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Flecainide arrhythmia with

Flecainide, as with other local anesthetics, is used for naturally occurring ventricular arrhythmia. A synonym of this drug is tambocor. [Pg.251]

In the National Heart, Lung, and Blood Institute s Cardiac Arrhythmia Suppression Trial (CAST), a long-term, multicenter, randomized, double-blind study in patients with asymptomatic non-life-threatening ventricular arrhythmias who had an Ml more than 6 days but less than 2 years previously, an excessive mortality or nonfatal cardiac arrest rate (7.7%) was seen in patients treated with encainide or flecainide compared with that seen in patients assigned to carefully matched placebo-treated groups (3%). The average duration of treatment with encainide or flecainide in this study was 10 months. [Pg.436]

The applicability of the CAST results to other populations (eg, those without recent Ml) is uncertain, but at present, it is prudent to consider the risks of Class 1C agents (including flecainide), coupled with the lack of any evidence of improved survival, generally unacceptable in patients without life-threatening ventricular arrhythmias, even if the patients are experiencing unpleasant, but not life-threatening, symptoms or signs. [Pg.456]

FLECAINIDE ANTIVIRALS - PROTEASE INHIBITORS Amprenavir, ritonavir and possibly saquinavir and tipranavir with ritonavir t flecainide levels, with risk of ventricular arrhythmias Uncertain possibly inhibition of CYP3A4- and CYP2D6-mediated metabolism of flecainide Manufacturers recommend avoiding co-administration of flecainide with amprenavir, ritonavir and saquinavir... [Pg.20]

Fleca.inide, Elecainide acetate, a fluorobenzamide, is a derivative of procainamide, and has been reported to be efficacious in suppressing both supraventricular and ventricular arrhythmias (26—29). The dmg is generally reserved for patients with serious and life-threatening ventricular arrhythmias. Elecainide depresses phase 0 depolarization of the action potential, slows conduction throughout the heart, and significantly prolongs repolarization (30). The latter effect indicates flecainide may possess some Class III antiarrhythmic-type properties (31). [Pg.114]

Flecainide is a drug used for arrhythmias and is of particular use in ventricular arrhythmias and paroxysmal atrial fibrillation. Flecainide has a membrane-stabilising activity. Use of flecainide may precipitate serious arrhythmias, even in patients with no history of cardiovascular disease and with otherwise normal hearts. [Pg.169]

Amiodarone is a drug used for arrhythmias, which has very similar properties to flecainide. Both drugs may cause pneumonitis as a side-effect but risk is lower with flecainide. Signs of pneumonitis include progressive shortness of breath or cough. [Pg.169]

Clinical use of encainide is primarily associated with the presence of serious ventricular tachycardia however, like flecainide, it is also sufficiently effective for atrial arrhythmia and is used for natural occurrences. A synonym of this drug is enkaid. [Pg.251]

Not recommended in patients with less severe ventricular arrhythmias even if the patients are symptomatic. Because of proarrhythmic effects of flecainide, reserve use for patients in whom benefits outweigh risks. [Pg.457]

Once the arrhythmia is controlled, it may be possible to reduce the dose, as necessary, to minimize side effects or effects on conduction. PSVT and PAF The recommended starting dose is 50 mg every 12 hours. Doses may be increased in increments of 50 mg twice daily every 4 days until efficacy is achieved. For PAF patients, a substantial increase in efficacy without a substantial increase in discontinuation for adverse experiences may be achieved by increasing the flecainide dose from 50 to 100 mg twice/day. The maximum recommended dose for patients with paroxysmal supraventricular arrhythmias is 300 mg/day. [Pg.457]

Approved indications for propafenone include treatment of supraventricular arrhythmias and life-threatening ventricular arrhythmias in the absence of structural heart disease. Propafenone has been shown to increase mortality in patients with structural heart disease, and so extreme caution must be used in this subset of patients. As with flecainide, the patient should be hospitalized for initiation of therapy. [Pg.181]

Because of mortality risks noted for flecainide and/or encainide (type 1C antiarrhyth-mics), this drug should be reserved for use in patients with life-threatening ventricular arrhythmias. [Pg.1042]

These are class IC drugs with similar pharmacological profiles and with the same indication range and adverse effects. They are mainly used for the treatment of severe, lifethreatening ventricular tachyarrhythmias, and non-sustained ventricular tachycardia or high-frequency premature ventricular beats. The main adverse effects are cardiovascular, including proarrhythmic actions and severe negative inotropic effects, especially in patients with impaired cardiac function. Both flecainide and encainide increase the risk of sudden death in patients with myocardial infarction and asymptomatic unsustained ventricular arrhythmias. [Pg.160]

Genetic polymorphism is clinically important e.g. in the CAST (Cardiac Arrhythmia Suppression Trial), serious problems were identified with encainide and flecainide, because of polymorphic metabolism by CYP2D6. [Pg.267]

Flecainide is a potent blocker of sodium and potassium channels with slow unblocking kinetics. (Note that although it does block certain potassium channels, it does not prolong the action potential or the QT interval.) It is currently used for patients with otherwise normal hearts who have supraventricular arrhythmias. It has no antimuscarinic effects. [Pg.288]

Flecainide is very effective in suppressing premature ventricular contractions. However, it may cause severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with a previous myocardial... [Pg.288]

Propafenone has some structural similarities to propranolol and possesses weak 3-blocking activity. Its spectrum of action is very similar to that of quinidine, but it does not prolong the action potential. Its sodium channel-blocking kinetics are similar to that of flecainide. Propafenone is metabolized in the liver, with an average half-life of 5-7 hours. The usual daily dosage of propafenone is 450-900 mg in three divided doses. The drug is used primarily for supraventricular arrhythmias. The most common adverse effects are a metallic taste and constipation arrhythmia exacerbation can also occur. [Pg.289]

Drugs that markedly slow conduction, such as flecainide, or high concentrations of quinidine, can result in an increased frequency of reentry arrhythmias, notably ventricular tachycardia in patients with prior myocardial infarction in whom a potential reentry circuit may be present. Treatment here consists of recognition, withdrawal of the offending agent, and intravenous sodium. [Pg.294]

Flecainide Sodium channel (INa) blockade Dissociates from channel with slow kinetics no change in action potential duration Supraventricular arrhythmias in patients with normal heart do not use in ischemic conditions (post-myocardial infarction) Oral hepatic, and kidney metabolism half life 20 h Toxicity Proarrhythmic... [Pg.295]

Flecainide is very effective in suppressing premature ventricular contractions. However, it may cause severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with a previous myocardial infarction and ventricular ectopy (see The Cardiac Arrhythmia Suppression Trial). The drug is well absorbed and has a half-life of approximately 20 hours. Elimination is both by hepatic metabolism and by the kidney. The usual dosage of flecainide is 100-200 mg twice a day. [Pg.334]

Proarrhythmic effects of antiarrhythmic drugs In the Cardiac Arrhythmia Suppression Trial (CAST) treatment with encainide and flecainide, two class IC antiarrhythmic agents, successfully prevented ventricular ectopic beats in patients who had myocardial infarction. However, continued therapy with either drug was associated with a two- to three-fold increase in death due to cardiac arrhythmias. Similar results were reported for moricizine. Increased death was probably due to drug-induced fatal arrhythmias triggered by recurrent myocardial ischemia. [Pg.177]

Asymptomatic Carotid Atherosclerosis Study Group (1995). Carotid endarterectomy for patients with asymptomatic internal carotid artery stenosis. Journal of the American Medical Association 273 1421-1428 Barnett HJ, Taylor DW, Ehasziw M etal. (1998). The final results of the NASCET trial. New England Journal of Medicine 339 1415-1425 Cardiac Arrhythmia Suppression Trial (CAST) Investigators (1989). Preliminary report effect of encainide and flecainide on mortality in a randomised trial of arrhythmia suppression after myocardial infarction. New England Journal of Medicine 321 406-412 Charleson ME, Horwitz RI (1984). Applying results of randomised trials to clinical practice impact of losses before randomisation. British Medical Journal 289 1281-1284... [Pg.237]

FLECAINIDE ANTIEMETICS-5-HT3-ANTAGONISTS Risk of arrhythmias Additive effect Manufacturers recommend avoiding co-administration of flecainide with dolasetron. Caution with other 5-HT3-antagonists monitor ECG closely... [Pg.20]

ARTEMETHER WITH LUMEFANTRINE ANTIARRHYTHMICS -FLECAINIDE Risk of arrhythmias Additive effect Avoid co-administration... [Pg.581]


See other pages where Flecainide arrhythmia with is mentioned: [Pg.1212]    [Pg.122]    [Pg.125]    [Pg.80]    [Pg.88]    [Pg.250]    [Pg.387]    [Pg.340]    [Pg.603]    [Pg.604]    [Pg.180]    [Pg.1264]    [Pg.1]    [Pg.192]    [Pg.131]    [Pg.67]   
See also in sourсe #XX -- [ Pg.112 , Pg.126 , Pg.129 ]




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