In many trials of antiarrhythmic therapy for non-life-threatening arrhythmias, active antiarrhythmic therapy has resulted in increased mortality; the risk of active therapy is probably greatest in patients with structural heart disease.
In the case of quinidine used to prevent or defer recurrence of atrial flutter/fibrillation, the best available data come from a meta-analysis described under CLINICAL PHARMACOLOGY/Clinical Effects above. In the patients studied in the trials there analyzed, the mortality associated with the use of quinidine was more than three times as great as the mortality associated with the use of placebo.
Another meta-analysis, also described under CLINICAL PHARMACOLOGY/Clinical Effects, showed that in patients with various non-life-threatening ventricular arrhythmias, the mortality associated with the use of quinidine was consistently greater than that associated with the use of any of a variety of alternative antiarrhythmics.
Quinidine is an antimalarial schizonticide and an antiarrhythmic agent with Class Ia activity; it is the d-isomer of quinine, and its molecular weight is 324.
Conversion of atrial fibrillation/flutter
In patients with symptomatic atrial fibrillation/flutter whose symptoms are not adequately controlled by measures that reduce the rate of ventricular response, quinidine gluconate is indicated as a means of restoring normal sinus rhythm. If this use of quinidine gluconate does not restore sinus rhythm within a reasonable time (see
DOSAGE AND ADMINISTRATION), then quinidine gluconate should be discontinued.
Reduction of frequency of relapse into atrial fibrillation/flutter
Chronic therapy with quinidine gluconate is indicated for some patients at high risk of symptomatic atrial fibrillation/flutter, generally patients who have had previous episodes of atrial fibrillation/flutter that were so frequent and poorly tolerated as to outweigh, in the judgment of the physician and the patient, the risks of prophylactic therapy with quinidine gluconate. The increased risk of death should specifically be considered. Quinidine gluconate should be used only after alternative measures (e.g., use of other drugs to control the ventricular rate) have been found to be inadequate.
In patients with histories of frequent symptomatic episodes of atrial fibrillation/flutter, the goal of therapy should be an increase in the average time between episodes. In most patients, the tachyarrhythmia will recur during therapy, and a single recurrence should not be interpreted as therapeutic failure.
Suppression of ventricular arrhythmias
Quinidine gluconate is also indicated for the suppression of recurrent documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgment of the physician are life-threatening. Because of the proarrhythmic effects of quinidine, its use with ventricular arrhythmias of lesser severity is generally not recommended, and treatment of patients with asymptomatic ventricular premature contractions should be avoided. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise.
Antiarrhythmic drugs (including quinidine gluconate) have not been shown to enhance survival in patients with ventricular arrhythmias.
Published Studies Related to Quinidine
Nonlinear pharmacokinetics of oral quinidine and verapamil in healthy subjects: a clinical microdosing study. [2011.08]
Microdosing studies are effective in enabling the early identification of the pharmacokinetic properties of compounds administered to humans. However, the nonlinearity of the pharmacokinetics between microdose and therapeutic dose, attributable to the saturation of metabolic enzymes and transporters, is a major concern.
Dextromethorphan/quinidine: in pseudobulbar affect. [2011.05.01]
Pseudobulbar affect is characterized by uncontrollable, inappropriate laughing and/or crying that is either unrelated or out of proportion to the emotions felt by the patient and occurs in patients with neurological disorders, such as amyotrophic lateral sclerosis (ALS), multiple sclerosis or traumatic brain injury...
Dextromethorphan plus ultra low-dose quinidine reduces pseudobulbar affect. [2010.11]
OBJECTIVE: To evaluate dextromethorphan combined with ultra low-dose quinidine (DMq) for treating pseudobulbar affect (PBA) in patients with amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS)... INTERPRETATION: DMq markedly reduced PBA frequency and severity, decreasing the condition's detrimental impact on a patient's life, with satisfactory safety and high tolerability. The findings expand the clinical evidence that DMq may be an important treatment for patients suffering from the socially debilitating symptoms of PBA.
Efficacy and tolerability of oral propafenone versus quinidine in the treatment of recent onset atrial fibrillation: A randomized, prospective study. 
BACKGROUND: A prospective, randomized study was conducted to evaluate the efficacy and tolerability of oral propafenone and quinidine for the conversion of paroxysmal atrial fibrillation (AF)... CONCLUSIONS: Although both drugs revealed the same effectiveness, the conversion to sinus rhythm in the group treated with propafenone was observed more quickly despite the longer paroxysmal AF episode duration.
Effects of ketoconazole and quinidine on pharmacokinetics of pactimibe and its plasma metabolite, R-125528, in humans. [2008.08]
Pactimibe sulfate is a novel acyl coenzyme A:cholesterol acyltransferase inhibitor developed for the treatment of hypercholesterolemia and atherosclerotic diseases. Pactimibe has two equally dominant clearance pathways forming R-125528 by CYP3A4 and M-1 by CYP2D6 in vitro... These values were well in accordance with the values observed in this study.
Clinical Trials Related to Quinidine
Empiric Quinidine for Asymptomatic Brugada Syndrome [Recruiting]
The purpose of this study is to determine if quinidine therapy (not guided by the results of
electrophysiologic studies) will reduce the long-term risk of arrhythmic events in
asymptomatic Brugada Syndrome.
Safety and Pharmacokinetics of Quinidine Alone and in Combination With Dabigatran Etexilate [Completed]
Open-label, two-way crossover design with a quinidine sulfate run-in period followed by a
randomised sequence of dabigatran etexilate plus quinidine sulfate or dabigatran etexilate
alone to evaluate the safety of co-administration of dabigatran etexilate and quinidine.
and the pharmacokinetic interaction between quinidine and dabigatran etexilate.
Study in Healthy Volunteers to Investigate the Effects of Quinidine on the Pharmacokinetics of NKTR-118 [Completed]
Relative Bioavailability of Dabigatran Etexilate Capsules With and Without Quinidine Sulfate Tablets and to Measure the Effect of Quinidine on the Absorption of Fexofenadine in Healthy Male and Female Volunteers [Terminated]
Study of the Electrocardiographic Effects of Ranolazine, Dofetilide, Verapamil, and Quinidine in Healthy Subjects [Completed]
This study seeks to compare 4 known QT prolonging drugs versus placebo to determine their
effects on electrophysiological and other clinical parameters. The underlying purpose is to
determine if depolarization and repolarization effects caused by drugs with differing ionic
channel mechanisms can be distinguished from one another, and to gauge the sensitivity and
specificity of novel signal analyses for detection of depolarization and repolarization
changes. Secondarily, to evaluate the exposure response relationship and drug induced
effects on the heart rate biomarker relationship.
Page last updated: 2011-12-09