blood mononuclear cells via alpha-adrenergic receptors. Am J Physiol Regul Integr Comp Physiol, 2013. 305(10): p. R1124-32.

2. Schraml, E., et al., Norepinephrine treatment and aging lead to systemic and intracellular oxidative stress in rats. Exp Gerontol, 2007. 42(11): p. 1072-8.

3. Carr, A.C., et al., Hypovitaminosis C and vitamin C deficiency in critically ill patients despite recommended enteral and parenteral intakes. Crit Care, 2017. 21(1): p. 300.

    This eLearning portal is powered by:
    This eLearning portal is powered by MULTIEPORTAL
Anonymous User Privacy Preferences

Strictly Necessary Cookies (Always Active)

MULTILEARNING platforms and tools hereinafter referred as “MLG SOFTWARE” are provided to you as pure educational platforms/services requiring cookies to operate. In the case of the MLG SOFTWARE, cookies are essential for the Platform to function properly for the provision of education. If these cookies are disabled, a large subset of the functionality provided by the Platform will either be unavailable or cease to work as expected. The MLG SOFTWARE do not capture non-essential activities such as menu items and listings you click on or pages viewed.


Performance Cookies

Performance cookies are used to analyse how visitors use a website in order to provide a better user experience.


Save Settings