Atrial fibrillation (AF) is becoming an increasing burden for health care systems worldwide owing to population aging.^1,2 Pharmacologic and electrical cardioversion are common therapies in emergency departments (EDs), especially for highly symptomatic patients. Each intervention has specific risks, and neither is considered cost-effective owing to frequent recurrence of AF.³ In addition, AF often terminates spontaneously.⁴ Thus, implementation of wait-and-watch strategies combined with scoring systems to estimate the probability of spontaneous conversion to sinus rhythm (SCV) might be an innovative approach to avoid unnecessary antiarrhythmic therapy and its potential adverse effects.⁵ Moreover, evidence suggests that hypokalemia and hypomagnesemia contribute to AF development.^6,7 Thus, the administration of potassium and magnesium could be a reasonable strategy to improve SCV rates.

Objectives: To assess the predictive value of N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitive troponin T (hs-TnT) serum levels for mid-term mortality in patients presenting with symptomatic atrial fibrillation (AF) to an emergency department.Methods: Non-interventional cohort/follow-up study, including consecutive patients presenting to a tertiary care university emergency department due to symptomatic AF between 2012 and 2016. Multivariable Cox proportional hazard regression models were used to estimate the mortality rates and hazards per 100 patient-years (pry) for NT-proBNP and hs-TnT serum levels in quintiles.Results: 2574 episodes of 1754 patients (age 68 (IQR 58–75) years, female gender 1199 (44%), CHA₂DS₂-VASc 3 (IQR 1–4)) were recorded. Following the exclusion of incomplete datasets, 1780 episodes were available for analysis. 162 patients deceased during the mid-term follow-up (median 23 (IQR 4–38) months); the mortality rate was 4.72/100 pry. Hazard for death increased with every quintile of NT-proBNP by 1.53 (HR; 95% CI 1.27 to 1.83; p<0.001) and by 1.31 (HR; 95% CI 1.10 to 1.55; p=0.002) with every quintile of hs-TnT in multivariate Cox-regression analysis. No interaction between NT-proBNP and hs-TnT levels could be observed.Conclusion: Elevated NT-proBNP and hs-TnT levels are independently associated with increased mid-term mortality in patients presenting to an emergency department due to symptomatic AF.Trial registration number: NCT03272620; Results.

Ischemia-reperfusion injury (IRI) causes vascular endothelial dysfunction. Preclinical data suggest that the SGLT2 inhibitor dapagliflozin may protect against vascular IRI. This trial has investigated if oral treatment with dapagliflozin can mitigate the transient impairment of IRI-induced-endothelial dysfunction in the forearm resistance vasculature. 32 healthy males (n = 16 per group, age: 27 ± 4 yrs) were studied in this randomized, placebo-controlled, parallel-group, double-blinded trial. Acetylcholine (ACh; endothelium-dependent vasodilator) and glyceryltrinitrate (GTN; endothelium-independent vasodilator) were administered into the brachial artery of the non-dominant arm. The response to stepwise increasing doses on forearm blood flow (FBF) was assessed. FBF was measured before and after a cuff-induced 20-minute forearm ischemia at pre-dose and following daily intake of 10 mg dapagliflozin or placebo over 15 days. IRI reduced endothelium-dependent vasodilatation by 29% (p < 0.001, paired t-test). After a 15-day treatment period, IRI-induced endothelial dysfunction was abrogated in participants receiving dapagliflozin (FBF ACh_AUC ratios post- vs. pre-ischemia: dapagliflozin: 0.93; 95% CI: 0.80–1.29) but unchanged with placebo (0.81; 95% CI: 0.68–0.92; p = 0.015 vs. pre-ischemia). GTN-induced vasodilation was not altered by IRI or treatment. Dapagliflozin treatment at standard clinical doses over 15 days prevents IRI-induced vascular endothelial dysfunction in the forearm resistance vasculature of healthy young males. The underlying mechanism and the potential clinical impact remain to be demonstrated. Clinical trial registration https://clinicaltrials.gov/study/NCT05217654 NCT05217654; EudraCT number: 2021-005002-95 Date of registration: 20/01/2022.

Atrial fibrillation (AF) is a globally evolving medical challenge with, currently, 4% prevalence in the European Union’s population

Aim: Medication for the pharmacological cardioversion of atrial fibrillation (AF) and atrial flutter (AFL) is applied either in a fixed dose or adapted to body weight. Individual body weight might be a relevant confounder for anti-arrhythmic treatment success. Therefore, the aim of this study was to elucidate the impact of body weight on pharmacological cardioversion success, comparing weight adapted (Vernakalant) and fixed dose (Ibutilide) pharmacotherapeutic cardioversion regimes. Methods: Within this prospective observational trial, a total of 316 episodes of AF and AFL were enrolled. Patients were stratified in either a Vernakalant (n = 181) or Ibutilide (n = 135) treatment arm, based on the chosen regime, for direct comparison of treatment efficacy. Results: Conversion to sinus rhythm was achieved in 76.3% of all cases. Of note, there was no difference comparing the Vernakalant and Ibutilide treatment arms (Vernakalant 76.2% vs. Ibutilide 76.3%; p = 0.991). Within the whole study population, decreasing conversion rates with increasing body weight (adjusted odds ratio (OR) = 0.69 (0.51–0.94); p = 0.018) were observed. An independent effect of body weight within the Ibutilide treatment arm was noted, which remained stable after adjustment for potential confounders (adjusted OR = 0.55 (0.38–0.92), p = 0.022. Conclusion: Both, the Vernakalant and Ibutilide treatment arms showed comparable rates of treatment success in pharmacotherapeutic cardioversion of AF and AFL. Of utmost importance, we observed that the fixed dose of Ibutilide—as compared to the weight-adapted dose of Vernakalant—showed a reduced treatment success with increasing body weight.