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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chemistry, electrophysiology, pharmacokinetics, clinical use and efficacy, adverse effects, drug interactions, and dosage of encainide hydrochloride and flecainide acetate are reviewed. Encainide and flecainide are class 1c antiarrhythmic agents that slow myocardial conduction and mildly prolong the duration of repolarization. Both agents block anterograde conduction over accessory pathways and prolong the effective refractory period of the accessory pathway. Bioavailability of encainide ranges from 7% to 82%, whereas that of flecainide is 90% to 95%. Encainide is metabolized by the liver to two major active metabolites that are slowly eliminated in the urine. About 23% of flecainide's total body clearance is dependent on renal elimination, and drug excretion is slowed in patients with renal dysfunction, requiring dosage adjustments. Both agents are effective in the suppression and prevention of ventricular arrhythmias, including premature ventricular contractions and sustained and nonsustained ventricular tachycardia. These agents may also be valuable in controlling supraventricular arrhythmias. The most common adverse effects of both agents involve the central nervous system and include dizziness, blurred vision, and headache. The potential for proarrhythmic effects is a concern with these agents. The risk is greater in patients with more severe arrhythmias, poor ventricular function, or high serum concentrations of drug. The usual initial oral dosage of encainide hydrochloride is 25 mg three times a day, with a usual dosage range of 100-200 mg/day. Flecainide acetate should be initiated at 100 mg every 12 hours and may be increased up to 400 mg/day. Encainide and flecainide could become useful therapeutic options in the treatment of a variety of arrhythmias.
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PMID:Encainide hydrochloride and flecainide acetate: two class 1c antiarrhythmic agents. 311 76

Flecainide acetate is a new orally active antidysrhythmic agent classified in the Ic category. Flecainide is effective in suppressing 88 to 100 percent of abnormal cardiac rhythms in the form of complex ventricular dysrhythmias, including couplets, ventricular tachycardia, reentrant junctional tachycardia, and Wolff-Parkinson-White syndrome. Flecainide appears to have a greater effect on conduction than on repolarization and only minimal effects on hemodynamic parameters. Flecainide is rapidly and completely absorbed after oral administration and has a 13-hour elimination half-life, allowing for twice-daily dosing regimens. Flecainide is generally well tolerated, with dizziness, blurred vision, nausea, and headache the most common side effects. Flecainide has been shown to be superior to quinidine and disopyramide in suppressing ventricular ectopic activity and may be considered a first-line oral agent for this indication. It is believe that flecainide has enough therapeutic advantages to be added to drug formularies.
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PMID:Flecainide: a new class Ic antidysrhythmic. 390 29

Flecainide acetate is a new class I antiarrhythmic agent which slows atrial, A-V nodal and ventricular conduction velocity, and prolongs refractoriness of these structures (Borchard et al., 1982; Hodess et al., 1979). Recent studies with oral flecainide therapy suggested its high potential for suppression of ventricular tachycardia in humans (Anderson et al., 1981; Duff et al., 1981; Hodges et al., 1982). Its favorable pharmacokinetics with an average plasma half-time of about 20 hours allows in most patients twice daily dosing (Duff et al., 1981). Usually, the drug seemed to be well tolerated and side-effects, such as blurred vision, could be resolved with smaller but still effective doses (Duff et al., 1981). Actually, the ideal antiarrhythmic agent which represents a high degree of effectiveness, a low level of toxicity, a wide therapeutic range, and a prolonged antiarrhythmic action does not exist (Dreifus and Ogawa, 1977). In this report we describe a patient with flecainide-induced aggravation of ventricular tachycardia necessitating resuscitation because of severe hemodynamic deterioration.
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PMID:Flecainide-induced aggravation of ventricular tachycardia. 685 Dec 74