Flecainide
Anti-Arrhythmia Agents
Disopyramide
Propafenone
Encainide
Quinidine
Sodium Channel Blockers
Tachycardia, Supraventricular
NAV1.5 Voltage-Gated Sodium Channel
Sodium Channels
Arrhythmias, Cardiac
Electrocardiography
Lidocaine
Mexiletine
Voltage-Gated Sodium Channel Blockers
Heart Conduction System
Cross Circulation
Ajmaline
Tachycardia, Ventricular
Atrial Fibrillation
Cardiac Complexes, Premature
Digoxin
Fetal tachycardias: management and outcome of 127 consecutive cases. (1/232)
OBJECTIVE: To review the management and outcome of fetal tachycardia, and to determine the problems encountered with various treatment protocols. STUDY DESIGN: Retrospective analysis. SUBJECTS: 127 consecutive fetuses with a tachycardia presenting between 1980 and 1996 to a single tertiary centre for fetal cardiology. The median gestational age at presentation was 32 weeks (range 18 to 42). RESULTS: 105 fetuses had a supraventricular tachycardia and 22 had atrial flutter. Overall, 52 fetuses were hydropic and 75 non-hydropic. Prenatal control of the tachycardia was achieved in 83% of treated non-hydropic fetuses compared with 66% of the treated hydropic fetuses. Digoxin monotherapy converted most (62%) of the treated non-hydropic fetuses, and 96% survived through the neonatal period. First line drug treatment for hydropic fetuses was more diverse, including digoxin (n = 5), digoxin plus verapamil (n = 14), and flecainide (n = 27). The response rates to these drugs were 20%, 57%, and 59%, respectively, confirming that digoxin monotherapy is a poor choice for the hydropic fetus. Response to flecainide was faster than to the other drugs. Direct fetal treatment was used in four fetuses, of whom two survived. Overall, 73% (n = 38) of the hydropic fetuses survived. Postnatally, 4% of the non-hydropic group had ECG evidence of pre-excitation, compared with 16% of the hydropic group; 57% of non-hydropic fetuses were treated with long term anti-arrhythmics compared with 79% of hydropic fetuses. CONCLUSIONS: Non-hydropic fetuses with tachycardias have a very good prognosis with transplacental treatment. Most arrhythmias associated with fetal hydrops can be controlled with transplacental treatment, but the mortality in this group is 27%. At present, there is no ideal treatment protocol for these fetuses and a large prospective multicentre trial is required to optimise treatment of both hydropic and non-hydropic fetuses. (+info)Intracoronary flecainide induces ST alternans and reentrant arrhythmia on intact canine heart: A role of 4-aminopyridine-sensitive current. (2/232)
BACKGROUND: The electrical alternans shown on an ST segment, ST alternans, is known as one of the most important predictors of ventricular fibrillation (VF). It has also been reported that sodium channel inhibition changes action potential configuration, especially on the repolarization phase. Thus, the sodium channel blocker may produce ST alternans and trigger reentrant arrhythmia. METHODS AND RESULTS: A sodium channel blocker (disopyramide, lidocaine, or flecainide) was infused selectively into the left anterior descending coronary artery in anesthetized, open-chest dogs. Sixty unipolar electrograms were simultaneously recorded from the entire cardiac surface of the heart. The amplitude of ST alternans (STa) was determined as the difference in the ST-segment magnitude between 2 consecutive electrograms. We accepted the greatest STa among 60 leads for evaluation. High-dose flecainide (100 microg. kg-1. min-1) increased STa and evoked a spontaneous VF. The STa in high-dose flecainide loading (8.7+/-3.4 mV; mean+/-SEM) was significantly greater than that in disopyramide or lidocaine (0. 9+/-0.4 and 0.8+/-0.2 mV, P<0.05). Treatment of 4-aminopyridine (4-AP) suppressed the increase in STa and the occurrence of VF evoked by flecainide, while E4031 or verapamil did not inhibit those. CONCLUSIONS: Flecainide caused the ST alternans that was closely correlated to the occurrence of VF. Because the ST alternans was suppressed by 4-AP treatment, a 4-AP-sensitive current such as Ito or Isus may play an important role on this phenomenon. (+info)Functional consequences of a domain 1/S6 segment sodium channel mutation associated with painful congenital myotonia. (3/232)
An unusual form of painful congenital myotonia is associated with a novel SCN4A mutation causing a valine to methionine substitution in the domain 1/S6 segment of the skeletal muscle sodium channel. We studied the functional characteristics of this mutant allele using a recombinant channel to gain understanding about the nature of the biophysical defect responsible for this unique phenotype. When expressed heterologously in a cultured mammalian cell line (tsA201), the mutant channel exhibits subtle defects in its gating properties similar, but not identical, to other myotonia-producing sodium channel mutations. The main abnormalities are the presence of a small non-inactivating current that occurs during short test depolarizations, a shift in the voltage-dependence of channel activation to more negative potentials, and a slowing of the time course of recovery from inactivation. Flecainide, a potent sodium channel blocker previously reported to benefit patients affected by this form of myotonia, effectively inhibits the abnormal sodium current associated with expression of the mutant channel. Our findings demonstrate the unique pattern of sodium channel dysfunction associated with a D1/S6 myotonia-producing sodium channel mutation, and provide a mechanism for the beneficial effects of flecainide in this setting. (+info)A case of vasospastic angina presenting Brugada-type ECG abnormalities. (4/232)
An electrophysiological study and a provocative test of coronary artery spasm was attempted in a 68-year-old man who was having syncopal attacks and chest pain. His electrocardiogram had the characteristics of Brugada syndrome and ventricular fibrillation (VF) was induced by programmed electrical stimulation. ST-segment elevation became exaggerated by procainamide, which could not prevent the induction of VF. Coronary angiography revealed no stenotic lesions, and spasm in the left coronary artery was induced by intracoronary administration of acetylcholine with similar chest pain to that experienced before. Under treatment with diltiazem and flecainide, which suppressed the induction of VF, the patient experienced no recurrence of symptoms despite persistent ST-segment elevation. No previous reports have described coronary spasm associated with Brugada-type ECG abnormalities, and patients with syncope should be evaluated carefully. (+info)Electrophysiological effects of flecainide and propafenone on atrial fibrillation cycle and relation with arrhythmia termination. (5/232)
OBJECTIVES: (1) To investigate the electrophysiological effects of flecainide and propafenone during atrial fibrillation, and their relation to arrhythmia termination; (2) to investigate the effects of isoprenaline on atrial fibrillation in basal conditions and during treatment with class 1C drugs to evaluate the role of adrenergic stimulation on proarrhythmic events occurring during this treatment. DESIGN: Prospective, single centre study. SETTING: University hospital. METHODS: 10 patients with lone paroxysmal atrial fibrillation underwent an electrophysiological study. The dynamic behaviour of MFF (the mean of 100 consecutive atrial fibrillation intervals) was evaluated at two atrial sites after induction of atrial fibrillation either at baseline or after class 1C drug administration (flecainide or propafenone 2 mg/kg). The effects of isoprenaline on MFF and RR interval were also investigated both under basal conditions and during class 1C drug treatment. RESULTS: After induction of atrial fibrillation, mean (SD) MFF shortened with time, and was further shortened by isoprenaline infusion (177 (22) v 162 (16) v 144 (11) ms, p < 0.05). The administration of class 1C drugs reversed this trend and significantly increased the MFF to an average of 295 (49) ms, leading to conversion to sinus rhythm within 10 minutes in all patients. Atrial fibrillation was then reinduced on class 1C drugs: isoprenaline shortened the MFF and RR interval with a trend to AV synchronisation (223 (43) v 269 (49) ms for the MFF, 347 (55) v 509 (92) ms for the RR, p < 0.05); 1:1 sustained AV conduction occurred in two patients, at 187 and 222 beats/min respectively. One of these patients underwent electrical cardioversion because of haemodynamic collapse. CONCLUSIONS: Class 1C drugs are effective at restoring sinus rhythm by increasing the MFF to a much greater extent than observed in self terminating atrial fibrillation episodes, and reversing the spontaneous atrial fibrillation behaviour (progressive shortening of MFF and self perpetuation of atrial fibrillation). MFF prolongation with 1:1 conduction at fast ventricular rates may lead to synchronisation during adrenergic stimulation, with a very short ventricular cycle; hence it is advisable to keep the patients at rest after acute class 1C drug loading or to consider pharmacological modulation of AV conduction for patients who are prone to a fast ventricular response. (+info)Chronotropic, inotropic, dromotropic and coronary vasodilator effects of bisaramil, a new class I antiarrhythmic drug, assessed using canine isolated, blood-perfused heart preparations. (6/232)
The cardiovascular effects of a new class I antiarrhythmic drug, bisaramil, were examined using canine isolated, blood-perfused heart preparations. Bisaramil exerted negative chronotropic, inotropic and dromotropic effects as well as coronary vasodilator action, which are qualitatively the same as those of classical class I drugs. The selectivity of bisaramil for the intraventricular conduction vs the other cardiac variables was compared with that of disopyramide and flecainide. Bisaramil was the most selective for intraventricular conduction, while it was the least selective for ventricular muscle contraction. We conclude that bisaramil may become a useful antiarrhythmic drug with less cardiac adverse effects. (+info)Relation between activation sequence fluctuation and arrhythmogenicity in sodium-channel blockades. (7/232)
To examine the correlation between activation sequence fluctuation and arrhythmogenicity, we investigated temporal changes in the activation sequence by measuring activation times [negative first derivative of voltage over time (-dV/dt) in QRS] from the entire heart in 18 dogs. The heart was paced by constant atrial stimulation. The character of the activation sequence fluctuation was established by a principal component analysis, in which the first principal component was defined as a stable component of the sequence and the second or third component as a fluctuated component. Steady state contained 2.2 +/- 0.6% (percent total principal component, mean +/- SD) of fluctuated components, which appeared in a beat-by-beat manner (activation sequence alternans). Activation sequence alternans was observed only during flecainide administration and not during lidocaine or disopyramide administration. Fluctuated components at a high dose of flecainide significantly increased (3.3 +/- 0.8%). Ventricular fibrillation ensued in all dogs (n = 6) exposed to flecainide after an increase in activation sequence alternans. In conclusion, flecainide evoked local activation sequence alternans. This phenomenon correlated with the occurrence of ventricular fibrillation. (+info)Lack of prevention of heart failure by serial electrical cardioversion in patients with persistent atrial fibrillation. (8/232)
OBJECTIVE: To investigate the occurrence of heart failure complications, and to identify variables that predict heart failure in patients with (recurrent) persistent atrial fibrillation, treated aggressively with serial electrical cardioversion and antiarrhythmic drugs to maintain sinus rhythm. DESIGN: Non-randomised controlled trial; cohort; case series; mean (SD) follow up duration 3.4 (1.6) years. SETTING: Tertiary care centre. SUBJECTS: Consecutive sampling of 342 patients with persistent atrial fibrillation (defined as > 24 hours duration) considered eligible for electrical cardioversion. INTERVENTIONS: Serial electrical cardioversions and serial antiarrhythmic drug treatment, after identification and treatment of underlying cardiovascular disease. MAIN OUTCOME MEASURES: heart failure complications: development or progression of heart failure requiring the institution or addition of drug treatment, hospital admission, or death from heart failure. RESULTS: Development or progression of heart failure occurred in 38 patients (11%), and 22 patients (6%) died from heart failure. These complications were related to the presence of coronary artery disease (p < 0.001, risk ratio 3.2, 95% confidence interval (CI) 1.6 to 6.5), rheumatic heart disease (p < 0.001, risk ratio 5.0, 95% CI 2.4 to 10.2), cardiomyopathy (p < 0.001, risk ratio 5.0, 95% CI 2.0 to 12.4), atrial fibrillation for < 3 months (p = 0.04, risk ratio 2.0, 95% CI 1.0 to 3.7), and poor exercise tolerance (New York Heart Association class III at inclusion, p < 0.001, risk ratio 3.5, 95% CI 1.9 to 6. 7). No heart failure complications were observed in patients with lone atrial fibrillation. CONCLUSIONS: Aggressive serial electrical cardioversion does not prevent heart failure complications in patients with persistent atrial fibrillation. These complications are predominantly observed in patients with more severe underlying cardiovascular disease. Randomised comparison with rate control treatment is needed to define the optimal treatment for persistent atrial fibrillation in relation to heart failure. (+info)Flecainide is an antiarrhythmic medication used to regularize abnormal heart rhythms, specifically certain types of irregular heartbeats called ventricular arrhythmias and paroxysmal atrial tachycardia/atrial fibrillation. It works by blocking sodium channels in the heart, which helps to slow down the conduction of electrical signals and reduces the likelihood of erratic heart rhythms.
Flecainide is available in oral forms such as tablets or capsules and is typically prescribed under the supervision of a healthcare professional experienced in managing heart rhythm disorders. It's important to note that flecainide can have serious side effects, including increasing the risk of dangerous arrhythmias in some patients, so it should only be used under close medical monitoring.
This definition is for informational purposes only and should not be considered a substitute for professional medical advice, diagnosis, or treatment. If you have any questions about your medications or health conditions, please consult with your healthcare provider.
Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:
1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.
It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.
Disopyramide is an antiarrhythmic medication that is primarily used to treat certain types of irregular heart rhythms (arrhythmias), such as ventricular tachycardia and atrial fibrillation. It works by blocking the activity of sodium channels in the heart, which helps to slow down and regulate the heart rate.
Disopyramide is available in immediate-release and extended-release forms, and it may be taken orally as a tablet or capsule. Common side effects of this medication include dry mouth, blurred vision, constipation, and difficulty urinating. More serious side effects can include dizziness, fainting, irregular heartbeat, and allergic reactions.
It is important to take disopyramide exactly as directed by a healthcare provider, as improper use or dosing can lead to serious complications. Additionally, individuals with certain medical conditions, such as heart failure, kidney disease, or myasthenia gravis, may not be able to safely take this medication.
Propafenone is an antiarrhythmic medication used to treat certain types of irregular heartbeats (such as atrial fibrillation, paroxysmal supraventricular tachycardia). It works by blocking certain electrical signals in the heart to help it beat regularly. Propafenone belongs to a class of drugs known as Class IC antiarrhythmics.
It is important to note that this definition provides an overview of what propafenone is and how it is used, but it does not cover all possible uses, precautions, side effects, and interactions related to the drug. For more detailed information about propafenone, including its specific indications, contraindications, and potential adverse effects, consult a reliable medical reference or speak with a healthcare professional.
Encainide is a Class Ic antiarrhythmic drug that was used to treat certain types of serious, life-threatening heart rhythm disorders (ventricular arrhythmias). It works by blocking the signals that cause the heart muscle to contract and thus help to normalize the heart rhythm. However, Encainide has been withdrawn from the market in many countries, including the United States, due to an increased risk of death associated with its use.
Quinidine is a Class IA antiarrhythmic medication that is primarily used to treat and prevent various types of cardiac arrhythmias (abnormal heart rhythms). It works by blocking the rapid sodium channels in the heart, which helps to slow down the conduction of electrical signals within the heart and stabilize its rhythm.
Quinidine is derived from the bark of the Cinchona tree and has been used for centuries as a treatment for malaria. However, its antiarrhythmic properties were discovered later, and it became an important medication in cardiology.
In addition to its use in treating arrhythmias, quinidine may also be used off-label for other indications such as the treatment of nocturnal leg cramps or myasthenia gravis. It is available in various forms, including tablets and injectable solutions.
It's important to note that quinidine has a narrow therapeutic index, meaning that there is only a small difference between an effective dose and a toxic one. Therefore, it must be carefully monitored to ensure that the patient is receiving a safe and effective dose. Common side effects of quinidine include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as visual disturbances, headache, and dizziness. More serious side effects can include QT prolongation, which can lead to dangerous arrhythmias, and hypersensitivity reactions.
Sodium channel blockers are a class of medications that work by blocking sodium channels in the heart, which prevents the rapid influx of sodium ions into the cells during depolarization. This action slows down the rate of impulse generation and propagation in the heart, which in turn decreases the heart rate and prolongs the refractory period.
Sodium channel blockers are primarily used to treat cardiac arrhythmias, including atrial fibrillation, atrial flutter, and ventricular tachycardia. They may also be used to treat certain types of neuropathic pain. Examples of sodium channel blockers include Class I antiarrhythmics such as flecainide, propafenone, lidocaine, and mexiletine.
It's important to note that sodium channel blockers can have potential side effects, including proarrhythmia (i.e., the development of new arrhythmias or worsening of existing ones), negative inotropy (decreased contractility of the heart muscle), and cardiac conduction abnormalities. Therefore, these medications should be used with caution and under the close supervision of a healthcare provider.
Supraventricular tachycardia (SVT) is a rapid heart rhythm that originates above the ventricles (the lower chambers of the heart). This type of tachycardia includes atrial tachycardia, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT). SVT usually causes a rapid heartbeat that starts and stops suddenly, and may not cause any other symptoms. However, some people may experience palpitations, shortness of breath, chest discomfort, dizziness, or fainting. SVT is typically diagnosed through an electrocardiogram (ECG) or Holter monitor, and can be treated with medications, cardioversion, or catheter ablation.
NAV1.5, also known as SCN5A, is a specific type of voltage-gated sodium channel found in the heart muscle cells (cardiomyocytes). These channels play a crucial role in the generation and transmission of electrical signals that coordinate the contraction of the heart.
More specifically, NAV1.5 channels are responsible for the rapid influx of sodium ions into cardiomyocytes during the initial phase of the action potential, which is the electrical excitation of the cell. This rapid influx of sodium ions helps to initiate and propagate the action potential throughout the heart muscle, allowing for coordinated contraction and proper heart function.
Mutations in the SCN5A gene, which encodes the NAV1.5 channel, have been associated with various cardiac arrhythmias, including long QT syndrome, Brugada syndrome, and familial atrial fibrillation, among others. These genetic disorders can lead to abnormal heart rhythms, syncope, and in some cases, sudden cardiac death.
Sotalol is a non-selective beta blocker and class III antiarrhythmic drug. It works by blocking the action of certain natural substances in your body, such as adrenaline, on the heart. This helps to decrease the heart's workload, slow the heart rate, and regulate certain types of irregular heartbeats (such as atrial fibrillation).
Sotalol is used to treat various types of irregular heartbeats (atrial fibrillation/flutter, ventricular tachycardia) and may also be used to help maintain a normal heart rhythm after a heart attack. It is important to note that Sotalol should only be prescribed by a healthcare professional who has experience in treating heart rhythm disorders.
This medical definition is based on the information provided by the National Library of Medicine (NLM).
Sodium channels are specialized protein structures that are embedded in the membranes of excitable cells, such as nerve and muscle cells. They play a crucial role in the generation and transmission of electrical signals in these cells. Sodium channels are responsible for the rapid influx of sodium ions into the cell during the initial phase of an action potential, which is the electrical signal that travels along the membrane of a neuron or muscle fiber. This sudden influx of sodium ions causes the membrane potential to rapidly reverse, leading to the depolarization of the cell. After the action potential, the sodium channels close and become inactivated, preventing further entry of sodium ions and helping to restore the resting membrane potential.
Sodium channels are composed of a large alpha subunit and one or two smaller beta subunits. The alpha subunit forms the ion-conducting pore, while the beta subunits play a role in modulating the function and stability of the channel. Mutations in sodium channel genes have been associated with various inherited diseases, including certain forms of epilepsy, cardiac arrhythmias, and muscle disorders.
Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.
An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.
There are several types of cardiac arrhythmias, including:
1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.
Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.
Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.
Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.
During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.
ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.
Lidocaine is a type of local anesthetic that numbs painful areas and is used to prevent pain during certain medical procedures. It works by blocking the nerves that transmit pain signals to the brain. In addition to its use as an anesthetic, lidocaine can also be used to treat irregular heart rates and relieve itching caused by allergic reactions or skin conditions such as eczema.
Lidocaine is available in various forms, including creams, gels, ointments, sprays, solutions, and injectable preparations. It can be applied directly to the skin or mucous membranes, or it can be administered by injection into a muscle or vein. The specific dosage and method of administration will depend on the reason for its use and the individual patient's medical history and current health status.
Like all medications, lidocaine can have side effects, including allergic reactions, numbness that lasts too long, and in rare cases, heart problems or seizures. It is important to follow the instructions of a healthcare provider carefully when using lidocaine to minimize the risk of adverse effects.
Mexiletine is defined as an antiarrhythmic agent, classified as a Class IB medication. It works by blocking sodium channels in the heart, which helps to stabilize cardiac membranes and reduces the rate of firing of cardiac cells. This makes it useful for treating certain types of irregular heart rhythms (ventricular arrhythmias).
Mexiletine is also known to have analgesic properties and is sometimes used off-label for the treatment of neuropathic pain. It is available in oral form, and its use should be under the close supervision of a healthcare provider due to its potential side effects, which can include gastrointestinal symptoms, dizziness, tremors, and cardiac arrhythmias.
Voltage-gated sodium channel blockers are a class of pharmaceutical drugs or toxins that work by inhibiting the function of voltage-gated sodium channels. These channels are crucial for the initiation and propagation of action potentials in excitable cells, such as neurons and muscle fibers. By blocking these channels, the drug reduces the flow of sodium ions into the cell, which stabilizes the membrane potential and prevents or reduces the generation of action potentials.
This class of drugs is used to treat a variety of medical conditions, including cardiac arrhythmias, neuropathic pain, and epilepsy. Examples of voltage-gated sodium channel blockers include Class I antiarrhythmics such as lidocaine, flecainide, and propafenone, as well as some antiepileptic drugs like carbamazepine and lamotrigine. Some toxins, such as those found in certain types of cone snails and spiders, also act as voltage-gated sodium channel blockers.
The heart conduction system is a group of specialized cardiac muscle cells that generate and conduct electrical impulses to coordinate the contraction of the heart chambers. The main components of the heart conduction system include:
1. Sinoatrial (SA) node: Also known as the sinus node, it is located in the right atrium near the entrance of the superior vena cava and functions as the primary pacemaker of the heart. It sets the heart rate by generating electrical impulses at regular intervals.
2. Atrioventricular (AV) node: Located in the interatrial septum, near the opening of the coronary sinus, it serves as a relay station for electrical signals between the atria and ventricles. The AV node delays the transmission of impulses to allow the atria to contract before the ventricles.
3. Bundle of His: A bundle of specialized cardiac muscle fibers that conducts electrical impulses from the AV node to the ventricles. It divides into two main branches, the right and left bundle branches, which further divide into smaller Purkinje fibers.
4. Right and left bundle branches: These are extensions of the Bundle of His that transmit electrical impulses to the respective right and left ventricular myocardium. They consist of specialized conducting tissue with large diameters and minimal resistance, allowing for rapid conduction of electrical signals.
5. Purkinje fibers: Fine, branching fibers that arise from the bundle branches and spread throughout the ventricular myocardium. They are responsible for transmitting electrical impulses to the working cardiac muscle cells, triggering coordinated ventricular contraction.
In summary, the heart conduction system is a complex network of specialized muscle cells responsible for generating and conducting electrical signals that coordinate the contraction of the atria and ventricles, ensuring efficient blood flow throughout the body.
Cross circulation is a medical procedure in which blood from one person (the donor) is circulated through the body of another person (the recipient) by connecting their cardiovascular systems. This technique was first developed and used in open-heart surgery during the 1950s, before the invention of heart-lung machines.
In cross circulation, the donor's and recipient's circulatory systems are connected through anastomoses (surgical connections) between their blood vessels. The most common configuration involved connecting the donor's femoral artery to the recipient's aorta and the donor's femoral vein to the recipient's vena cava. This allowed the donor's heart to pump oxygenated blood to both the donor and the recipient during the surgery.
Cross circulation was used as a temporary measure to maintain the recipient's circulation and oxygenation while their own heart was stopped and repaired during open-heart surgery. However, this technique had several limitations and risks, including potential complications for the donor (such as bleeding, infection, or reactions to the recipient's blood) and ethical concerns related to using one person as a "human bridge" to save another.
With the development of more advanced and safer heart-lung machines in the early 1960s, cross circulation became obsolete in cardiac surgery. Nowadays, it is rarely used and mainly of historical interest.
Phenothiazines are a class of heterocyclic organic compounds that contain a phenothiazine nucleus, which consists of a pair of benzene rings fused to a thiazine ring. They have been widely used in medicine as antipsychotic drugs for the treatment of various mental disorders such as schizophrenia and bipolar disorder.
Phenothiazines work by blocking dopamine receptors in the brain, which helps to reduce the symptoms of psychosis such as hallucinations, delusions, and disordered thinking. They also have sedative and antiemetic (anti-nausea) effects. However, they can cause a range of side effects including extrapyramidal symptoms (involuntary muscle movements), tardive dyskinesia (irreversible movement disorder), and neuroleptic malignant syndrome (a rare but potentially fatal reaction to antipsychotic drugs).
Examples of phenothiazine drugs include chlorpromazine, thioridazine, and promethazine. While they have been largely replaced by newer atypical antipsychotics, phenothiazines are still used in some cases due to their lower cost and effectiveness in treating certain symptoms.
Ajmaline is a type of medication known as a Class I antiarrhythmic agent, which is used to treat certain types of abnormal heart rhythms. It works by blocking the sodium channels in the heart muscle, which helps to slow down the conduction of electrical signals within the heart and can help to restore a normal heart rhythm.
Ajmaline is typically administered intravenously (through a vein) in a hospital setting, as it acts quickly and its effects can be closely monitored by healthcare professionals. It may be used to diagnose certain types of heart rhythm disturbances or to treat acute episodes of arrhythmias that are not responding to other treatments.
Like all medications, ajmaline can have side effects, including dizziness, headache, nausea, and chest pain. It is important for patients to be closely monitored while taking this medication and to report any unusual symptoms to their healthcare provider. Ajmaline should only be used under the close supervision of a qualified healthcare professional.
Ventricular Tachycardia (VT) is a rapid heart rhythm that originates from the ventricles, the lower chambers of the heart. It is defined as three or more consecutive ventricular beats at a rate of 120 beats per minute or greater in a resting adult. This abnormal heart rhythm can cause the heart to pump less effectively, leading to inadequate blood flow to the body and potentially life-threatening conditions such as hypotension, shock, or cardiac arrest.
VT can be classified into three types based on its duration, hemodynamic stability, and response to treatment:
1. Non-sustained VT (NSVT): It lasts for less than 30 seconds and is usually well tolerated without causing significant symptoms or hemodynamic instability.
2. Sustained VT (SVT): It lasts for more than 30 seconds, causes symptoms such as palpitations, dizziness, shortness of breath, or chest pain, and may lead to hemodynamic instability.
3. Pulseless VT: It is a type of sustained VT that does not produce a pulse, blood pressure, or adequate cardiac output, requiring immediate electrical cardioversion or defibrillation to restore a normal heart rhythm.
VT can occur in people with various underlying heart conditions such as coronary artery disease, cardiomyopathy, valvular heart disease, congenital heart defects, and electrolyte imbalances. It can also be triggered by certain medications, substance abuse, or electrical abnormalities in the heart. Prompt diagnosis and treatment of VT are crucial to prevent complications and improve outcomes.
Atrial fibrillation (A-tre-al fi-bru-la'shun) is a type of abnormal heart rhythm characterized by rapid and irregular beating of the atria, the upper chambers of the heart. In this condition, the electrical signals that coordinate heartbeats don't function properly, causing the atria to quiver instead of contracting effectively. As a result, blood may not be pumped efficiently into the ventricles, which can lead to blood clots, stroke, and other complications. Atrial fibrillation is a common type of arrhythmia and can cause symptoms such as palpitations, shortness of breath, fatigue, and dizziness. It can be caused by various factors, including heart disease, high blood pressure, age, and genetics. Treatment options include medications, electrical cardioversion, and surgical procedures to restore normal heart rhythm.
Premature cardiac complexes, also known as premature heartbeats or premature ventricular contractions (PVCs), refer to extra or early heartbeats that originate in the lower chambers of the heart (the ventricles). These extra beats disrupt the normal rhythm and sequence of heartbeats, causing the heart to beat earlier than expected.
Premature cardiac complexes can occur in healthy individuals as well as those with heart disease. They are usually harmless and do not cause any symptoms, but in some cases, they may cause palpitations, skipped beats, or a fluttering sensation in the chest. In rare cases, frequent premature cardiac complexes can lead to more serious heart rhythm disorders or decreased heart function.
The diagnosis of premature cardiac complexes is usually made through an electrocardiogram (ECG) or Holter monitoring, which records the electrical activity of the heart over a period of time. Treatment is typically not necessary unless the premature complexes are frequent, symptomatic, or associated with underlying heart disease. In such cases, medications, cardioversion, or catheter ablation may be recommended.
Digoxin is a medication that belongs to a class of drugs called cardiac glycosides. It is used to treat various heart conditions, such as heart failure and atrial fibrillation, by helping the heart beat stronger and more regularly. Digoxin works by inhibiting the sodium-potassium pump in heart muscle cells, which leads to an increase in intracellular calcium and a strengthening of heart contractions. It is important to monitor digoxin levels closely, as too much can lead to toxicity and serious side effects.
Paroxysmal Tachycardia is a type of arrhythmia (abnormal heart rhythm) characterized by rapid and abrupt onset and offset of episodes of tachycardia, which are faster than normal heart rates. The term "paroxysmal" refers to the sudden and recurring nature of these episodes.
Paroxysmal Tachycardia can occur in various parts of the heart, including the atria (small upper chambers) or ventricles (larger lower chambers). The two most common types are Atrial Paroxysmal Tachycardia (APT) and Ventricular Paroxysmal Tachycardia (VPT).
APT is more common and typically results in a rapid heart rate of 100-250 beats per minute. It usually begins and ends suddenly, lasting for seconds to hours. APT can cause symptoms such as palpitations, lightheadedness, shortness of breath, chest discomfort, or anxiety.
VPT is less common but more serious because it involves the ventricles, which are responsible for pumping blood to the rest of the body. VPT can lead to decreased cardiac output and potentially life-threatening conditions such as syncope (fainting) or even cardiac arrest.
Treatment options for Paroxysmal Tachycardia depend on the underlying cause, severity, and frequency of symptoms. These may include lifestyle modifications, medications, cardioversion (electrical shock to restore normal rhythm), catheter ablation (destroying problematic heart tissue), or implantable devices such as pacemakers or defibrillators.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Flecainide
Cardioversion
Sodium channel blocker
Encainide
Channel blocker
Cardiac Arrhythmia Suppression Trial
Catecholaminergic polymorphic ventricular tachycardia
Andersen-Tawil syndrome
Brugada syndrome
Aconitum carmichaelii
Aconitum
Aconitum coreanum
Potassium channel
Aconitum napellus
Management of atrial fibrillation
Premature ventricular contraction
Randomized controlled trial
Moracizine
Heart rate variability
Atrial fibrillation
Propafenone
Myotonia congenita
Accessory pathway
Junctional ectopic tachycardia
Cimetidine
Romano-Ward syndrome
Ebstein's anomaly
List of MeSH codes (D03)
ATC code C01
List of investigational sleep drugs
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TAMBOCOR3
- TAMBOCOR™ (flecainide acetate) is an antiarrhythmic drug available in tablets of 50, 100, or 150 mg for oral administration. (nih.gov)
- Flecainide (Tambocor) Flecainide is used to reduce irregular heartbeat. (nih.gov)
- A recent study showed that short-term treatment with flecainide ( Tambocor ), following electrical cardioversion appears to lower the chance of relapses within weeks of the procedure. (rxwiki.com)
Acetate7
- A flecainide acetate inhalation solution was self-administered by each patient using a nebulizer, with 10 patients inhaling a 30 mg flecainide solution, 22 inhaling a 60 mg solution, 21 inhaling 90 mg solution and 19 inhaling a 120 mg solution. (medscape.com)
- Flecainide acetate is a white crystalline substance with a pKa of 9.3. (nih.gov)
- Flecainide acetate is a membrane-stabilizing antiarrhythmic agent that exhibits a local anesthetic effects. (medscape.com)
- Flecainide acetate is rapidly and almost completely absorbed from the gastrointestinal tract following oral administration. (medscape.com)
- Acute electrophysiological effects of flecainide acetate on cardiac conduction and refractoriness in man. (bmj.com)
- The electrophysiological effects of flecainide acetate (2 mg/kg as an intravenous infusion over five minutes) were assessed in 47 patients undergoing electrophysiological study. (bmj.com)
- Flecainide acetate treatment of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation: dose-response studies. (bvsalud.org)
Atrial fibrillation12
- People with atrial fibrillation or atrial flutter who take flecainide may have a higher risk of developing certain types of irregular heartbeats. (medlineplus.gov)
- NEW YORK (Reuters Health) - Inhaled flecainide shows promise for returning patients with recent-onset atrial fibrillation (AF) to sinus rhythm, a new study suggests. (medscape.com)
- A lower concentration of flecainide is possible via inhalation because the drug is absorbed from the lungs into the pulmonary venous system, which flows to the heart's left atrium, where atrial fibrillation often occurs. (medscape.com)
- Flecainide is used mainly for treatment and prevention of ventricular arrhythmia, paroxysmal supraventricular tachycardia , paroxysmal atrial fibrillation , and paroxysmal atrial flutter . (medscape.com)
- Intravenous flecainide administration for conversion of paroxysmal atrial fibrillation in the emergency room]. (nih.gov)
- Tachycardia due to atrial flutter with rapid 1:1 conduction following treatment of atrial fibrillation with flecainide. (nih.gov)
- A short cut review was carried out to establish whether amiodarone is better than flecainide at restoring sinus rhythm in patients with atrial fibrillation. (bmj.com)
- Flecainide is an IC antiarrhythmic drug approved in 1984 from Food and Drug Administration for the suppression of sustained ventricular tachycardia and later for acute cardioversion of atrial fibrillation (AF) and for sinus rhythm maintenance. (encyclopedia.pub)
- Currently, flecainide is mostly used for sinus rhythm maintenance in atrial fibrillation patients without structural cardiomyopathy although recent studies enrolling different patient population demonstrated a good effectiveness and safety profile. (encyclopedia.pub)
- Currently, the use of flecainide in atrial fibrillation represents the main indication of the drug. (encyclopedia.pub)
- Flecainide should not be used to treat a certain type of irregular heartbeat ( persistent atrial fibrillation /flutter). (webmd.com)
- Flecainide can increase QRS duration especially with tachycardia (positive use dependence) and organize atrial fibrillation to atrial flutter. (towerhealth.org)
Antiarrhythmic4
- Flecainide is a class Ic antiarrhythmic agent. (wikipedia.org)
- As with all other antiarrhythmic agents, there is a risk of proarrhythmia associated with the use of flecainide. (wikipedia.org)
- As with all class I antiarrhythmic agents, flecainide increases the capture thresholds of pacemakers. (wikipedia.org)
- Flecainide is a class IC antiarrhythmic drug (AAD). (encyclopedia.pub)
Negative inotropic effect1
- In animals and isolated myocardium, a negative inotropic effect of flecainide has been demonstrated. (nih.gov)
Effects of flecainide2
- Because of the negative inotropic effects of flecainide, it should be used with caution in individuals with depressed ejection fraction, and may worsen congestive heart failure in these individuals. (wikipedia.org)
- While the toxic effects of flecainide are closely related to the plasma levels of the drug, it is unfeasible to check the plasma concentration in an individual on a regular basis. (wikipedia.org)
Pharmacist if you are allergic1
- tell your doctor and pharmacist if you are allergic to flecainide or any other medications. (medlineplus.gov)
Quinidine3
- In a randomized placebo-controlled double-blind trial, we compared flecainide to quinidine for treatment of ventricular ectopic depolarizations in 19 patients. (annals.org)
- A greater than 80% reduction of total ventricular ectopic depolarizations was obtained in eight of nine patients given flecainide and in five of ten patients given quinidine ( p = 0.09). (annals.org)
- Side effects were commoner with quinidine than flecainide ( p = 0.06). (annals.org)
Intravenous2
- Inhaled flecainide converts patients to sinus rhythm at a much lower - read 'safer' - plasma concentration compared to oral or intravenous treatments," said Dr. Crijns, a cardiologist at Maastricht University Medical Center in the Netherlands. (medscape.com)
- Four patients had serious adverse cardiac events, deemed related to the flecainide solution because they were consistent with those observed for oral and intravenous flecainide: Two cases of transient sinus arrest, one case of atrial flutter, and one case of bradycardia. (medscape.com)
Arrhythmias6
- Flecainide has been introduced into the treatment of arrhythmias in children. (wikipedia.org)
- Due to the narrow therapeutic index of flecainide, physicians should be alert for signs of toxicity before life-threatening arrhythmias occur like torsades de pointes. (wikipedia.org)
- Treatment of flecainide cardiac toxicity involves increasing the excretion of flecainide, blocking its effects in the heart, and (rarely) institution of cardiovascular support to avoid impending lethal arrhythmias. (wikipedia.org)
- Plasma levels of flecainide should be monitored, when feasible, especially in patients with severe liver or kidney failure, severe congestive heart failure, or life-threatening ventricular arrhythmias. (medscape.com)
- These electrophysiological properties strongly suggest that flecainide will be useful in the management of a wide variety of cardiac arrhythmias. (bmj.com)
- Because repolarization is not delayed flecainide is unlikely to induce ventricular arrhythmias related to prolongation of the QT interval. (bmj.com)
Ventricular tachycardia2
- Flecainide produced 100% suppression of nonsustained ventricular tachycardia and 99.5% suppression of paired ventricular depolarizations. (annals.org)
- Flecainide was first synthesized in 1972 and approved in 1984 from the Food and Drug Administration (FDA) for the suppression of sustained ventricular tachycardia [ 1 ] and later for acute cardioversion of AF and for sinus rhythm maintenance. (encyclopedia.pub)
Cardiac2
- Studies (notably the Cardiac Arrhythmia Suppression Trial) have shown an increased mortality when flecainide is used to suppress ventricular extrasystoles in the setting of acute myocardial infarction. (wikipedia.org)
- The researchers obtained electrocardiograms and flecainide-blood-plasma concentrations for each patient and tracked their cardiac rhythms for four hours using a Holter monitor to record adverse events. (medscape.com)
Sinus rhythm1
- Nearly half the patients (48%) who self-administered flecainide plus saccharin converted to sinus rhythm within 90 minutes of initiating inhalation. (medscape.com)
Cardioversion1
- Randomly selected patients took flecainide for four weeks or six months following electrical cardioversion. (rxwiki.com)
Pharmacodynamics1
- The pharmacodynamics of inhaled flecainide is different. (medscape.com)
CYP2D63
- Flecainide is metabolized in the liver via cytochrome (CYP2D6 and CYP1A2) in meta-O-dealkylated flecainide (active, but about one-fifth as potent) and meta-O-dealkylated lactam (inactive form), then excreted in the urine. (encyclopedia.pub)
- CYP2D6 genotype affects age-related decline in flecainide clearance: a population pharmacokinetic analysis. (cdc.gov)
- Serum flecainide S/R ratio reflects the CYP2D6 genotype and changes in CYP2D6 activity. (cdc.gov)
Allergic1
- On the assumption of a drug-induced allergic reaction, flecainide was withdrawn, after which liver enzymes rapidly returned to control values. (nih.gov)
Antiarrhythmics2
- This risk is probably increased when flecainide is co-administered with other class Ic antiarrhythmics, such as encainide. (wikipedia.org)
- Flecainide is in a class of medications called antiarrhythmics. (medlineplus.gov)
Serum1
- Maternal doses of flecainide up to 200 mg daily produce low levels in milk and undetectable infant serum levels. (nih.gov)
Concentrations2
- One-hour conversion rates back to normal rhythm increased with dosage as well as with the maximum plasma concentrations of flecainide. (medscape.com)
- Trough plasma concentrations are 0.2-1 µg/mL in most patients successfully treated with flecainide. (medscape.com)
20231
- Flecainide" Encyclopedia , https://encyclopedia.pub/entry/15951 (accessed November 28, 2023). (encyclopedia.pub)
Myocardial2
- Prospective participants were screened for their potential adverse responses, based on personal contraindications to flecainide such as heart failure, myocardial ischemia, or structural heart disease. (medscape.com)
- Flecainide works blocking the open-state fast inward Na+ channel Nav 1.5 [ 8 ] in a rate- and voltage-dependent manner, reducing the maximum rate of phase 0 rise of the action potential (Vmax) in fast channel-dependent myocardial fibers (mostly in His-Purkinje tissue and ventricular muscle, followed by atrial muscle) [ 9 ] . (encyclopedia.pub)
Increases1
- There is not enough information to tell whether taking flecainide also increases the risk of heart attack or death in people who have not had heart attacks within the past 2 years. (medlineplus.gov)
Toxicity1
- Signs of flecainide toxicity include marked prolongation of the PR interval and widening of the QRS duration on the surface ECG. (wikipedia.org)
Therapeutic2
- In adults, the reference range of the therapeutic trough of flecainide is 0.2-1 µg/mL. (medscape.com)
- The goal is to control or prevent arrhythmia with the lowest therapeutic plasma flecainide level. (medscape.com)
Prolongation1
- Flecainide may cause a condition that affects the heart rhythm (QT prolongation). (webmd.com)
Medication2
- Flecainide is a medication used to prevent and treat abnormally fast heart rates. (wikipedia.org)
- The flecainide trough level should be checked 3-5 days after starting the medication and less than one hour before the following dose. (medscape.com)
Liver2
- Because of the role of both the liver and the kidneys in the elimination of flecainide, the dosing of flecainide may need to be adjusted in individuals who develop either liver failure or kidney failure. (wikipedia.org)
- Although neither a reexposition with flecainide nor a liver biopsy was obtained, a flecainide-induced hepatitis seems probable. (nih.gov)
Tablet1
- Flecainide comes as a tablet to take by mouth. (medlineplus.gov)
Treatment4
- Flecainide is used in the treatment of many types of supraventricular tachycardias, including AV nodal re-entrant tachycardia (AVNRT) and Wolff-Parkinson-White syndrome (WPW). (wikipedia.org)
- In particular, flecainide has been useful in the treatment of ventricular tachycardias that are not in the setting of an acute ischemic event. (wikipedia.org)
- You may be hospitalized when you begin your treatment with flecainide. (medlineplus.gov)
- Arrhythmogenic effect of flecainide--treatment with i.v. magnesium]. (nih.gov)
Absorbed from the gastrointestinal tract1
- Flecainide, administered bis in die (immediate-release form) or once daily (controlled-release form), is nearly completely absorbed from the gastrointestinal tract with very high bioavailability (from 85% to 90%) [ 3 ] . (encyclopedia.pub)
Dose1
- Your doctor will probably start you on a low dose of flecainide and gradually increase your dose, not more than once every 4 days. (medlineplus.gov)
Cytochrome1
- In vitro metabolic studies have confirmed that cytochrome P450IID6 is involved in the metabolism of flecainide. (nih.gov)
Patients3
- A final group of 29 patients self-administered 120 mg flecainide in a solution that also contained saccharin. (medscape.com)
- The percentage of patients with successful conversion were 10% in the 30 mg group, 35% in the 60 mg group, 33% in the 90 mg group, 35% in the 120 mg group and 44% in the flecainide-plus-saccharin solution. (medscape.com)
- Given the 90-minute conversion rate for inhaled flecainide (per our study result) and the well-known low placebo conversion rate within the 90-minute time frame, the formal sample size in a randomized trial would be 250 patients," Dr. Crijns said. (medscape.com)
Adverse1
- Flecainide is not expected to cause any adverse effects in breastfed infants, especially if the infant is older than 2 months. (nih.gov)
Heart3
- In the long-term, flecainide seems to be safe in people with a healthy heart with no signs of left ventricular hypertrophy, ischemic heart disease, or heart failure. (wikipedia.org)
- In a study of people who had experienced heart attacks within the past 2 years, people who took flecainide were more likely to have another heart attack or to die than people who did not take flecainide. (medlineplus.gov)
- Had you had a heart attack in the 1980s, you might've been given a drug called encainide or flecainide to prevent irregular heart beats, which are common potentially fatal after-effects of heart attacks. (abc.net.au)
Prevent1
- Flecainide is used to prevent certain types of life-threatening irregular heartbeats. (medlineplus.gov)
Effect2
- Flecainide does not undergo any consequential presystemic biotransformation (first-pass effect). (nih.gov)
- Flecainide exerts a variable effect in terms of action potential duration (APD) and effective refractory period (ERP) on ventricular fibers and the Purkinje fibers. (encyclopedia.pub)
Administration1
- In individuals suspected of having the Brugada syndrome, the administration of flecainide may help reveal the ECG findings that are characteristic of the disease process. (wikipedia.org)
Hours2
- Some people may take flecainide once every 8 hours if they experience side effects or if their condition cannot be controlled by taking flecainide every 12 hours. (medlineplus.gov)
- The peak flecainide plasma concentration is generally reached within 2-3 hours. (medscape.com)
Plasma1
- A flecainide plasma trough level of less than 0.2 µg/mL is considered subtherapeutic. (medscape.com)
Risk2
- The risk of proarrhythmia is not necessarily associated with the length of time an individual is taking flecainide, and cases of late proarrhythmia have been reported. (wikipedia.org)
- Because of this serious risk and because flecainide has not been shown to help people with irregular heartbeats to live longer, flecainide should be used only to treat people with life-threatening irregular heartbeats. (medlineplus.gov)
Levels1
- Goji might increase the levels of flecainide in the body. (nih.gov)