Flecainide was originally sold under the trade name Tambocor (manufactured by 3M pharmaceuticals). Flecainide went off-patent on February 10th, 2004, and is now available under the trade names Almarytm, Apocard, Ecrinal, and Flécaine. It is also available generically.
It also has limited use in the treatment of certain forms of ventricular tachycardia (VT). In particular, flecainide has been useful in the treatment of ventricular tachycardias that are not in the setting of an acute ischemic event. It has use in the treatment of right ventricular outflow tract (RVOT) tachycardia and in the suppression of arrhythmias in arrhythmogenic right ventricular dysplasia (ARVD). However, studies have shown an increased mortality when flecainide is used to suppress ventricular extrasystoles in the setting of acute myocardial infarction.
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. This may help make the diagnosis of the disease in equivocal cases.
Flecainide has been introduced into the treatment of arrhythmias in the pediatric population.
Given the variable half life of flecainide and the characteristic QRS prolongation on ECG elicited in flecainide toxicity, especially at rapid heart rates , starting flecainide or changing the level of the drug is done under telemetry monitoring (preferably in a hospital telemetry unit) until a steady state plasma level has been achieved, typically three to five days after the dose has been increased.
For the treatment of supraventricular tachycardias and paroxysmal atrial fibrillation or flutter in individuals without significant structural heart disease, a starting dose of 50 mg twice a day may be appropriate. The dose may be increased (once a steady state level has been reached) if breakthrough dysrhythmias occur.
For the treatment of life-threatening ventricular arrhythmias (ie: ventricular tachycardia), a starting dose of 100 mg twice a day may be appropriate. As with the treatment of benign arrhythmias, the dose of flecainide given for the treatment of life-threatening ventricular dysrhythmias should not be increased until a steady state has been achieved.
The effect of flecainide on the sodium channels of the heart increases as the heart rate increases. This is known as use-dependence. This means that flecainide is potentially more useful to break a tachyarrhythmia (because it has increased effect during the fast heart rate) than to prevent a bradyarrhythmia from occurring (because of its lowered effectiveness during slower heart rates).
The majority of flecainide is eliminated by the kidneys, with the remainder metabolised by the cytochrome P450 2D6 isoenzyme in the liver. Therefore, alterations in renal function or urine pH will greatly affect the elimination of flecainide, as more is eliminated by the hepatic route.
Because of the dual elimination routes of flecainide and its tendency to decrease myocardial contractility, flecainide interacts with numerous pharmaceuticals and can potentiate the effects of other myocardial depressants and AV node blocking agents. In addition, flecainide can decrease the metabolism or elimination of many (but not all) agents that use the cytochrome P450 enzyme system.
A full list of drug interactions with flecainide can be obtained from the manufacturer. Some important drug interactions with flecainide include:
The dose may need to be adjusted in certain clinical scenarios. As with all other antiarrhythmic agents, there is a risk of proarrhythmia associated with the use of flecainide. This risk is probably increased when flecainide is co-administered with other class Ic antiarrhythmics, such as encainide. The risk of proarrhythmia may also be increased by hypokalemia. 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. 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 renal failure.
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.It should be avoided in people with ischaemic heart disease and the elderly.
As with all class I antiarrhythmic agents, Flecainide increases the capture thresholds of pacemakers. Therefore, capture thresholds should be remeasured in individuals with pacemakers after the steady-state flecainide dose is changed.
Signs of flecainide toxicity include marked prolongation of the PR interval and widening of the QRS duration on the surface ECG. There may be signs and symptoms attributable to overt heart failure secondary to sudden decreased myocardial contractility.
It also causes the heart to beat below par, meaning low pulse rate in some patients
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