No abstract available.
Amiodarone*

No abstract available.
Amiodarone* ; Arrhythmias, Cardiac* ; Child* ; Humans

Humans ; Thyrotoxicosis/chemically induced* ; Amiodarone

Although amiodarone is generally regarded as safe with a low incidence of associated arrhythmias, torsade de pointes (TdP) has been observed usually in the presence of predisposing factors. We report a case of amiodarone-induced TdP after long-term administration of a low dose of oral amiodarone in the absence of predisposing factors.
Amiodarone ; Arrhythmias, Cardiac ; Incidence ; Torsades de Pointes

Amiodarone hydrochloride is a benzofuran derivative used for the treatment of cardiac arrhythmias. It is associated with a number of side effects, including thyroidopathy, neuropathy, cutaneous pigmentation, photosensitivity, pulmonary toxicity, hepatotoxicity and keratopathy. Amiodarone keratopathy hasbeen classified into four stages. Corneal pigmentation varies from stage 0, which is a clear cornea without pigment deposition, to stage 3, that is, corneal pigmentation encroaching upon the pupil. We present a case of amiodarone induced keratopathy of stage 3 who received low dose oral amiodarone maintain therapy.
Amiodarone* ; Arrhythmias, Cardiac ; Cornea ; Pigmentation ; Pupil

Amiodarone is one of the most commonly prescribed antiarrhythmic drug for almost all atrial or ventricular arrythmias. Amiodarone-induced pulmonary toxicity (APT) was first described in 1980 and has potentially serious side effects that are believed to develop in 5% of patients. In general, APT occurs only when high amiodarone doses are used for a long time. However, during short-term therapy of amiodarone, APT is rarely reported. In this report, we describe a case of amiodarone-induced pulmonary toxicity after a short course of amiodarone therapy for atrial fibrillation.
Amiodarone ; Arrhythmias, Cardiac ; Atrial Fibrillation ; Dimaprit ; Humans

BACKGROUND/AIMS: Long-term antiarrhythmic drug therapy remains the principal approach for suppressing atrial fibrillation (AF) and maintaining sinus rhythm. In this study, we examined the differing electrophysiological effects of various antiarrhythmic drugs on the cardiac chamber and atrial selectivity in patients with AF. METHODS: We analyzed 134 patients (60.4 +/- 12.5 years, M:F = 1.14:1) who were administered a single antiarrhythmic agent for AF over 6 months: amiodarone (group A), flecainide (group F), or propafenone (group P). The P wave, QRS complex duration and dispersion, and QT interval and its dispersion were evaluated using a standard 12-lead electrocardiogram. RESULTS: There was no significant difference in age, gender ratio, or associated diseases among the three groups. In group A, Pmax, Pmin, P dispersion, QRSmax, QRSmin, and QRS dispersion were shorter than in groups F and P, whereas Pmax/QRSmax was the highest in group A (A = 1.2, F = 0.9, P = 1.0; p < 0.01). QTcmax and QTcmin were longer in group A, whereas QTc dispersion and the QT peak to end (A = 13.3 +/- 11.2, F = 30.7 +/- 24.9, P = 31.8 +/- 21.6; p < 0.01) were shorter in group A than in the other groups. CONCLUSIONS: Amiodarone had a weaker, but more selective, inhibitory effect on intra-atrial conduction, and inhibited ventricular repolarization more effectively and homogenously than flecainide or propafenone. These differing electrophysiological effects may contribute to the superior effectiveness and safety of amiodarone over flecainide or propafenone.
Amiodarone ; Anti-Arrhythmia Agents ; Atrial Fibrillation ; Electrophysiology ; Flecainide ; Humans ; Propafenone

Amidarone hydrochloride, benzofuran derivatives, particularly effective for the treatment of arrythmias by prolong the duration of the action potential in all cardiac-conducting tissues. We studied the 25 patients with typical amiodarone keratopathy, retrospectively. In 25 patients, ten patients developed grade 1, eleven patients developed grade 2, and four patients developed grade 3 keratopathy. They complained of decreased best corrected visual acuity(1 patient), halos(1 patient), hypothyroidism(3 patients), pulmonary toxicity(2 patients), thpatic dysfunction(5 patients) and sleep dusturbance(3 patients). Therefore ophthalmologists should be alert for the complications of amiodarone and regular careful slit-lamp examination will be helpful in minimizing amidarone toxicity.
Action Potentials ; Amiodarone* ; Arrhythmias, Cardiac ; Humans ; Retrospective Studies

To assess the efficacy of amiodarone on chronic atral fibrillation(AF) and to evaluate the relation between the ability to convert AF to sinus rhythm (SR) with amiodarone therapy and left atrial(LA) size and atrial fibrillatory wave forms, 22 patients with AF, aged 40 to 60 years(mean 47.5 years), were studied. Nine patients(40.9%) had mitral valvaular heart disease, 6(27.3%) hypertension, 5(18.2%) lone AF and 2 (9.1%) cadiomyopathy. Amiodarone therapy with either 600mg for 1 week, 200mg for 4 weeks in 5 consecutive patients, or 800mg for 1 week, 400mg for 4 weeks and 200mg for 6 weeks in 17 patients, converted AF to SR in 9(40.9%) patients 3 to 6 weeks after amiodarone was started on. In either group, patients who achieved conversion had smaller LA size(mean 43.7mm) than those who failed conversion(mean50.2mm)(P<0.05). Those who had LA size less than 45mm achieved conversion of AF to SR in 70%, comparing to 16.7% in patients with LA size more than 46mm(P<0.05). Among patients who achieved conversion, LA size was less than 46mm in 77.8% comparing to 23.1% in patients who failed conversion on Amiodarone. Those with coarse AF(46.2mm), althogh the difference was not significant statistically. There was no converstion in patients with LA size greater then 58mm and in patients with coarse AF who concomittantly had MVD. These findings suggest that the efficacy of amiodarone was related to LA size, and to the atrial fibrillation wave form in patients with mitral valvular heart disease.
Amiodarone* ; Atrial Fibrillation* ; Heart Diseases ; Heart Valve Diseases ; Humans ; Hypertension

Amiodarone is widely used to control fatal arrhythmia. However, amiodarone therapy is associated with a relatively high incidence of pulmonary toxicity, up to 5 to 10%. Typical symptoms are nonspecific and often manifest as nonproductive cough, dyspnea and interstitial infiltrates in patients with acute pneumonitis or chronic fibrosis. However, hemoptysis is a very rare symptom of amiodarone pulmonary toxicity. We report a case of amiodarone pulmonary toxicity, who presented with hemoptysis and was successfully treated with the cessation of amiodarone, with review of the relevant literature.
Amiodarone* ; Arrhythmias, Cardiac ; Cough ; Dyspnea ; Fibrosis ; Hemoptysis* ; Humans ; Incidence ; Pneumonia