Ciprofloxacin induced acquired long QT syndrome in a patient under class III antiarrhythmic therapy.
نویسندگان
چکیده
We report one case of cardiac arrest related to ciprofloxacin administration. One female patient (aged 70 years old) developed a marked QTc prolongation (QTc = 0.62 s) within 24 hours of ciprofloxacin administration, with documented torsades de pointes and recurrent syncope that required defibrillation. The patient was under amiodarone and sotalol therapy for atrial fibrillation, with no obvious QT prolongation prior to ciprofloxacin therapy. QT prolongation and subsequent torsades de pointes appeared only after initiation of ciprofloxacin and normalized after drug discontinuation. Even though ciprofloxacin is thought to be safer than other agents in its class, it may cause QT prolongation and torsades de pointes, particularly in high risk patients with predisposing factors. Prolongation of the QT interval related to the effect of fluoroquinolones on rapid potassium channels (IKr) may result on potentially serious proarrhythmic effect, leading to torsades de pointes.
منابع مشابه
گزارش یک مورد سندرم ژرول- لانژنلسون
Long QT syndrome, which is defined by corrected QT interval longer than 0.45 seconds in men and o. 47 sec in women , could be divided into idiopathic (congenital ) and acquired forms. The idiopathic form is a familial disorder that can be associated with sensorineural deafness (Jervell and Lange- Neelson syndrome), which is transmitted with an autosomal recessive pattern. Although this syndrome...
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Long QT syndrome (LQTS) is characterized by inherited or acquired prolonged QT interval on the surface electrocardiogram. This can lead to torsade de pointes ventricular tachycardia (TdP VT) and ventricular fibrillation. In the acquired form of the disease, medications from several classes can cause TdP VT or potentiate the electrocardiographic findings. These include class IA and III antiarrhy...
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Drug-induced torsades de pointes (TdP) is common with class III antiarrhythmic drugs. Increased transmural dispersion of repolarization (TDR) contributes significantly to the development of TdP. Gap junctions play an important role in maintaining TDR in long QT syndrome. The present study examined the effect of a gap junction enhancer, antiarrhythmic peptide 10 (AAP10), on ibutilide-induced TdP...
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ورودعنوان ژورنال:
- Cardiology journal
دوره 16 2 شماره
صفحات -
تاریخ انتشار 2009