Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiarrhythmic effects of Encainide in acute intravenous and long-term oral therapy were investigated in 10 patients suffering from chronic atrial ectopic beats previously non-responsive to conventional therapy. The efficacy of Encainide was assessed by 24-hour ECG monitoring during the acute i.v. application and in 4 week intervals over a period of 4 to 6 months. Plasma concentrations of Encainide and the O-demethyl- (ODE) and 3-methoxy-O-demethyl metabolites (3-MODE) were determined after i.v. administration and during oral therapy. A significant reduction of arrhythmias by 76% was found after 1.0 mg/kg Encainide given intravenously. Atrial ectopic beats with bundle branch block QRS-morphology were reduced by more than 90% after only 0.5 mg/kg. During long-term oral therapy 6 of the 9 patients were treated successfully. Following i.v. administration Encainide-plasma concentrations rapidly decreased with a half life of approximately 75 min in the final distribution phase. During oral therapy Encainide levels were not detectable under steady state conditions 4 to 6 hours after the last dose, or they were only minimal, but the average concentrations of ODE and 3-MODE were 71.3 +/- 21.3 and 75.6 +/- 13.5 ng/ml. Encainide increased PR interval and QRS duration significantly. QT-interval changed as a result of the QRS-prolongation. Encainide was well tolerated during acute and chronic therapy. No severe side effects were seen, except in one case, in which dose reduction by 50% was necessary because of blurred vision.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Acute and long-term antiarrhythmia effect of encainide in chronic atrial extrasystole]. 240 92

Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
 ...
PMID:Encainide. 251 80

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.
 ...
PMID:Encainide hydrochloride and flecainide acetate: two class 1c antiarrhythmic agents. 311 76

Encainide is an antiarrhythmic drug with class IC activity which has been used in the treatment of life-threatening ventricular arrhythmias, symptomatic ventricular arrhythmias and supraventricular arrhythmias. The antiarrhythmic activity is due to the parent drug and its two principal active metabolites, and in the extensive metabolising phenotype (90% of patients), metabolites are present in plasma at higher concentrations than encainide itself. Encainide produces little haemodynamic change in patients with left ventricular dysfunction and thus has considerable therapeutic potential in view of its efficacy in patients with ventricular tachycardia, premature ventricular complexes and the Wolff-Parkinson-White syndrome. However, this potential is reduced by a tendency for encainide to aggravate arrhythmia in a proportion of patients. At present there is no reliable method of identifying patients at risk for this potentially serious side effect. The most common non-cardiac side effects are dizziness and blurred vision which seldom necessitate withdrawal of treatment. Thus, encainide has proved effective in controlling ventricular tachyarrhythmias including those which have not been controlled by other antiarrhythmic drugs.
 ...
PMID:Encainide. A review of its pharmacological properties and therapeutic efficacy. 312 Dec 75

Encainide is a class IC antiarrhythmic agent that has been under clinical investigation for the last decade. Laboratory and clinical studies have demonstrated it to be a potent suppressor of ventricular extrasystoles. It is effective in approximately one-half of patients with malignant ventricular arrhythmias. The preliminary experience in patients with supraventricular arrhythmias indicates that the drug is particularly effective in arrhythmias associated with an accessory pathway. Side effects most commonly include blurred vision, nausea, heart block, and proarrhythmic effects. The hemodynamic effect of oral encainide are insignificant in patients with well-preserved left ventricular function. Despite minimal myocardial depression in patients with left ventricular dysfunction, there is the potential for worsening of heart failure. Encainide has a short half-life of 3 hours, but has 2 active metabolites with longer half-lives. No clinically significant drug interaction has been demonstrated with encainide therapy.
 ...
PMID:Encainide: its electrophysiologic and antiarrhythmic effects, pharmacokinetics, and safety. 312 82