NEW YORK (Reuters Health) - Quinidine prolongs the QT interval and prevents induced ventricular fibrillation in patients with QT syndrome, according to a report in the April 21st issue of the Journal of the American College of Cardiology.
Implantation of an automatic cardioverter-defibrillator (ICD) is the only available therapy for this recently described genetic syndrome, the authors point out, and little is known about the effects of antiarrhythmic drugs in these patients.
Accordingly, Dr. Fiorenzo Gaita from Ospedale Civile di Asti, Italy and colleagues evaluated the effects of various antiarrhythmic drugs in 6 patients (one child, five adults) with short QT syndrome. The patients were members of 2 different families. The 5 adults received ICDs.
However, as Dr Gaita told Reuters Health, ICD implantation “is not feasible in young children. “The next step, he added, will be to obtain the results of follow-up of quinidine therapy in “these young patients and of those patients who refuse the ICD.”
Among findings of the current study were that flecainide slightly increased the QT interval by prolonging the QRS interval, whereas ibutilide and sotalol caused no changes of QT interval.
Quinidine prolonged the QT interval into the normal range, the authors report, and increased the ventricular effective refractory period to at least 200 milliseconds in all 5 adult patients. Quinidine was discontinued in the child because of asthma and diarrhea.
A mean 11 months after ICD implantation, all patients remained asymptomatic and no ventricular arrhythmias were detected by the ICD. At that time, 2 additional patients had been switched to flecainide after developing diarrhea on quinidine.
“Quinidine should be considered he most effective pharmacologic therapy in these patients,” the investigators conclude. “Flecainide may be the second choice when quinidine is not tolerated.”
Source: J Am Coll Cardiol 2004;43:1494-1499. [ Google search on this article ]
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