IntroductionLong QT syndrome (LQTS) is a disorder of myocardial repolarization characterized by a prolonged QT interval on the electrocardiogram (ECG). This syndrome is associated with an increased risk of polymorphic ventricular tachycardia (VT) and a characteristic life-threatening cardiac arrhythmia also known as torsade de pointes (TdP). TdP is an uncommon and fatal polymorphic ventricular tachyarrhythmia, which often occurs in association with a prolonged QT interval. It is usually asymptomatic and terminates spontaneously; nevertheless it can cause syncope, dizziness, palpitations, seizures, and sudden cardiac death (SCD).QT prolongation has traditionally been separated into two general categories: congenital LQTS and acquired LQTS. The acquired causes include drugs (antiarrhythmic, antibiotic, antipsychotic, antihistamines, and antiemetic), electrolyte abnormality (hypokalemia, hypocalcemia, and hypomagnesemia), bradycardia, ischemia, stroke, and structural heart disease [1-3].Quinolone antibiotics are frequently prescribed agents due to their broad-spectrum antimicrobial efficacy. QT prolongation is a class effect of fluoroquinolones, but there are great differences between the various members of this group in their proarrhythmic potential. Ciprofloxacin is considered to be safer than the other agents in this class [4]. Current clinical studies suggest that among quinolones, ciprofloxacin has no effect on QT interval in healthy subjects with no predisposing factors [5-6] and a weak effect in patients with preexisting risk factors for torsade de Pointes [4, 7].We report a case 40-years old Ethiopian man with no previous history of cardiac disease who died due to recurrent cardiac arrest secondary to ciprofloxacin-induced torsade de pointes.