A prediction tool for initial out-of-hospital cardiac arrest survivors.

AIM: Improvement in predicting survival after out-of-hospital cardiac arrest is of major medical, scientific and socioeconomic interest. The current study aimed at developing an accurate outcome-prediction tool for patients following out-of-hospital cardiac arrests. METHODS: This retrospective cohort study was based on a cardiac arrest registry. From out-of-hospital cardiac arrest patients (n=1932), a set of variables established before restoration of spontaneous circulation was explored using multivariable logistic regression. To obtain reliable estimates of the classification performance the patients were allocated to training (oldest 80%) and validation (most recent 20%) sets. The main performance parameter was the area under the ROC curve (AUC), classifying patients into survivors/non-survivors after 30 days. Based on rankings of importance, a subset of variables was selected that would have the same predictive power as the entire set. This reduced-variable set was used to derive a comprehensive score to predict mortality. RESULTS: The average AUC was 0.827 (CI 0.793-0.861) for a logistic regression model using all 21 variables. This was significantly better than the AUC for any single considered variable. The total amount of adrenaline, number of minutes to sustained restoration of spontaneous circulation, patient age and first rhythm had the same predictive power as all 21 variables. Based on this finding, our score was built and had excellent predictive accuracy (the AUC was 0.810), discriminating patients into 10%, 30%, 50%, 70%, and 90% survival probabilities. CONCLUSION: The current results are promising to increase prognostication accuracy, and we are confident that our score will be helpful in the daily clinical routine.

Effect of systemic high dose vitamin C therapy on forearm blood flow reactivity during endotoxemia in healthy human subjects.

OBJECTIVE: Acute inflammation induced by administration of Escherichia coli lipopolysaccharide endotoxin (LPS) reduces plasma concentrations of vitamin C and impairs vascular endothelium-derived nitric oxide (NO) bioactivity. We tested the hypothesis that systemically administered high dose vitamin C restores the endogenous anti-oxidant potential and improves NO-dependent vasodilatation in the forearm vasculature. DESIGN & SETTING: 36 male subjects were enrolled in this balanced, placebo controlled cross-over study. Forearm blood flow (FBF) reactivity to acetylcholine (ACh) and glyceryl-trinitrate (GTN), a sensitive test for endothelial function, was assessed at baseline and 4h after LPS-administration (20 IU/kg i.v). The effect of two different doses of intravenous vitamin C (Vitamin C-Injektopas®), 320 mg/kg and 480 mg/kg over 2h, or placebo on forearm vascular function was studied after LPS. MAIN RESULTS: LPS caused transient flu-like symptoms, decreased plasma vitamin C concentrations and reduced the ACh-dependent increase in FBF by up to 76%. Vitamin C at a mean plasma concentration of 3.2 or 4.9 mmol/L restored the response to ACh compared to baseline. CONCLUSION: High dose systemic vitamin C recovers LPS-induced endothelium-dependent vasodilation in the forearm resistance vasculature. This provides a rationale for a further clinical study of the systemic vitamin C effect under inflammatory conditions.

Hypertensive emergencies are associated with elevated markers of inflammation, coagulation, platelet activation and fibrinolysis.

Data from in vitro and animal experiments suggest that progressive endothelial damage with subsequent activation of coagulation and inflammation have a key role in hypertensive crisis. However, clinical investigations are scarce. We hypothesized that hypertensive emergencies are associated with enhanced inflammation, endothelial- and coagulation activation. Thus, we enrolled 60 patients admitted to an emergency department in a prospective, cross-sectional study. We compared markers of coagulation, fibrinolysis (prothrombin fragment F(1+2), plasmin-antiplasmin complexes, plasmin-activator inhibitor, tissue plasminogen activator), platelet- and endothelial activation and inflammation (P-selectin, C-reactive protein, leukocyte counts, fibrinogen, soluble vascular adhesion molecule-1, intercellular adhesion molecule-1, myeloperoxidase and asymmetric dimethylarginine) between hypertensive emergencies, urgencies and normotensive patients. In hypertensive emergencies, markers of inflammation and endothelial activation were significantly higher as compared with urgencies and controls (P<0.05). Likewise, plasmin-antiplasmin complexes were 75% higher in emergencies as compared with urgencies (P<0.001), as were tissue plasminogen-activator levels (∼30%; P<0.05) and sP-selectin (∼40%; P<0.05). In contrast, similar levels of all parameters were found between urgencies and controls. We consistently observed elevated markers of thrombogenesis, fibrinolysis and inflammation in hypertensive emergencies as compared with urgencies. Further studies will be needed to clarify if these alterations are cause or consequence of target organ damage.