View clinical trials related to Post Cardiac Arrest Syndrome.
Filter by:Only half of the patients suffering from cardiac arrest arrive at the hospital alive. Of these survivors, more than 50% will still die or remain severely disabled. During cardiac arrest ischemia causes damage to the vital organs, especially the brain. When with return of spontaneous circulation oxygen is re-offered to the ischemic organs, massive amounts of reactive oxygen species (ROS) are produced. These ROS can further increase the damage to the myocardium and brain (reperfusion injury). Vitamin C is the primary circulating antioxidant. It scavenges free radicals and reduces the production of ROS. In a recent study we demonstrated that vitamin C plasma levels are deficient in ~60% of the patients after cardiac arrest, probably due to massive consumption. Vitamin C deficiency reduces the protection against oxidative stress. Intravenous supplementation is needed to restore deficiency and the antioxidative effect of vitamin C is much more potent if it is administered in a supraphysiological dose (≥ 3 g per day). Its strong antioxidative effect may reduce damage to the circulation and to brain, heart and other organs. Beneficial effects of high dose i.v. vitamin C after cardiac arrest have been demonstrated in preclinical studies, but not in patients. The investigators hypothesize that vitamin C can reduce organ damage, especially cerebral injury, if administered for a short period as a high i.v. dose during the very early phase of reperfusion after cardiac arrest. Objectives: - To determine whether an early high dose i.v. vitamin C can improve organ function, especially neurological outcome, in patients after cardiac arrest - To explore the optimal dosing regimen for high dose i.v. vitamin C - To investigate in vitro the difference in effect of plasma obtained from post cardiac arrest patients treated with placebo, 3 gr/day or 10 gr/day vitamin C on endothelial cell viability and underlying oxidative pathways.
This study includes comatose survivors of out-of-hospital cardiac arrest treated with 24 hours or 48 hours of targeted temperature management. The overall aim is to evaluate the importance of plasma complement protein concentrations in patients resuscitated after out-of-hospital cardiac arrest and treated with 24 hours or 48 hours of targeted temperature management. The specific aim is to evaluate: - the concentration of plasma lectin pathway proteins the first, second and third day after cardiac arrest - the relation between concentration of plasma lectin pathway proteins and mortality - if prolonged targeted temperature management influences the concentration of plasma lectin pathway proteins This study is a sub-study to the trial entitled: "Time-differentiated targeted temperature management (TTH48) (ClinicalTrials.gov Identifier: NCT01689077)" The following Complement Lectin Pathway proteins will be measured: Mannan-Binding-Lectin, M-ficolin, H-ficolin, CL-L1, MASP-1, MASP-2, MASP-3, MAp19 and MAp44.