PURPOSE: Although the economic and mortality burden of atrial fibrillation (AF) is substantial, it remains unclear which treatment strategies for rate and rhythm control are most cost-effective. Consequently, economic factors can play an adjunctive role in guiding treatment selection. MATERIALS AND METHODS: We built a Markov chain Monte Carlo model using the Korean Health Insurance Review & Assessment Service database. Drugs for rate control and rhythm control in AF were analyzed. Cost-effective therapies were selected using a cost-effectiveness ratio, calculated by net cost and quality-adjusted life years (QALY). RESULTS: In the National Health Insurance Service data, 268149 patients with prevalent AF (age ≥18 years) were identified between January 1, 2013 and December 31, 2015. Among them, 212459 and 55690 patients were taking drugs for rate and rhythm control, respectively. Atenolol cost $714/QALY. Among the rate-control medications, the cost of propranolol was lowest at $487/QALY, while that of carvedilol was highest at $1363/QALY. Among the rhythm-control medications, the cost of pilsicainide was lowest at $638/QALY, while that of amiodarone was highest at $986/QALY. Flecainide and propafenone cost $834 and $830/QALY, respectively. The cost-effectiveness threshold of all drugs was lower than $30000/QALY. Compared with atenolol, the rate-control drugs propranolol, betaxolol, bevantolol, bisoprolol, diltiazem, and verapamil, as well as the rhythm-control drugs sotalol, pilsicainide, flecainide, propafenone, and dronedarone, showed better incremental cost-effectiveness ratios. CONCLUSION: Propranolol and pilsicainide appear to be cost-effective in patients with AF in Korea assuming that drug usage or compliance is the same.
Amiodarone ; Atenolol ; Atrial Fibrillation ; Betaxolol ; Bisoprolol ; Compliance ; Cost-Benefit Analysis ; Diltiazem ; Flecainide ; Humans ; Insurance, Health ; Korea ; Markov Chains ; Mortality ; National Health Programs ; Propafenone ; Propranolol ; Quality-Adjusted Life Years ; Sotalol ; Verapamil

Concealed bypass tract (CBT) results from incomplete development of the atrioventricular (AV) annulus. CBT conducts only in a retrograde direction, and therefore does not cause pre-excitation on standard electrocardiograms. The most common tachycardia associated with CBT is an orthodromic atrioventricular reentrant tachycardia (AVRT): a pathway involving anterograde circuitry through the AV node and His Purkinje system and retrograde conduction over the accessory pathway. Orthodromic AVRT accounts for approximately 90%-95% cases of AVRT. Most incidences of CBT occur at the left free wall. Vagal maneuvers and/or intravenous (IV) adenosine are recommended for first line acute management of AVRT. However, pharmacological therapy with IV diltiazem, verapamil, or beta blockers can also be effective for acute treatment for orthodromic AVRT in patients who do not show pre-excitation on their resting ECG during sinus rhythm. The first-line ongoing therapy for AVRT is catheter ablation of CBT; when catheter ablation is not indicated or preferred, oral beta blockers, diltiazem, verapamil, flecainide, propafenone, or amiodarone are recommended.
Adenosine ; Amiodarone ; Atrioventricular Node ; Catheter Ablation ; Diltiazem ; Electrocardiography ; Flecainide ; Humans ; Incidence ; Propafenone ; Tachycardia ; Tachycardia, Supraventricular* ; Verapamil

Dronedarone is a new antiarrhythmic drug for the treatment of nonpermanent atrial fibrillation. Compared with amiodarone, it is regarded as a safe medication due to its structural differences. In this report, we describe a 56-year-old man who developed photosensitivity due to dronedarone. He presented with itchy skin rashes for 1 week. Maculopapular exanthema was localized on the neck, both arms, and both hands, with sparing of the other parts of the body. Dronedarone was prescribed 4 weeks ago when atrial fibrillation occurred. After development of skin rashes, dronedarone was discontinued, and systemic steroid, antihistamine, and topical corticosteroid were administered for 1 week, with improvement in skin rashes. The photopatch test was performed with antiarrhythmic drugs, including dronedarone, amiodarone, and flecainide, 4 weeks after withdrawal of dronedarone. Positive reactions were recorded only to dronedarone at the site exposed to ultraviolet A. He was diagnosed with dronedarone-induced photosensitivity and advised to change the antiarrhythmic medication to others. There have been a few case reports on photosensitivity reactions due to dronedarone, which were diagnosed only by clinical suspicion. However, we suspected photosensitivity and proved it by the photopatch test. Photosensitivity should be considered in patients having skin rashes on the exposed area and taking antiarrhythmic medication, including dronedarone.
Amiodarone ; Anti-Arrhythmia Agents ; Arm ; Atrial Fibrillation ; Exanthema ; Flecainide ; Hand ; Humans ; Middle Aged ; Neck

Although Atrial flutter (AFL) in newborn infant with normal cardiac anatomy has benign clinical course, an intractable AFL is associated with an increased risk of development of heart failure and sudden death, and is still difficult to manage. It requires multiple external electrical cardioversions, and it shows a poor response to antiarrhythmic drug therapy. We report a case of a premature infant with an intractable AFL, which we successfully treated with oral flecainide and propranolol in spite of recurred AFL. A 1-month-old, 34-week gestation, premature baby presented with an irregular heart beat and irritability. An AFL with 2:1 atrioventricular conduction was documented. Because of the intractable AFL, repeated electrical cardioversion and amiodarone were continued for 14 days. However, amiodarone was discontinued in favour of flecainide and propranolol because of the recurrent AFL and newly developed transient hypothyroidism. During 1-year follow-up period, in which oral flecainide and propranolol were continued, no AFL was observed.
Amiodarone ; Atrial Flutter* ; Death, Sudden ; Drug Therapy ; Electric Countershock ; Flecainide* ; Follow-Up Studies ; Heart ; Heart Failure ; Humans ; Hypothyroidism ; Infant, Newborn ; Infant, Premature* ; Pregnancy ; Propranolol*

BACKGROUND: Flecainide is an antiarrhythmic agent that is used primarily in the treatment of cardiac arrhythmias. Some evidences also suggest that flecainide can participate in alveolar fluid clearance and inflammatory responses. This experiment was aimed to evaluate the effects of flecainide on sepsis induced acute lung injury in a rat model. METHODS: Rats were treated with subcutaneous infusion of saline or flecainide (0.1 or 0.2 mg/kg/hr) by a mini-osmotic pump. Subcutaneous infusion was started 3 hours before and continued until 8 hours after intraperitoneal injection of saline or endotoxin. Animals were sacrificed for analyses of severity of acute lung injury with wet to dry (W/D) ratio and lung injury score (LIS) in lung and inflammatory responses with level of leukocyte, polymorphonuclear neutrophils (PMNs) and inteleukin-8 (IL-8) in bronchoalveolar lavages fluid (BALF). RESULTS: Flecainide markedly improved dose dependently sepsis induced acute lung injury as analysed by W/D ratio (from 2.24 ± 0.11 to 1.76 ± 0.09, p < 0.05) and LIS (from 3 to 1, p < 0.05), and inflammatory response as determined by leukocyte (from 443 ± 127 to 229 ± 95, p < 0.05), PMNs (from 41.43 ± 17.63 to 2.43 ± 2.61, p < 0.05) and IL-8 (from 95.00 ± 15.28 to 40.00 ± 10.21, p < 0.05) in BALF. CONCLUSIONS: Flecanide improve sepsis induced acute lung injury in rats by controlling inflammatory responses.
Acute Lung Injury* ; Animals ; Arrhythmias, Cardiac ; Bronchoalveolar Lavage ; Flecainide* ; Infusions, Subcutaneous ; Injections, Intraperitoneal ; Interleukin-8 ; Leukocytes ; Lung ; Lung Injury ; Models, Animal ; Neutrophils ; Rats ; Sepsis*

Flecainide acetate is a potent class IC anti-arrhythmic drug with a major sodium channel blocking effect. Flecainide toxicity can cause myocardial impairment and precipitate circulatory collapse. It may also result in life-threatening arrhythmia, although cases of flecainide-induced torsades de pointes are rare. Furthermore, the electrical and hemodynamic deteriorations observed during flecainide toxicity may not respond to conventional treatments. In the present study, we report the case of a 20-year-old Korean man with flecainide poisoning, who presented with hypotension. The patient was successfully treated with sodium bicarbonate, amiodarone, MgSO₄, and lidocaine, with no recourse to extracorporeal therapy. Although there is no standard therapy for flecainide toxicity, this report demonstrates that intensive pharmacological treatment is beneficial in cases of flecainide overdose.
Amiodarone ; Arrhythmias, Cardiac ; Drug-Related Side Effects and Adverse Reactions ; Flecainide ; Hemodynamics ; Humans ; Hypotension ; Lidocaine ; Poisoning ; Shock ; Sodium Bicarbonate ; Sodium Channels ; Torsades de Pointes* ; Young Adult

BACKGROUND: Flecainide is an antiarrhythmic agent that is used primarily in the treatment of cardiac arrhythmias. Some evidences also suggest that flecainide can participate in alveolar fluid clearance and inflammatory responses. This experiment was aimed to evaluate the effects of flecainide on sepsis induced acute lung injury in a rat model. METHODS: Rats were treated with subcutaneous infusion of saline or flecainide (0.1 or 0.2 mg/kg/hr) by a mini-osmotic pump. Subcutaneous infusion was started 3 hours before and continued until 8 hours after intraperitoneal injection of saline or endotoxin. Animals were sacrificed for analyses of severity of acute lung injury with wet to dry (W/D) ratio and lung injury score (LIS) in lung and inflammatory responses with level of leukocyte, polymorphonuclear neutrophils (PMNs) and inteleukin-8 (IL-8) in bronchoalveolar lavages fluid (BALF). RESULTS: Flecainide markedly improved dose dependently sepsis induced acute lung injury as analysed by W/D ratio (from 2.24 ± 0.11 to 1.76 ± 0.09, p < 0.05) and LIS (from 3 to 1, p < 0.05), and inflammatory response as determined by leukocyte (from 443 ± 127 to 229 ± 95, p < 0.05), PMNs (from 41.43 ± 17.63 to 2.43 ± 2.61, p < 0.05) and IL-8 (from 95.00 ± 15.28 to 40.00 ± 10.21, p < 0.05) in BALF. CONCLUSIONS: Flecanide improve sepsis induced acute lung injury in rats by controlling inflammatory responses.
Acute Lung Injury ; Animals ; Arrhythmias, Cardiac ; Bronchoalveolar Lavage ; Flecainide ; Infusions, Subcutaneous ; Injections, Intraperitoneal ; Interleukin-8 ; Leukocytes ; Lung ; Lung Injury ; Models, Animal ; Neutrophils ; Rats ; Sepsis

To study the transport mechanisms of drugs for transplacental treatment of fetal tachyarrhythmia, MDCKII-BCRP and MDCKII cell models was used. MDCKII-BCRP and MDCKII cell monolayer model was used to investigate the bi-direction transport of sotalol, propranolol, propafenone, procainamide and flecainide. Drug concentrations were measured by HPLC-UV or chemiluminescence. The apparent permeability coefficient (P(app)), efflux rate (R(E)) and net efflux rate (R(net)) were calculated. Drugs with R(net) greater than 1.5 were further investigated using cellular accumulation experiments with or without a BCRP inhibitor. The R(net) of sotalol, propranolol, propafenone and procainamide were less than 1.5, while R(net) of flecainide with concentrations of 20 and 5 μmol x L(-1) were 1.6 and 1.9, respectively. The results showed that the transport of flecainide on MDCKII-BCRP cell monolayer could be mediated by BCRP; and the affinity increased when the concentration of flecainide decreased. Cellular accumulation experiments further suggested that accumulation of flecainide in MDCKII-BCRP cells was significantly lower than that in MDCKII cells in a concentration-dependent manner. BCRP inhibitor quercetin (50 μmol x L(-1)) significantly increased the accumulation of flecainide in MDCKII-BCRP cells (P < 0.05). Our preliminary data showed that flecainide but not sotalol, propranolol, propafenone or procainamide can be a substrate of BCRP. Thus the effect of flecainide may be affected by the BCRP in the maternal placental trophoblast membrane layer when treating fetal tachyarrhythmia.
Animals ; Biological Transport ; Cell Membrane Permeability ; Dogs ; Female ; Flecainide ; metabolism ; Madin Darby Canine Kidney Cells ; metabolism ; Placenta ; physiology ; Pregnancy ; Tachycardia ; drug therapy

Flecainide acetate is a potent class Ic anti-arrhythmic drug with a major sodium channel-blocking effect. Flecainide toxicity can cause myocardial impairment and precipitate circulatory collapse, particularly in patients with renal failure. Electrical and hemodynamic deterioration during flecainide toxicity may not respond to conventional treatments. We report the successful management of flecainide toxicity using extracorporeal membrane oxygenation (ECMO), hemoperfusion, and bicarbonate administration maintaining alkalinity.
Extracorporeal Membrane Oxygenation ; Flecainide* ; Hemodynamics ; Hemoperfusion ; Humans ; Renal Insufficiency ; Shock ; Sodium ; Tachycardia, Supraventricular*

We describe here a woman with Brugada syndrome revealed in postoperative period. A 48-year-old woman who underwent open biopsy of a tumor on her left distal femur under general anesthesia experienced post-surgical palpitations and chest discomfort. On the following day, an electrocardiogram showed coved type ST elevation with T inversion on V1 and V2 without any structural heart disease. After we confirmed it by a flecainide provocation test, the patient was diagnosed with Brugada syndrome. Genetic analysis showed c.3578G > A (p.Arg1193Gln) variant in the SCN5A gene. She underwent successful curettage and internal fixation under a single-shot spinal anesthesia without any adverse events.
Anesthesia, General ; Anesthesia, Spinal ; Biopsy ; Brugada Syndrome ; Curettage ; Electrocardiography ; Female ; Femur ; Flecainide ; Heart Diseases ; Humans ; Postoperative Period ; Thorax