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BACKGROUND: Cardiac arrest and cardiopulmonary resuscitation (CPR) are associated with activated coagulation and microvascular fibrin deposition with subsequent multiorgan failure and adverse outcome.OBJECTIVES: Activated Factor XI-antithrombin (FXIa-AT) complex, activated Factor IX-antithrombin (FIXa-AT) complex and thrombin-antithrombin (TAT) complex were measured as markers of coagulation activation, and evaluated as independent prognostic indicators in out-of-hospital cardiac arrest (OHCA) patients.METHODS: From February 2007 until December 2010 blood samples were collected in close approximation to CPR from patients with OHCA of assumed cardiac origin. Follow-up samples in survivors were drawn 8-12 h and 24-48 h after hospital admission. All measurements were determined by ELISA.RESULTS: Thirty-seven patients presented with asystole and 77 with ventricular fibrillation as first recorded heart rhythm. At 30-days follow-up, 70 patients (61.4%) had died. All patients had elevated levels of FXIa-AT complex, FIXa-AT complex and TAT. Initial levels were significantly higher in non-survivors compared to 30-days survivors. A significant increase in risk of 30-days all-cause mortality was observed through increasing quartiles of all three biomarkers in univariate Cox regression analysis. Compared to the lowest quartile (Q1), only FXIa-AT complex levels in Q3 (HR 3.17, p = 0.011) and Q2 (HR 3.02, p = 0.016) were independently associated with all-cause mortality in the multivariable analysis. FIXa-AT complex and TAT-complex did not behave as independent predictors.CONCLUSIONS: Complexes of FXIa-AT were independently associated with 30-days survival in OHCA-patients.CLINICAL TRIAL REGISTRATION: ClinicalTrials. gov, NCT02886273.

AimSudden cardiac arrest (SCA) secondary to ventricular fibrillation (VF) may be due to different cardiac conditions. We investigated whether copeptin, hs-cTnT and NT-proBNP in addition to clinical assessment may help to identify the etiology of SCA and yield prognostic information.Methods and ResultsEDTA-blood was collected prior to or at hospital admission from patients with SCA of assumed cardiac origin. Clinical data were obtained from hospital records. VF was the primary heart rhythm in 77 patients who initially were divided into 2 groups based on whether they had an ischemic or non-ischemic mechanism as the most likely cause of SCA. They were further divided into 4 groups according to whether or not they had a history of previous heart disease. The patients were categorized by baseline clinical information, ECG, echocardiography and coronary angiography; Group 1 (n = 43): SCA with first AMI, Group 2 (n = 10): SCA with AMI and previous MI, Group 3 (n = 3): SCA without AMI and without former heart disease, Group 4 (n = 18): SCA without AMI and with known heart disease. Copeptin and hs-cTNT did not differ between patient groups, whereas NT-proBNP was significantly higher in patients with established heart disease without AMI and differed between non-AMI and AMI. Furthermore, NT-proBNP was significantly elevated in non-survivors as compared to survivors.ConclusionNT-proBNP provided both diagnostic and prognostic information in blood samples collected close to out-of-hospital resuscitation of VF patients, whereas copeptin and hs-cTnT failed to do so.Clinical Trial RegistrationClinicalTrials.gov, NCT02886273.

To evaluate whether low levels of holotranscobalamin (holoTC) or elevated levels of methylmalonic acid (MMA), both indicators of vitamin B12 deficiency, might predispose to new cardiovascular events following an acute myocardial infarction (MI). A prospective prognostic study. One hospital center in Stavanger, Norway. A total of 300 patients admitted with an acute MI. Registration of new TnT positive coronary events (defined as TnT>0.05 μg/l and a typical MI pattern) and/or cardiac death during a median follow-up time of 45 months. We compared the recurrence of events in the lowest quartile of holoTC (Q1

Objective: In the last few years the genetic influence on health and disease outcome has become more apparent. The ACE genotype appears to play a significant role in the pathophysiology of several disease processes. This pilot study aims at showing the feasibility to examine the genetic influence of the ACE genotype on return of spontaneous circulation (ROSC) in out-of-hospital cardiac arrest (OHCA). Methods: We performed a prospective observational study of all OHCAs of presumed cardiac origin in a well-defined population. We collected prehospital blood samples for the determination of ACE genotype and used this information together with Utstein template parameters in a multivariable analysis to examine the relationship between ROSC and ACE genotype. Results: We collect blood samples in 156 of 361 patients with OHCA of presumed cardiac origin, 127 samples were analysed (mean age 67 years, 86% male, 79% witnessed OHCA, 80% bystander CPR, 62% had a shockable rhythm, ROSC 77%). Distribution of the ACE gene polymorphisms: insertion polymorphism (II) n=22, 17%, insertion/deletion polymorphism (ID) n=66, 52% and deletion polymorphism (DD) n=39, 31%. We found no significant association between ACE II vs ACE DD/DI and ROSC (OR 1.72; CI 0.52 to 5.73; p=0.38). Other ACE genotype groupings (II/ID vs DD or II vs DD) did not change the overall finding of lack of impact of ACE genotype on ROSC. Conclusions: This pilot study did not indicate a significant association between ACE gene polymorphism and ROSC. However, it has demonstrated that prehospital genetic studies including blood sampling are feasible and ethically acceptable. publishedVersion