Flecainide acetate is a class IC antiarrhythmic agent and its clinical efficacy has been confirmed by the results of several clinical trials. Nowadays, flecainide is recommended as one of the first line therapies for ...Flecainide acetate is a class IC antiarrhythmic agent and its clinical efficacy has been confirmed by the results of several clinical trials. Nowadays, flecainide is recommended as one of the first line therapies for pharmacological conversion as well as maintenance of sinus rhythm in patients with atrial fibrillation and/or supraventricular tachycardias. Based on the Cardiac Arrhythmia Suppression Trial study results, flecainide is not recommended in patients with structural heart disease due to high proarrhythmic risk. Recent data support the role of flecainide in preventing ventricular tachyarrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia associated both with ryanodine receptor and calsequestrin mutations. We herein review the current clinical data related to flecainide use in clinical practice and some concerns about its role in the management of patients with coronary artery disease.展开更多
In this report, we described a death caused by a deliberate overdose of Flecainide acetate （Almarytm^（R））, an antiarrhythmic agent. The patient had taken a box of 20 Almarytm^（R） 100 mg tablets. The Flecainide c...In this report, we described a death caused by a deliberate overdose of Flecainide acetate （Almarytm^（R））, an antiarrhythmic agent. The patient had taken a box of 20 Almarytm^（R） 100 mg tablets. The Flecainide concentration found in the post-mortem cardiac blood was 10.16 mg/L. This concentration could not have been determined by post-mortem diffusion of the drug from gastric residue because the patient was previously given activated carbon during the emergency procedure. In fact, in the peripheral blood, the Flecainide concentration was 8.64 mg/L, therefore, this concentration is overlapping with the concentration in the cardiac blood; the gastric content was negative at the screening of Flecainide, while the liver tissue concentration of Flecaiuide was 59.6 mg/L and the bile concentration was 128 mg/L. The brain tissue concentration of Flecainide was 4.19 mg/L. In this case, the cause of death, excluding that toxicity was depending on post-mortem gastric diffusion of the drug, because of the absorbing activity of the administered carbon at the recovery.展开更多
文摘Flecainide acetate is a class IC antiarrhythmic agent and its clinical efficacy has been confirmed by the results of several clinical trials. Nowadays, flecainide is recommended as one of the first line therapies for pharmacological conversion as well as maintenance of sinus rhythm in patients with atrial fibrillation and/or supraventricular tachycardias. Based on the Cardiac Arrhythmia Suppression Trial study results, flecainide is not recommended in patients with structural heart disease due to high proarrhythmic risk. Recent data support the role of flecainide in preventing ventricular tachyarrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia associated both with ryanodine receptor and calsequestrin mutations. We herein review the current clinical data related to flecainide use in clinical practice and some concerns about its role in the management of patients with coronary artery disease.
文摘In this report, we described a death caused by a deliberate overdose of Flecainide acetate （Almarytm^（R））, an antiarrhythmic agent. The patient had taken a box of 20 Almarytm^（R） 100 mg tablets. The Flecainide concentration found in the post-mortem cardiac blood was 10.16 mg/L. This concentration could not have been determined by post-mortem diffusion of the drug from gastric residue because the patient was previously given activated carbon during the emergency procedure. In fact, in the peripheral blood, the Flecainide concentration was 8.64 mg/L, therefore, this concentration is overlapping with the concentration in the cardiac blood; the gastric content was negative at the screening of Flecainide, while the liver tissue concentration of Flecaiuide was 59.6 mg/L and the bile concentration was 128 mg/L. The brain tissue concentration of Flecainide was 4.19 mg/L. In this case, the cause of death, excluding that toxicity was depending on post-mortem gastric diffusion of the drug, because of the absorbing activity of the administered carbon at the recovery.
