(Circulation. 1995;92:2944-2950.)
© 1995 American Heart Association, Inc.
Articles |
From the Cardiovascular Research Group, University of Calgary, Calgary, Alberta, Canada.
Correspondence to Dr Robert Sheldon, Division of Cardiology, Calgary General Hospital, 841 Centre Avenue East, Calgary, Alberta, Canada T2E 0A1.
Background Quinine is the diastereomer of quinidine. In dogs, it has similar effects on conduction time but does not prolong epicardial repolarization time or ventricular refractoriness. It has antiarrhythmic effects in both cats and dogs. We assessed the antiarrhythmic potential of quinine in suppressing ventricular arrhythmias in humans.
Methods and Results Patients underwent open-label, dose-ranging trials of quinine with daily doses of 600, 1200, and 1800 mg in a twice-daily dosing regimen. In 17 patients with frequent spontaneous ventricular ectopy, oral quinine suppressed arrhythmia in 11 of 12 patients who finished the study and was not tolerated by 4 patients, and 1 patient withdrew from the study. The mean effective daily dosage was 927 mg, the mean effect trough serum level was 11 µmol/L (range, 4 to 17 µmol/L), and the half-life was 20±7 hours. In a second open-label, dose-ranging trial in 10 patients with inducible ventricular tachycardia and reduced left ventricular systolic function (left ventricular ejection fraction, 35±16%), quinine suppressed inducibility of ventricular tachycardia in 3 of 10 patients. At a basic pacing cycle length of 500 milliseconds, ventricular effective refractory period was prolonged (279±21 versus 247±10 milliseconds, quinine versus drug free, P=.003). In the remaining patients, ventricular tachycardia cycle length was prolonged (373±48 versus 253±30 milliseconds, quinine versus drug free, P<.001). The corrected QT interval was not prolonged.
Conclusions Quinine is an effective and convenient antiarrhythmic drug for the suppression of ventricular arrhythmias in humans.
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