The Canadian Community Utilization of Stroke Prevention Study in Atrial Fibrillation in the Emergency Department (C-CUSP ED).

STUDY OBJECTIVE: Lack of oral anticoagulation prescription in the emergency department (ED) has been identified as a care gap in atrial fibrillation patients. This study seeks to determine whether the use of a tool kit for emergency physicians with a follow-up community-based atrial fibrillation clinic resulted in greater oral anticoagulation prescription at ED discharge than usual care. METHODS: This was a before-after study in 5 Canadian EDs in 3 cities. Patients who presented to the ED with atrial fibrillation were eligible for inclusion. The before phase (1) was retrospective; 2 after phases (2 and 3) were prospective: phase 2 used an oral anticoagulation prescription tool for emergency physicians and patient education materials, whereas phase 3 used the same prescription tool, patient materials, atrial fibrillation educational session, and follow-up in an atrial fibrillation clinic. Each phase was 1 year long. The primary outcome was the rate of new oral anticoagulation prescription at ED discharge for patients who were oral anticoagulation eligible and not receiving oral anticoagulation at presentation. RESULTS: A total of 631 patients were included. Mean age was 69 years (SD 14 years), 47.4% were women, and 69.6% of patients had a CHADS2 score greater than or equal to 1. The rate of new oral anticoagulation prescription in phase 1 was 15.8% compared with 54.1% and 47.2%, in phases 2 and 3, respectively. After multivariable adjustment, the odds ratio for new oral anticoagulation prescription was 8.03 (95% confidence interval 3.52 to 18.29) for phase 3 versus 1. The 6-month rate of oral anticoagulation use was numerically but not significantly higher in phase 3 compared with phase 2 (71.6% versus 79.4%; adjusted odds ratio 2.30; 95% confidence interval 0.89 to 5.96). The rate of major bleeding at 6 months was 0%, 0.8%, and 1% in phases 1, 2, and 3, respectively. CONCLUSION: An oral anticoagulation prescription tool was associated with an increase in new oral anticoagulation prescription in the ED, irrespective of whether an atrial fibrillation clinic follow-up was scheduled. The use of an atrial fibrillation clinic was associated with a trend to a higher rate of oral anticoagulation at 6-month follow-up.

Small-molecule complement inhibitors cannot prevent the development of the platelet storage lesion.

BACKGROUND: Suppression of the platelet (PLT) storage lesion would maintain PLT quality over longer storage times. An increased storage period would greatly improve the ability of blood agencies and hospitals to manage PLT inventories and minimize product wastage. Activation of the complement system has been proposed to play a role in initiating or potentiating the PLT storage lesion. This study examines the effect of complement inhibition on the development of the PLT storage lesion. STUDY DESIGN AND METHODS: Leukofiltered PLT concentrates (PCs) were split into miniunits containing the complement inhibitors N-acetylaspartylglutamic acid (NAAGA) or compstatin, a control peptide, or saline. Samples were collected up to Day 11 of storage. Complement activation was monitored as C3a generation. PLT quality was assessed by morphology, CD62 and CD63 expression, fibrinogen binding, pH, mean PLT volume, annexin V binding, and PLT viability. Caspase-3 activity served as a measure of PLT apoptosis. RESULTS: At concentrations of NAAGA required to achieve approximately 50 percent complement inhibition, PLT activation, and caspase-3 activity were increased. Complement inhibition by compstatin was highly variable. Compstatin addition consistently resulted in a 37 to 55 percent inhibition of PLT caspase-3 activity, but PLT quality and viability were no different between compstatin PCs and control PCs over the storage time. CONCLUSIONS: Neither NAAGA nor compstatin provided complete inhibition of complement over the storage period. Addition of these small-peptide inhibitors to PCs did not slow PLT storage lesion development, in spite of the partial inhibition of caspase-3 activity in the compstatin-treated PCs.