Quinidine

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 sulfate is indicated as a means of restoring normal sinus rhythm. If this use of quinidine sulfate does not restore sinus rhythm within a reasonable time, then quinidine sulfate should be discontinued. Reduction of Frequency of Relapse Into Atrial Fibrillation/Flutter Chronic therapy with quinidine sulfate 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 judgement of the physician and the patient, the risks of prophylactic therapy with quinidine sulfate.

Treatment of P. Falcipum Malaria Quinidine sulfate tablets are used in one of the approved regimens for the treatment of life-threatening P. falciparum malaria. The central component of the regimen is Quinidine Gluconate Injection, and the regimen is described in the package insert of Quinidine Gluconate Injection. Conversion of Atrial Fibrillation/Flutter to Sinus Rhythm Especially in patients with known structural heart disease or other risk factors for toxicity, initiation or dose-adjustment of treatment with quinidine sulfate should generally be performed in a setting where facilities and personnel for monitoring and resuscitation are continuously available. Patients with symptomatic atrial fibrillation/flutter should be treated with quinidine sulfate only after ventricular rate control (e.g., with digitalis or β-blockers) has failed to provide satisfactory control of symptoms.

Quinidine is contraindicated in patients who are known to be allergic to it, or who have developed thrombocytopenic purpura during prior therapy with quinidine or quinine. In the absence of a functioning artificial pacemaker, quinidine is also contraindicated in any patient whose cardiac rhythm is dependent upon a junctional or idioventricular pacemaker, including patients in complete atrioventricular block. Quinidine is also contraindicated in patients who, like those with myasthenia gravis, might be adversely affected by an anticholinergic agent.

Mortality 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 metaanalysis 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.

Quinidine preparations have been used for many years, but there are only sparse data from which to estimate the incidence of various adverse reactions. The adverse reactions most frequently reported have consistently been gastrointestinal, including diarrhea, nausea, vomiting, and heartburn/esophagitis. In one study of 245 adult outpatients who received quinidine to suppress premature ventricular contractions, the incidences of reported adverse experiences were as shown in the table below. The most serious quinidine-associated adverse reactions are described above under WARNINGS. Adverse Experiences in a 245-Patient PVC Trial Incidence (%) Incidence (%) diarrhea 85 “upper gastrointestinal distress” 55 lightheadedness 37 headache 18 fatigue 17 palpitations 16 angina-like pain 14 weakness 13 rash 11 visual problems 8 change in sleep habits 7 tremor 6 nervousness 5 discoordination 3.

Altered Pharmacokinetics of Quinidine Drugs that alkalinize the urine ( carbonic-anhydrase inhibitors, sodium bicarbonate, thiazide diuretics ) reduce renal elimination of quinidine. By pharmacokinetic mechanisms that are not well understood, quinidine levels are increased by coadministration of amiodarone or cimetidine. Very rarely, and again by mechanisms not understood, quinidine levels are decreased by coadministration of nifedipine. Hepatic elimination of quinidine may be accelerated by coadministration of drugs ( phenobarbital, phenytoin, rifampin ) that induce production of cytochrome P450 IIIA4. Perhaps because of competition for the P450 IIIA4 metabolic pathway, quinidine levels rise when ketaconazole is coadministered.

Store at 20° to 25°C (68° to 77°F).