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

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.
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PMID:Encainide. 251 80

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

It is important for women to understand the risk of first onset and symptomatic exacerbation of paroxysmal supraventricular tachycardia (SVT) during pregnancy. Reports regarding the effects of pregnancy on first onset and symptomatic exacerbation of paroxysmal SVT have been controversial, and have not been conducted in a systematic fashion. Two hundred seven consecutive female patients diagnosed with symptomatic paroxysmal SVT were requested to respond to multiple questionnaires before electrophysiologic study and catheter ablation. A person-years data method was used to estimate risk of first onset of paroxysmal SVT during pregnancy. Exacerbation of paroxysmal SVT was assessed by a score scale including each of the following symptoms: palpitation, fatigue, rest dyspnea, effort dyspnea, dizziness, chest oppression, blurred vision, and syncope (total score change > 2 points). In the 107 patients with accessory pathway-mediated tachycardia, 7 patients had had a first onset of tachycardia during pregnancy (relative risk ratio 0.86, confidence interval 0.4 to 1.9, p = 0.35). In the 100 patients with atrioventricular nodal reentrant tachycardia, 1 patient had had the first onset of tachycardia during pregnancy (relative risk ratio 0.11, confidence interval 0.02 to 0.56, p = 0.004). Otherwise, 14 of the 63 patients (22%) with tachycardia in the pregnant and nonpregnant periods had exacerbation of symptoms during pregnancy. Thus, first onset of paroxysmal SVT during pregnancy was rare (3.9%), and pregnancy was associated with a low risk of first onset of paroxysmal SVT. However, symptoms of paroxysmal SVT were exacerbated during pregnancy in some patients.
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PMID:Effects of pregnancy on first onset and symptoms of paroxysmal supraventricular tachycardia. 757 23

In 102 patients with inducible supraventricular tachycardia (SVT), 56 women and 46 men aged 20-86 (mean, 52) years, underwent electrophysiologic study. SVTs observed at electrophysiologic study were atrial flutter or atrial fibrillation (32%), the "slow-fast" form of atrioventricular (AV) nodal reentrant tachycardia (45%), orthodromic AV reentrant tachycardia (25%), and atrial tachycardia (9%). More than 1 SVT occurred in some patients. Spontaneous symptomatic SVT frequency prior to oral flecainide varied from 3/day to 1/3 months (mean, 3/month). At electrophysiologic study and during SVT, intravenous flecainide, 2 mg/kg body weight, was given at an infusion rate of 10 mg/min up to a maximum dose of 150 mg. Patients were commenced on oral flecainide if SVT termination occurred during intravenous flecainide administration and if reinitiation was not possible after the total dose of flecainide had been given. In patients with AV nodal reentrant tachycardia and AV reentrant tachycardia further criteria for commencing oral flecainide were SVT termination by ventricular-atrial conduction block and persistent ventricular-atrial block after intravenous flecainide administration. Initial oral flecainide dosage was determined by assessing ability to reinitiate SVT after 50 mg, 100 mg, and the total dose of intravenous flecainide had been given. Eighty-nine patients (87%) remained free of symptomatic SVT over a mean follow-up period of 3.9 years (range, 3 months to 6.5 years). Two thirds were still taking the original dosage of flecainide and the rest were SVT-free on a higher dosage. Oral dosages ranged from 50 to 300 mg/day (median dosage, 100 mg twice daily) Nine patients experienced minor side effects, including, lethargy, dizziness, headache, and blurred vision. There were no deaths and no reports of major proarrhythmic events or other major adverse effects.
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PMID:Efficacy and safety of long-term oral flecainide acetate in patients with responsive supraventricular tachycardia. 860 96

We present the imaging findings pretreatment and posttreatment in a 58-year-old woman with recurrent thymic carcinoma. Two years after treatment, the patient presented with a 3-week history of right eye pain and blurred vision. Ophthalmological examination and MRI of the orbits showed a right superolateral choroidal lesion. Neurologic and whole-body FDG PET/CT scans showed a markedly glucose-avid right choroidal mass and extensive lung parenchymal, pleural, and thoracic nodal disease. There was a good response to chemoradiotherapy with a reduction in size and metabolism at all sites.
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PMID:An Intraocular Thymic Metastasis Identified on 18F-FDG PET/CT Before and After Treatment. 3323 36