Advanced searches left 3/3

Flecainide - Crossref

Summarized by Plex Scholar
Last Updated: 07 August 2022

* If you want to update the article please login/register

Increased early sodium current causes familial atrial fibrillation and dampens effect of flecainide

Methods We created a new murine model with the Scn5a-M1875T mutation, enabling us to investigate the effect of the Na v 1. 5 mutation in vivo and in vitro using patch clamp and microelectrode recording of atrial cardiomyocytes, optical mapping, epidemiology, histology, and biochemistry. Initial cardiac sodium current from newly isolated adult Scn5a -M1875T +/- mice showed a selective rise in the early cardiac sodium current, larger action potential amplitude, and a faster peak-upstroke velocity. Our results indicate that elevated atrial peak sodium current as a potential source of elevated atrial excitability and therefore AF. What's new The point mutation M1875T in the cardiac sodium channel's C-terminal domain of the cardiac sodium channel Na v1. 5 leads to an increase in early peak sodium current in left atria. Our results point to a possible explanation for the inconsistent use of sodium channel blockers in patients with AF.

Source link: https://doi.org/10.1101/2022.01.18.476646


Common Structural Pattern for Flecainide Binding in Atrial-Selective K v 1.5 and Na v 1.5 Channels: A Computational Approach

The most common cardiac rhythm is atrial fibrillation. Combining blockade of Nav1. 5 and Kv1. 5 ion channels produced a synergistic anti-arrhythmic effect without effect on ventricles, according to theoretical models. As a first step toward prospective multi-target directed ligand design goals, we concentrated on Kv1. 5 and Nav1. 5 to look for structural similarities in their binding site for flecainide. In a flecainide-Kv1. 5 docking model and a solved structure of flecainide-Nav1. 5 complicated, we described a computational workflow for comparing flecainide BS comparisons. Since the logical MTDL design for AF is still incipient, our results may help advance multi-target selective strategies for AF treatment.

Source link: https://doi.org/10.20944/preprints202205.0392.v1


Common Structural Pattern for Flecainide Binding in Atrial-Selective Kv1.5 and Nav1.5 Channels: A Computational Approach

A combined blockade of Nav1. 5 and Kv1. 5 ion channels produced a synergistic anti-arrhythmic effect without changes in ventricles, according to Theoretical studies. As a first step for potential multi-target directed ligand design strategies, we concentrated on Kv1. 5 and Nav1. 5 to look for structural similarities in their binding site for flecainide. We present a computational workflow for a flecainide BS comparison in a flecainide-Kv1. 5 docking model and a fully integrated flecainide-Nav1. 5 complex. Our results may help with multi-target atrial-selective strategies for AF treatment since the logical MTDL pattern for AF is still incipient.

Source link: https://doi.org/10.3390/pharmaceutics14071356


Successful Treatment of Supraventricular Tachycardia Exhibiting Hydrops fetalis with Flecainide Acetate

BACKGROUND: The effectiveness of flecainide acetate for the treatment of fetal supraventricular tachycardia with hydrops fetalis, as well as shifts in venous blood flow patterns in the fetus during therapy have been documented. Oral flecainide therapy was initiated at 30 weeks of gestation. Conclusion: And after cardioversion in the fetus with supraventricular tachycardia, which could be measured more precisely by venous Doppler analysis, reversible cardiac dysfunction was observed.

Source link: https://doi.org/10.1159/000068066


How does flecainide impact RyR2 channel function?

Flecainide, a surface membrane sodium channel blocker, has also been shown to reduce cardiac ryanodine receptor-mediated sarcoplasmic reticulum Ca2+ production by a cardiac class 1C blocker, according to the author. Flecainide can bind to at least four separate inhibitory sites on RyR2 and one activation site, in contrast to its single NaV1. 5 pore binding site. Flecainide binding to voltage-dependent inhibition sites reduces cation fluxes in a direction opposite to physiological Ca2+ flow from SR lumen to cytosol, according to a confounding finding. Flemis may reduce Ca2+ efflux by blocking counter currents through the pore, which would otherwise limit SR membrane potential variation during systolic Ca2+ efflux. This may mean that, rather than explicitly blocking Ca2+ efflux, flecainide can reduce Ca2+ efflux by blocking counter currents through the pore that otherwise limit SR membrane potential changes during systolic Ca2+ efflux. In summary, the antiarrhythmic consequences of flecainide in CPVT seem to involve multiple aspects of EC coupling and several actions on RyR2. Their clarification may help identify novel drug targets and enhance flecainideu2019s clinical use in CPVT.

Source link: https://doi.org/10.1085/jgp.202213089


Elimination of Benign Ventricular Premature Beats or Ventricular Tachycardia with Catheter Ablation versus Two Different Optimal Antiarrhythmic Drug Treatment Regimens (Sotalol or Verapamil/Flecainide)

Hypothesis: The evaluation of catheter ablation in patients with symptomatic idiopathic VA, as well as optimal AAD therapy with sotalol or flecainide/verapamil is a randomized, multicenter, prospective clinical trial. There will be a burden of 200,000 percent on 24-h ambulatory rhythm monitoring. One hundred eighty patients with persistent symptomatic VA in the absence of structural heart disease or underlying cardiac ischemia are eligible for catheter ablation with a monomorphic VA origin, with a burden u2265 percent. Patients randomized to one of the two AAD arms will cross-over to the other AAD treatment arm in order to find differences in drug safety and QoL in individual patients.

Source link: https://doi.org/10.1159/000509661


Description of flecainide usage from 2005-2018 in the Danish population

BACKGROUND - Introduction: Flecainide is an antiarrhythmic class 1C drug used to treat cardiac arrhythmias. Methods Using the National Danish Registers, all Danish patients over the age of 18 years with a redeemed prescription for flecainide between January 1st, 2005 and December 31st, 2018, and included at the time of the first prescription. Agents who were enrolled in the period from 180 days prior to and 180 days after the inclusion date were recorded. Results The study cohort included 6,594 patients with a median [IQR] age change from 2005 to 63 [56-69] in 2018, with 56% being women, with the most common arrhythmia diagnosis being AF. The number of patients using flecainide was down by 0. 3 percent this year relative to the 144,215 patients with widespread atrial fibrillation in Denmark in 2018. The percentage of patients on concomitant AVNB therapy varied throughout the study period, with 93% in 2005 and 95% in 2018, with an average increase of 0. 3% per year over time. The number of patients with concomitant AVNB treatment to flecainide decreased from 94% in the first year to 90% between the second and third years. In 2005, the number of patients with a diagnosis of ischemic heart disease was 10% in 2005, down to 6% in 2018. Conclusions Flecainide use increased from 2005 to 2018 was up from 2005 to 2018. The use of AVNB was high in patients treated with flecainide and escalated over time, with beta-blocker being the most common.

Source link: https://doi.org/10.1093/europace/euac053.054


P406 UNMASKING A PATTERN OF BRUGADA: FLECAINIDE VS AJMALINA

Abstract Brugada syndrome is mainly present in males in the third and fourth decade of life. With Propafenone, a previous paroxysmal tachycardia from atrio-u2013ventricular reentry emerged in antiarrhythmic prophylaxis for several years, and subsequently treated with catheter ablation of the right lateral accessory path. We conducted a Flecainide test in the following days, considering the lack of documentation of complex ventricular arrhythmias during transport to the hospital and during the stay in the UTIC, the long-term antiarrhythmic therapy with sodium channel inhibitors, and the absence of a typical Brugada pattern during fever, we decided against testing type 1 for Brugada type 1 in the absence of atypical Brugada pattern during fever.

Source link: https://doi.org/10.1093/eurheartj/suac012.392


Flecainide toxicity with high pacemaker capture thresholds and associated takotsubo syndrome

At atrioventricular nodal ablation, very high right ventricular capture thresholds resulted in abortion of the procedure as back-up ventricular pacing could not be assured with sufficient margin for safety. The patient suffered cardiogenic shock after the electrophysiology study, but not soon after, the patient developed apical left ventricular regional wall motion abnormality, indicating new apical ballooning and a wide QRS complex electrocardiogram. After 2 days of therapy, the regional wall motion abnormalities and EKG changes improved along with normalization of capture thresholds.

Source link: https://doi.org/10.1136/bcr-2021-243326


Flecainide increases Kir2.1 currents by interacting with cysteine 311, decreasing the polyamine-induced rectification

Both increase and decrease of cardiac inward rectifier currents are connected to severe cardiac arrestrhythmias. Flecainide, a commonly used antiarrhythmic drug, has ventricular proarrhythmic activity while still effectively controlling ventricular arrhythmias linked to gene encoding Kir2. 1 channels, which decrease I K1 decreases. Here we describe the electrophysiological and molecular basis of the new generated by Kir2. 1 channels and I K1 in ventricular myocytes, as well as an enzyme, molecular basis. That increases the outward I Kir2. 1 channel produced by homotetrameric Kir2. 1 channels by lowering their affinity for intracellular polyamines, which reduces the current's inward rectification. Because Kir2. 2 and Kir2. 3 channels do not have a Cys residue at the same level, this explains why flecainide does not raise I Kir2. 2 and I Kir2. 3. Incubation with flecainide increases the presence of functional Kir2. 1 channels in the membrane, a function that was also observed by Cys311.

Source link: https://doi.org/10.1073/pnas.1004021107

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions