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

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

The antiarrhythmic efficacy if low dose amiodarone treatment was studied in 30 cases of ventricular premature beats(VPBs). Amiodarone was administered 600mg daily in three divided doses for for initial 7-10 days as loadihg dosage,then 100-200mg once daily as maintenance. The results obtained were as follow : 1) The complete control of VPBs was achieved by amiodarone treatment in 90%, 27cases of 30 cases(all 11 cases with simple VPBs and 16 cases of the remainders with complex VPBs). 2) The QT interval and QTc were significantly prolonged, whereas heart rate was reduced significantly after amiodarone treatment. 3) In 27 cases of responder, the frequency of VPBs began to decrease overtly 2-3 days after amiodarone administration, then relatively stablized in 6 days, and complete cnotrol of VPBs was achieved in all cases about 10 days after treatment. 4) No significant side-reaction was observed except the decrease of serm T3 level after treatment.
Amiodarone* ; Arrhythmias, Cardiac* ; Heart Rate ; Selective Estrogen Receptor Modulators

Amiodarone is an antiarrhythmic drug containing 37% iodine by weight ; during long-term therapy the drugaccumulates in the liver, lung and various other organs. We describe two cases in which high attenuation of theliver due to the accumulation of amiodarone was seen on abdominal CT.
Amiodarone* ; Iodine ; Liver* ; Lung ; Tomography, X-Ray Computed

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