Vernakalant Research Articles

Abstract 11662: Efficacy And Safety Outcome Of Intravenous Vernakalant For Recent-onset Atrial Fibrillation: A Systematic Review And Meta-analysis

Introduction: Vernakalant hydrochloride is a relatively new atrial-selective antiarrhythmic approved in >40 countries to pharmacologically cardiovert patients with recent-onset atrial fibrillation (ROAF). Due to safety concerns, it is yet to be approved in the USA. Objectives: To determine the effectiveness and safety of vernakalant in patients with ROAF. Methods: We systematically searched PubMed, EMBASE, Ovid MEDLINE, and CENTRAL from inception to December 2022 for studies that compared intravenous vernakalant to another drug(s) or placebo in patients with ROAF (onset ≤7 days). The pre-specified efficacy endpoint was conversion to sinus rhythm within 90minutes of administering interventions. Safety outcome of interest was mortality rate. Random-effects model meta-analysis was performed on extracted quantitative data. Results: 886 patients got vernakalant, 353 received placebo, and 401 got an antiarrhythmic agent. Vernakalant was significantly superior to placebo (conversion rate: 49.5% vs 6.2%, OR: 14.94, 95% CI: 7.18-31.07, P<0.001, I 2 : 49%), Flecainide (72.3% vs 53.8%, OR: 2.44, 95% CI: 1.46-4.06, p<0.001, I 2 : 0%), Amiodarone (55.7% vs 8.5%, OR: 17.42, 95% CI: 7.75-39.13, p<0.001, I 2 : 0%), but not Ibutilide (62.4% vs 47.3%, OR: 1.77, 95% CI: 0.61-5.08, p=0.29, I 2 : 67%) in efficacy endpoint. In the vernakalant group, there was significantly lower incidence of ventricular arrhythmia (OR:0.65, 95% CI: 0.45-0.95, p=0.027) but higher incidence of bradycardia (OR:8.58, 95% CI: 4.69-15.67, p<0.0001) and dysgeusia (OR:14.51, 95% CI: 7.03-29.95, p<0.0001). No significant difference in mortality rate between vernakalant and other groups combined (OR: 2.51, 95% CI: 0.26-24.21, p=0.427). Conclusions: This hypothesis-generating study showed that intravenous vernakalant, though associated with a higher incidence of bradycardia and dysgeusia, is superior to placebo, Flecainide, and Amiodarone not Ibutilide in converting ROAF to sinus rhythm.

Characterization of electropharmacological profile of an anti-atrial fibrillatory drug vernakalant along with potential risk toward torsade de pointes: Translational studies using isoflurane-anesthetized dogs and isolated rat aortic preparations

We simultaneously assessed electropharmacological effects of anti-atrial fibrillatory drug vernakalant and its potential risk toward torsade de pointes. Vernakalant hydrochloride in doses of 0.3 and 3 mg/kg/10 min was intravenously administered to isoflurane-anesthetized beagle dogs without (n = 5) and with (n = 4) α-adrenoceptor blockade. Its vascular effect was analyzed using the rat aortae (n = 12). Vernakalant increased total peripheral vascular resistance and preload to left ventricle, leading to transient elevation of mean blood pressure indirectly via non-adrenergic pathway. Vernakalant suppressed sinus automaticity, ventricular contractility and intra-atrial/atrioventricular nodal/intraventricular conductions, and decreased cardiac output. Moreover, vernakalant prolonged atrial/ventricular effective refractory period by 53/55 ms, respectively, whereas it delayed ventricular repolarization in a reverse frequency-dependent manner. The extent of prolongation in early/late ventricular repolarization and electrically vulnerable period was 26/32 and 9 ms, respectively when QT-interval prolongation was the greatest. We compared them with those of known anti-atrial fibrillatory drugs; ranolazine, amiodarone, dronedarone, dl-sotalol and bepridil. The magnitude of vernakalant to alter those variables was the greater among those drugs except that the atrial selectivity was the lesser of those. Thus, vernakalant is expected to be efficacious against atrial fibrillation, but caution should be excised on its use for patients having labile ventricular function and repolarization.

Abstract 15506: Optical Mapping in Atrial Engineered Heart Tissues Reveals Proarrhythmic Potential of the Anti-AF Agent Vernakalant

Pharmacotherapy for atrial fibrillation (AF) is confounded by ventricular proarrhythmia. Vernakalant (VER) belongs to a class of atrial selective channel blockers developed in attempts to convert AF safely. Yet, robust analysis of the effects of VER in human based tissues has not been performed. We hypothesized that engineered heart tissues (EHT) composed of atrial (A) or ventricular (V) human iPSCs would provide a robust platform for quantitative analysis of chamber specific electrophysiological (EP) effects of VER. Methods: iPSCs were differentiated into cardiomyocytes using biphasic Wnt signaling, insulin, and lactate purification. Atrial-like myocytes were enriched by adding 0.75 μM retinoic acid on days 4-6 to promote atrial gene expression and specification. Myocytes were seeded onto cryosectioned, laser cut and decellularized myocardial tissues and cultured under isometric conditions. EHTs were stained with high dose, water soluble di-2-ANEPEQ to enhance signal-to-noise while avoiding toxicity. Results: Staining with 25 μM di-2-ANEPEQ provided high fidelity optical AP signals that allowed comprehensive characterization of the EP substrate. A-EHT exhibited significantly shorter AP durations than V-EHT reflecting greater repolarizing drive (APD80, 180 ms vs 367 ms; p < 0.0001, n = 4-5). Consistent with its role as an atrial-selective blocker, VER increased APD80 only in A-EHTs (180 ms vs 258 ms, p = 0.0027, n = 5). This beneficial property for combatting AF was countered by marked slowing of A-EHT conduction and AP upstroke velocity (20.6 cm/s vs 11.7 cm/s, p = 0.027, n = 5). Conclusions: Optical mapping of chamber specific EHTs confirms atrial specific nature of VER as an atrial repolarization prolonging agent but raises unexpected concerns regarding potential proarrhythmic toxicity related to atrial conduction slowing.

A rare case of vernakalant-induced 1:1 atrial flutter during chemical cardioversion of atrial fibrillation requiring emergency direct current cardioversion

Vernakalant is an atrial-selective, multi-channel anti-arrhythmic that offers a safe alternative to traditional approaches to chemical cardioversion of recent-onset, non-valvular atrial fibrillation. This case report describes a very rare occurrence of unstable accelerated 1:1 atrial flutter during an attempted cardioversion of non-valvular atrial fibrillation using vernakalant hydrochloride that required emergent direct current cardioversion. This case report highlights the need for clinicians to remain vigilant and be prepared to treat rare consequences of vernakalant administration.

Vernakalant hydrochloride for the treatment of atrial fibrillation: evaluation of its place in clinical practice.

Vernakalant is an intravenous anti-arrhythmic drug available in Europe, Canada and some countries in Asia for the restoration of sinus rhythm in acute onset atrial fibrillation. Currently, it is not available in USA because the US FDA have ongoing concerns about its safety. Vernakalant has a unique pharmacological profile of multi-ion channel activity and atrial-specificity that distinguishes it from other anti-arrhythmic drugs. This is thought to enhance efficacy but there are concerns of adverse events stemming from its diverse pharmacology. This ambiguity has prompted a review of the available clinical evidence on efficacy and safety to help re-evaluate its place in clinical practice.

Human medicines European public assessment report (EPAR): Brinavess, vernakalant hydrochloride, Atrial Fibrillation, Date of authorisation: 01/09/2010, Revision: 12, Status: Authorised

Human medicines European public assessment report (EPAR): Brinavess, vernakalant hydrochloride, Atrial Fibrillation, Date of authorisation: 01/09/2010, Revision: 12, Status: Authorised

Human medicines European public assessment report (EPAR): Brinavess, vernakalant hydrochloride, Atrial Fibrillation, Date of authorisation: 01/09/2010, Revision: 12, Status: Authorised

Human medicines European public assessment report (EPAR): Brinavess, vernakalant hydrochloride, Atrial Fibrillation, Date of authorisation: 01/09/2010, Revision: 12, Status: Authorised

Chemical cardioversion of recent-onset atrial fibrillation in the emergency department using vernakalant hydrochloride achieves safe and rapid restoration of sinus rhythm and facilitates same day discharge.

Vernakalant hydrochloride is a rapid-acting antiarrhythmic drug licensed in the EU since 2010 for the conversion of recent-onset atrial fibrillation with proven efficacy and safety when compared with placebo and amiodarone in randomized clinical trials. The aim of our study was to determine the feasibility of same day discharge (following 2h monitoring) from the emergency department after successful cardioversion using vernakalant hydrochloride. Patients with recent-onset atrial fibrillation treated in the emergency department of a large Dublin academic teaching hospital. Patients received a maximum of two weight based 10min infusions of vernakalant. Hypotensive events (>30% initial blood pressure), arrhythmias, conversion rates, and time to conversion were recorded. Sinus rhythm was restored in 35 out of 42 patients (83%) in an average of 8.8min (median 8min), average CHA2DS2-VASc of 0.92, HAS-BLED of 0.21 and average symptoms duration of 12h. There were no hypotensive or arrhythmogenic events. 41 out of 42 patients were discharged after 2h of monitoring. Vernakalant hydrochloride has provided a quick, safe, and practical means of achieving rapid restoration of sinus rhythm in our ED population with stable recent-onset AF who would otherwise not have undergone routine electrically cardioversion and same day discharge.

Vernakalant in Atrial Fibrillation: 2-Year Experience

Introduccion: El vernakalant es una nueva droga utilizada para el tratamiento de la fibrilacion auricular. Se encuentra disponible en nuestro pais para su uso desde el ano 2012. El objetivo de nuestro trabajo fue analizar los resultados luego de 2 anos de utilizacion del vernakalant para la reversion de la fibrilacion auricular aguda. Materiales y Metodos: Se registraron 121 pacientes con fibrilacion auricular aguda sin descompensacion hemodinamica, a los que se les decidio administrar un tratamiento farmacologico con vernakalant. Se recabaron variables clinicas, antecedentes cardiovasculares y datos ecocardiograficos. Resultados: La edad media de los pacientes fue de 58.1 ± 13.9 anos, con un 13,2 % de los pacientes que padecia cardiopatia estructural. La tasa de reversion a ritmo sinusal fue del 84,3 % con un 45,4 % que requirio de una segunda dosis del vernakalant. El tiempo a la reversion fue de 9 minutos (6-18), con un tiempo de estadia en el servicio de Emergencias hasta el alta de 165 minutos (110-210) . La tasa de eventos adversos serios fue de 2,5 %. Conclusion: En nuestra experiencia el Vernakalant resulto una droga efectiva y segura para el tratamiento de la fibrilacion auricular aguda que permitio una rapida resolucion y externacion de estos pacientes.

Vernakalant IV approved for reimbursement in Belgium

Vernakalant IV approved for reimbursement in Belgium

Vernakalant in an Experimental Model of Pacing-Induced Heart Failure: Lack of Proarrhythmia Despite Prolongation of Repolarization

BackgroundThe present ESC guidelines on atrial fibrillation have introduced vernakalant (VER) for pharmacologic cardioversion of atrial fibrillation. The aim of the present study was to investigate possible proarrhythmic effects of vernakalant in an experimental model of heart failure (HF). Methods and ResultsIn 12 female rabbits, HF was induced with the use of 4 weeks of rapid ventricular pacing. Twelve rabbits were sham operated. Isolated hearts demonstrated a significant prolongation of myocardial repolarization after induction of HF. Vernakalant caused a concentration-dependent (10 μmol/L and 30 μmol/L) increase of action potential duration (APD90) and QT interval without affecting spatial and temporal dispersion of repolarization. The increase in APD90 was accompanied by a greater increase in refractory period resulting in a significant increase in post-repolarization refractoriness. In control conditions, programmed ventricular stimulation and burst pacing led to ventricular fibrillation (VF) in 2 of the 12 sham (4 episodes) and in 3 of the 12 HF (24 episodes) subjects. In the presence of 30 μmol/L vernakalant, VF was no longer inducible in both groups (0 episodes). In the presence of low K+ concentration, neither sham nor HF vernakalant-treated subjects developed early after-depolarizations or ventricular tachyarrhythmias. ConclusionIn the present study, application of vernakalant led to a significant prolongation of myocardial repolarization and increased post-repolarization refractoriness but did not induce early after-depolarization and therefore did not cause proarrhythmia in failing hearts.

Synthesis of Vernakalant

Synthesis of Vernakalant

Electrophysiological profile of vernakalant in an experimental whole-heart model: the absence of proarrhythmia despite significant effect on myocardial repolarization

The most recent European Society of Cardiology (ESC) update on atrial fibrillation has introduced vernakalant (VER) for pharmacological cardioversion of atrial fibrillation. The aim of the present study was to investigate the safety profile of VER in a sensitive model of proarrhythmia. In 36 Langendorff-perfused rabbit hearts, VER (10, 30 µM, n = 12); ranolazine (RAN, 10, 30 µM, n = 12), or sotalol (SOT, 50; 100 µM, n = 12) were infused after obtaining baseline data. Monophasic action potentials and a 12-lead electrocardiogram showed a significant QT prolongation after application of VER as compared with baseline (10 µM: +25 ms, 30 µM: +50 ms, P < 0.05) accompanied by an increase of action potential duration (APD). The increase in APD90 was accompanied by a more marked increase in effective refractory period (ERP) leading to a significant increase in post-repolarization refractoriness (PRR, 10 µM: +30 ms, 30 µM: +36 ms, P < 0.05). Vernakalant did not affect the dispersion of repolarization. Lowered potassium concentration in bradycardic hearts did not provoke early afterdepolarizations (EADs) or polymorphic ventricular tachycardia (pVT). Comparable results were obtained with RAN. Hundred micromolars of SOT led to an increase in QT interval (+49 ms) and APD90 combined with an increased ERP and PRR (+23 ms). In contrast to VER, 100 µM SOT led to a significant increase in dispersion of repolarization and to the occurrence of EAD in 10 of 12 and pVT in 8 of 12 hearts. In the present study, application of VER and SOT led to a comparable prolongation of myocardial repolarization. Both drugs increased the PRR. However, VER neither affect the dispersion of repolarization nor induce EAD and therefore did not cause proarrhythmia.

Conversion of Recent-Onset Atrial Fibrillation: Which Drug is the Best?

Introduction: Vernakalant is a new, safe and effective drug used intravenously. It has proven to be more rapid in converting recent onset atrial fibrillation (AF) to sinus rhythm compared to placebo, amiodarone, propafenone and flecainide in clinical studies with few patients. At present no study has been conducted comparing these three drugs with a more substantial number of patients. The aim of our study is to compare the time to conversion to sinus rhythm, hospital stay and adverse events between vernakalant versus flecainide and propafenone in patients with a recent-onset AF. Materials and Methods: 150 hemodynamically stable patients with recent onset AF without structural heart disease were prospectively included. A single oral dose of propafenone 600 mg was administered to 50 patients; 50 patients received intravenous vernakalant; and 50 patients received a single oral dose of flecainide 300 mg. Clinical and laboratory variables were recorded. Results: Baseline characteristics were similar in the three groups.Time to conversion to sinus rhythm was 12 minutes in the vernakalant group versus 151 minutes in the propafenone group and 162 minutes in flecainide group (p< 0.01) The hospital stay was 243 minutes in the vernakalant group versus 422 minutes in the propafenone group and 410 minutes in flecainide group (p<0.01) (Figure 2). No adverse events were reported. Conclusion: The time to conversion to sinus rhythm and hospital stay were statistically shorter in vernakalant group compared to flecainide and to propafenone. There were no adverse events in the three groups.

Clinical efficacy of antazoline in rapid cardioversion of paroxysmal atrial fibrillation -- a protocol of a single center, randomized, double-blind, placebo-controlled study (the AnPAF Study)

BackgroundRapid conversion of atrial fibrillation (AF) to sinus rhythm may be achieved by the administration of class IA, IC and III antiarrhythmic drugs or vernakalant hydrochloride. However, that treatment may be related to potential pro-arrhythmia, lack of efficacy or the exceptionally high cost of a compound used. Antazoline is a first generation antihistaminic agent with chinidin-like properties. When administered intravenously, antazoline exerts a strong antiarrhythmic effect on supraventricular arrhythmia, especially on AF, facilitating rapid conversion to sinus rhythm. Despite a relative lack of published data antazoline has been marketed in Poland and widely used in cardiology wards and emergency rooms for many years due to its efficacy, safety and rapid onset of action within minutes of administration.Methods/designA randomized, double blind, placebo-controlled, superiority clinical trial was designed to assess clinical efficacy of antazoline in rapid conversion of AF to sinus rhythm. Eligible patients will present AF lasting less than 43 hours, will be in stable cardio-pulmonary condition and will have no prior history of advanced heart failure or significant valvular disease. Long-term antiarrhythmic therapy is not considered an exclusion criterion. Subjects who fulfill selection criteria will be randomly assigned to receive intravenously either antazoline or placebo in divided doses and observed for 1.5 hours after conversion to sinus rhythm or after the last i.v. bolus. Primary end point will be the conversion of AF to sinus rhythm confirmed in an electrocardiogram (ECG) during the observation period. Secondary end points will be comprised of time to conversion and return of AF during the observation period. Special consideration will be given to the observation of any adverse events. A sample size of 80 patients was calculated based on the following assumptions: two-tailed test, a type I error of 0.01, a power of 90%, efficacy of placebo 5%, efficacy of antazoline 50% and 20% drop-out rate to fulfill the criteria of intention-to-treat analysis. Due to the presumed lack of statistical power, the secondary end points and safety endpoints will be considered exploratory.Clinical trials registryClinicalTrials.gov, NCT01527279

Population Pharmacokinetics of Vernakalant Hydrochloride Injection (RSD1235) in Patients With Atrial Fibrillation or Atrial Flutter

Vernakalant hydrochloride is a novel, predominantly atrial-selective antiarrhythmic drug that effectively and rapidly terminates atrial fibrillation (AF). Plasma vernakalant concentration data from 5 phase 2 and 3 clinical trials of vernakalant in patients with AF or atrial flutter and a phase 1 study in healthy volunteers were used to construct a population pharmacokinetic model. Plasma vernakalant concentration-time data were best fit by a 2-compartment mammillary model, with rapid first-order elimination from the central compartment. Median systemic clearance was 0.35 L/h/kg (or 28 L/h for an 80-kg patient), with intersubject variability estimated to be 40%. Clearance was significantly influenced by CYP2D6 genotype, age, serum creatinine concentration, and subject status (patient vs volunteer). The intercompartmental clearance was also influenced by subject status, whereas the volumes of the central compartment and peripheral compartment were unaffected by any covariates. Based on the final pharmacokinetic model, the area under the plasma vernakalant concentration-time curve from 0 to 90 minutes was estimated to be 15% higher in CYP2D6 poor metabolizers than extensive metabolizers, with age and serum creatinine having much smaller influences on exposure. These data suggest that dose adjustments based on patient characteristics, including use of concomitant drugs, are unnecessary for intravenous vernakalant.

Population pharmacokinetic–pharmacodynamic analysis of vernakalant hydrochloride injection (RSD1235) in atrial fibrillation or atrial flutter

Vernakalant hydrochloride is a novel, relatively atrial-selective antiarrhythmic agent that rapidly converts atrial fibrillation (AF) to sinus rhythm (SR). This analysis integrates pharmacokinetic (PK) and safety data from 5 clinical trials of patients with AF or atrial flutter (AFL). Patients were initially given a 10-min intravenous (IV) infusion of vernakalant 3 mg/kg or placebo. If SR was not evident after a 15-min observation, then a second 10-min IV infusion of vernakalant 2 mg/kg or placebo was given. Population pharmacokinetic/pharmacodynamic (PK/PD) models were constructed for QT interval prolongation corrected for heart rate by Fridericia's formula (QTcF) and for changes in systolic blood pressure (SBP). The exposure-response relationships for QTcF and SBP were best described by sigmoidal maximum-effect (E (max)) models. For QTcF, the model was characterized by a typical E (max) of 20.3 ms, and by a vernakalant median effective concentration dependent (EC₅₀) on conversion status (4,222 ng/ml for patients converting to SR and 2,276 ng/ml for those remaining in AF/AFL). For SBP, the model was characterized by E (max) of 3.05 mmHg and EC₅₀ of 1,141 ng/ml. Risk of hypotension (SBP <90 mmHg) was primarily associated with low baseline SBP and to a smaller extent with a history of congestive heart failure (CHF); plasma vernakalant concentrations showed a small contribution to the risk of hypotension (relative risk = 1.4 at 4,000 ng/ml), which may be significant with a baseline SBP of <105 mmHg. These results show that vernakalant had a smaller effect on QTcF in patients who demonstrated conversion to SR than those remaining in AF or AFL, and it had a relatively small effect on SBP.

Disposition and Mass Balance of [&lt;sup&gt;14&lt;/sup&gt;C]Vernakalant After Single Intravenous and Oral Doses in Healthy Volunteers

Vernakalant hydrochloride is a novel antiarrhythmic drug for the rapid conversion of atrial fibrillation to sinus rhythm and prevention of relapse. In this open-label, parallel design study, 8 healthy men received single 240-mg doses of [(14)C]vernakalant hydrochloride, given as a 10-minute intravenous (IV) infusion on day 1, and as an oral gel capsule on day 22. Plasma, urine, and fecal samples were collected for 7 days after dosing to measure vernakalant and its metabolites and to estimate mass balance of total [(14)C] recovery. The disposition and metabolic profile of vernakalant after both IV and oral administration, depended on cytochrome P450 (CYP)2D6 genotype. Vernakalant underwent rapid and extensive distribution during infusion, which resulted in similar maximum plasma concentrations in extensive metabolizers (EMs) and poor metabolizers (PMs) for IV but not oral administration. Vernakalant was metabolized rapidly and extensively to a 4-O-demethylated metabolite with glucuronidation in EMs; direct glucuronidation predominated in PMs. Slower clearance in PMs contributed to 3- and 6-fold higher drug exposure (AUC(0-∞); IV and oral dosing, respectively). Urinary recovery of unchanged vernakalant was higher in PMs as well. Total [(14)C] was recovered predominantly in urine, while lower levels were recovered in feces. Mass balance was achieved, with a mean recovery of 99.7% of the IV dose and 98.7% of the oral dose, in EMs, and 89.2% and 88.2% of the IV and oral doses, respectively, in PMs. Vernakalant was well tolerated. The pharmacokinetics and metabolism of vernakalant depend on CYP2D6 genotype with more pronounced effects on exposure following oral administration; however, the differences between EMs and PMs are unlikely to be clinically significant following short-term IV infusion.

Vernakalant hydrochloride in the treatment of atrial fibrillation: a review of the latest clinical evidence

Pharmacological cardioversion is still a fundamental and readily available instrument to control symptoms and promptly restore sinus rhythm in atrial fibrillation. A rapidly acting, efficacious and safe agent that targets the fibrillating atria without affecting ventricular refractoriness is highly desirable. Among newer atrial-selective antiarrhythmic agents, vernakalant is in the most advanced phase of investigation and its intravenous formulation has recently been approved in the EU for atrial fibrillation pharmacological cardioversion. The present article reviews vernakalant’s pharmacological features and safety and efficacy as emerged from clinical trials performed so far to give a comprehensive vision of available data and to discuss implications for the clinical practice in atrial fibrillation management.

Vernakalant Hydrochloride: A NovelAtrial‐selective Agent for the Cardioversionof Recent‐onset Atrial Fibrillation in the Emergency Department

AbstractObjectives: Vernakalant is a relatively atrial‐selective antiarrhythmic agent that has been shown to successfully convert atrial fibrillation (AF) to normal sinus rhythm for some patients whose onset of dysrhythmia occurred less than 7 days previously. This study sought to evaluate the efficacy and safety of vernakalant for patients with recent‐onset AF.Methods: This was a post hoc analysis of patients with recent‐onset AF (&gt; 3 to ≤ 48 hours) enrolled in the double‐blind, placebo‐controlled Atrial arrhythmia Conversion Trial (ACT) I and the open‐label ACT IV trials. The studies enrolled adults presenting with AF to 78 emergency departments (ED) and cardiac clinics in six countries. Patients received a 10‐minute intravenous infusion of vernakalant or placebo, followed by an additional infusion if necessary. Efficacy assessments included conversion to sinus rhythm within 90 minutes and median time to conversion. Safety evaluations included telemetry, Holter monitoring, and adverse events (AEs).Results: Of the 290 patients, 229 received vernakalant, 61 received placebo, and the overall mean age was 59 years. The vernakalant and placebo groups were similar. Of all patients given vernakalant, 136 (59.4%) converted to sinus rhythm within 90 minutes, compared with three (4.9%) placebo patients. The median time to conversion with vernakalant was 12 minutes (interquartile range = 7–24.5 minutes). Clinically significant bradycardia and hypotension were uncommon, and no cases of torsade de pointes or ventricular fibrillation occurred.Conclusions: Vernakalant rapidly converted recent‐onset AF to sinus rhythm in over half of patients, was well tolerated, and has the potential to offer an important therapeutic option for rhythm control of recent‐onset AF in the ED.ACADEMIC EMERGENCY MEDICINE 2010; 17:1175–1182 © 2010 by the Society for Academic Emergency Medicine