Introduction
Long 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.