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Quinidine: Is it a good drug or a bad drug? David M. Salerno MD, PhD To cite this article: David M. Salerno MD, PhD (1992) Quinidine: Is it a good drug or a bad drug?, Postgraduate Medicine, 92:4, 131-140, DOI: 10.1080/00325481.1992.11701470 To link to this article:

Published online: 17 May 2016.

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Quinidine: Is it a good drug or a bad drug?

David M. Salerno, MD, PhD

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Preview Are you a good witch or a bad witch? DOROTHY: Who, me? Why ... I'm not a witch at all. From the movie, The Wizard of Oz, 1939 GUNDA:

Recently, the level of concern about the safety of quinidine has been raised because of the risk of nonfatal and fatal proarrhythmic complications. Like Glinda, physicians must ask, Is quinidine a good drug or a bad drug?

Quinidine has been in clinical use for several decades. Its approved indications, according to Food and Drug Administration (FDA) labeling for 1992, include practically all cardiac arrhythmias. However, two recent metaanalyses have emphasized the potential for dangerous side effects, 1-3 and FDA-approved indications may soon be restricted. Quinidine is the most commonly prescribed class I antiarrhythmic drug in the United States. 1 Its use actually increased after the Cardiac Arrhythmia Suppression Trial (CAST) investigators reported adverse outcomes with flecainide acetate and encainide hydrochloride in 1989. 2·4 Therefore, it is timely to review its effectiveness and safety in the light of newer information.

Phannacologic considerations Quinidine is well absorbed from the gastrointestinal tract and is

metabolized in the liver, primarily to 3-hydroxyquinidine. 5 Because this metabolite has an active antiarrhythmic effect and accumulates in the body in measurable quantity, quinidine levels may not reliably indicate the antiarrhythmic effect. Quinidine levels may be increased in patients with liver failure, whereas metabolite levels may be increased in patients with renal failure. Furthermore, the unbound (and therefore pharmacologically "available") fraction of quinidine varies in patients with certain disease states. 6 Commonly used oral preparations include quinidine sulfate, which is taken four times daily but is by far the least expensive class I antiarrhythmic drug; quinidine gluconate, which usually is taken three times daily; and quinidine sulfate in dextrose tablets for extended release, which usually is taken only twice daily.

Quinidine is also available in intravenous form.

Effectiveness Oral quinidine has been studied extensively for treatment of ventricular premature contractions (VPCs). In many reports, it was used as the comparison agent for newer antiarrhythmic drugs. Because of this, there are more published data on quinidine than on any other antiarrhythmic agent for suppression ofVPCs. 7 The drug appears to be adequately tolerated when prescribed for long-term use, and it effectively suppresses VPCs in about 50% of patients. In other patients, oral quinidine either cannot be tolerated or does not achieve adequate levels for suppression. Quinidine suppresses sustained ventricular tachycardia during electrophysiologic testing in 25% to 33% of patients. 8'9 Little information is available on the long-term effectiveness of the drug for prevention of ventricular tachycardia. Quinidine prevents recurrence of supraventricular tachycardia in some patients, although controlled studies of its success rate are unavailable. The drug converts atrial fibrillation to sinus rhythm in up to 60% of patients. 10 In addition, according to a recent




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Little information is available on the long-term effectiveness of quinidine for prevention of ventricular tachycardia.

Table 1. Effectiveness of oral quinidine therapy for various arrhythmias Arrhythmia

Patients treated successfully (%)

Symptomatic ventricular premature contractions


Sustained ventricular tachycardia


Supraventricular tachycardia*


Atrial fibrillation or fluttert


tion of ventricular tachycardia in 26% of patients. Table 1 shows the effectiveness of oral quinidine therapy for various arrhythmias.


*Success rate estimated. tMaintenance of sinus rhythm.

Table 2. Side effects of oral quinidine Non cardiac

Diarrhea and other gastrointestinal symptoms Central nervous system symptoms (eg, fatigue, loss of concentration) Fever and increased liver enzyme levels Cinchonism (tinnitus, loss of hearing, blurred vision, dizziness, lightheadedness, nausea, headache) Rashes Thrombocytopenia (infrequent) Cardiac

Proarrhythmia (nonfatal and fatal) Torsades des pointes with syncope Bradycardia (sinus pauses, atrioventricular block) Congestive heart failure (very uncommon)

Two to three decades ago, intravenous quinidine was commonly used. However, this form fell out of favor because intravenous bolus therapy often caused hypotension. Subsequently, it was reponed that the incidence of side effects was much lower when the drug was given as a gradual infusion over about 30 minutes. 9 When this slow-infusion loading regimen was used, only 10% of patients had significant hypotension. In all cases, hypotension was promptly relieved when infusion was stopped or saline solution was administered. The loading dose of intravenous quinidine is 8 to 10 mg/kg, and the maintenance dose is 1 to 2 mg/ min. Considerably more information is known about the side effects of oral quinidine (table 2) and is examined here. NONCARDIAC SIDE EFFECI'S--

meta-analysis of several published randomized, placebo-controlled trials, 1 quinidine prevents recurrence of paroxysmal atrial fibrillation in approximately 50% of pa-


tients over a period of 1 year. The intravenous form of quinidine has been studied much less extensively. In one electrophysiologic study, 9 it prevented indue-

The noncardiac side effects of oral quinidine are most common and, although troublesome, are rarely life-endangering. Gastrointestinal side effects are the main problem, with diarrhea occurring


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Even though the cardiac side effects of quinidine are less common than the noncardiac effects, they are considerably more dangerous.

in 25% or more of patients. 11 Diarrhea often appears after the first dose of quinidine and usually is not controlled by reducing the amount. Agents that lower gastric motility or increase stool bulk also are not very effective. It is my impression that discontinuation of quinidine is the only truly effective management. A syndrome of fever, malaise, and flulike symptoms may develop in some patients during the first month of therapy. This is accompanied by an increase in liver enzyme levels. The illness is promptly reversed by discontinuing quinidine. 12 Central nervous system side effects are seen infrequently but do include fatigue and loss of concentration. Cinchonism (tinnitus, loss of hearing, blurred vision, dizziness, light-headedness, nausea, headache) is distinctly uncommon. It is often idiosyncratic, occurring soon after the initiation of quinidine therapy. Thrombocytopenia is noted infrequently. Cutaneous rashes may occur. Other noncardiac side effects are quite uncommon. CARDIAC SIDE EFFE~Even

though the cardiac side effects of oral quinidine are less common than noncardiac effects, they are considerably more dangerous. Ventricular proarrhythmia may

Figure 1. Electrocardiographic tracings in patient with recent anterior myocardial infarction complicated by ventricular fibrillation. a. QT interval is normal (375 msec) on 6/27/82. b. Oral quinidine was started on 6/28/82 for ventricular premature contractions. OT interval is markedly prolonged to 700 msec after two doses. c. Frequent episodes of nonsustained polymorphic ventricular tachycardia developed on same night. Some episodes had rapid rate and were typical of torsades des pointes. Problem resolved when quinidine was withdrawn.

become manifest as an increased frequency of ventricular beats or as episodes of syncope due to torsades des pointes, a form of very rapid polymorphic ventricular tachycardia. 1311 Although torsades des pointes is usually selfterminating, the runs can be lengthy and accompanied by transient loss of consciousness. In a few cases, sustained runs result in death unless cardioversion is done. Nonsustained runs may be frequent and are difficult to control. Therapy includes a trial of lidocaine (Xylocaine) hydro-


chloride and, if necessary, the initiation of ventricular pacing. Patients often have underlying sinus bradycardia that triggers torsades des pointes, and increasing the heart rate appears to suppress the propensity to tachyarrhythmia. Other conditions may predispose to torsades des pointes, including hypokalemia and acute myocar~ dial infarction (figure 1). Bradycardia occurs much less commonly as a side effect of quinidine than does tachycardia. Both sinus node dysfunction and atrioventricular block can occur



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Because ventricular proarrhythmia may occur later than the first 3 days of quinidine therapy, hospitalization for monitoring is not practical.

Figure 2. Electrocardiographic tracings in patient with acute inferior myocardial infarction. a. Tracing on 10/25/82. b. Because of ventricular premature contractions, oral quinidine was started on 10/28/82. A 3:2 atrioventricular block developed on same day. c. Rhythm soon progressed to complete atrioventricular block. Problem resolved when quinidine was withdrawn.

(figure 2). Bradycardias can be worsened by the interaction of quinidine with digoxin (Lanoxicaps, Lanoxin), beta-adrenergic blockers, and calcium channel blockers. 16' 17 An uncommon form of proarrhythmia is acceleration of ventricular rate in the presence of David M. Salerno, MD, PhD Dr Salerno is associate professor of medicine, University of Minnesota Medical School-Minneapolis, and director, electrocardiography laboratory, Hennepin County Medical Center, Minneapolis.

atrial fibrillation or flutter. This is particularly dangerous if quinidine is given to a patient in atrial flutter with 2: 1 atrioventricular block and a ventricular rate of 150 beats a minute. The result may be 1: 1 atrioventricular conduction with a ventricular rate of 300 beats a minute. Therefore, before quinidine is given, administration of atrioventricular blocking medications is strongly indicated for atrial flutter and fibrillation with rapid ventricular response.

The timing of ventricular proarrhythmia is a problem. Although it often appears during the first 1 to 3 days of quinidine therapy, it may occur later. 13-15 Thus, it is not practical to hospitalize patients long enough to be assured that ventricular proarrhythmia will not develop after discharge. Underscoring this concern are the results of two recent metaanalyses of quinidine therapy. The firse reported the 1-year mortality rates from six randomized trials in which patients with paroxysmal atrial fibrillation received either placebo or quinidine to maintain sinus rhythm. Although quinidine significantly increased the number of patients maintained in sinus rhythm for 1 year compared with placebo, it also caused a statistically significant increase in the mortality rate at 1 year (2.9% versus 0.8% with placebo). The second metaanalysis2 involved patients given either quinidine or one of four newer antiarrhythmic drugs to suppress ventricular beats. Again, the mortality rate with quinidine was significantly higher than that with other antiarrhythmic drugs (relative risk, 3.0). 2 The other antiarrhythmic drugs studied included flecainide, tocainide hydrochloride, propafenone hydro-




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The use of any antiarrhythmic drug to suppress VPCs is questionable.

chloride, and mexiletine hydrochloride. These fatal events occurred during the outpatient phases of therapy. In quinidine's favor, it appears to have fewer effects on left ventricular function than does any other class I antiarrhythmic drug. 18 It is quite unusual for quinidine to cause clinical congestive heart failure.

Reassessment and recommendations Clearly, quinidine is both a good drug and a bad drug. Among its advantages are its minimal effects on left ventricular function. It also appears to be effective in maintaining sinus rhythm in patients with atrial fibrillation who truly need this therapy. In carefully selected patients, it may suppress sustained ventricular tachycardia. However, it causes nonfatal and fatal (even delayed fatal) complications in some patients. Patients must be selected carefully for quinidine therapy. Current recommendations for its use in various arrhythmias (table 3) are discussed here. VPCs-The use of any antiarrhythmic drug to suppress VPCs is questionable. CAST investigators clearly established that there is no benefit from class I antiar-

Table 3. Indications for quinidine in treatment of arrhythmias Arrhythmia

Indication for quinidine

Symptomatic ventricular premature contractions

Very rarely needed

Sustained ventricular tachycardia

When effectiveness and safety are confirmed by electrophysiologic testing and in-hospital monitoring

Supraventricular tachycardia

When tachycardia is refractory, frequent, or severe (also consider radiofrequency ablation)

Atrial fibrillation or flutter

Frequent recurrences or severe hemodynamic compromise

rhythmic drug therapy after myocardial infarction for suppression of asymptomatic or minimally symptomatic VPCs (including runs of nonsustained ventricular tachycardia). 4 Although unproven, this finding also probably applies to patients with other forms of heart disease. Antiarrhythmic drugs cannot be administered to patients who have VPCs with the idea of preventing sustained ventricular tachycardia. However, some patients complain of symptoms, which, in most cases, are modest. It is my impression that the severity of these symptoms is inversely proportional to the time that I spend with a patient dis-

cussing the risks of antiarrhythmic drug therapy to suppress these beats! Most patients feel they can get along quite well with their palpitations once they have been reassured that their risk is small and that nothing can really be done to alter it. If treatment of symptomatic VPCs is deemed necessary, betaadrenergic blockers are probably the drugs of first choice. If these fail, class I antiarrhythmic drugs can be administered with caution. Quinidine may be used in this very uncommon situation. SUSTAINED VENTRICUlAR

TACHYCARDIA-In most cases, the use of quinidine for sustained ventricular tachycardia should be




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In most patients with supraventricular tachycardia, the arrhythmia can be controlled with calcium channel blockers or beta blockers; if these fail, radiofrequency ablation should be considered.

guided by electrophysiologic documentation of its effectiveness. Rarely do patients have such frequent episodes of spontaneous sustained ventricular tachycardia during cardiac monitoring that conclusions can be made about the effectiveness of a drug without provocative testing. In addition to documentation of effectiveness, inpatient observation for the development of torsades des poimes should be done for a reasonable period, even though, as mentioned, this proarrhythmia may develop after discharge from the hospital in some patients. Although physicians generally watch for prolongation of the QT interval as a predictor of this arrhythmia in patients receiving quinidine, there is little scientific validation for this approach. 14 SUPRAVENTRICULAR TACHY-

CARDIA-Quinidine can suppress supraventricular tachycardia, but the drug is rarely needed. In most patients, this arrhythmia is controlled with calcium channel blockers or beta-adrenergic blockers. If these agents fail and use of class I antiarrhythmic drugs is being considered, radiofrequency ablation should also be considered, because this approach is highly successful in eliminating tachycardia and, in turn, the need for long-term class I drug therapy. 19'20


FLUITER-My approach to treating atrial fibrillation and atrial flutter has clearly changed in light of the meta-analyses mentioned here. If atrial fibrillation or flutter is not causing severe hemodynamic collapse (which neither rarely does), it is reasonable to prescribe quinidine as short-term therapy in the hospital in an attempt to restore sinus rhythm. However, I believe that the use of quinidine or any other class I antiarrhythmic drug for a first episode of atrial fibrillation or flutter is contraindicated after discharge from the hospital in patients whose symptoms were moderate. In some cases, atrial fibrillation or flutter recurs only infrequently, and occasional brief hospitalizations for cardioversion may be the safest approach. If recurrences are frequent, it may be necessary to decide between leaving the patient in atrial fibrillation or trying long-term amiarrhythmic drug therapy. These approaches must be individualized, however, because there are no controlled trials to guide this decision. If atrial fibrillation causes severe hemodynamic collapse, as may occur with aortic stenosis, mitral stenosis, or hypertrophic cardiomyopathy, it may be neces-

sary to (1) restore sinus rhythm promptly with cardioversion and (2) maintain sinus rhythm (even after the first episode of atrial fibrillation) to minimize the risk of recurrent episodes of atrial fibrillation. In this case, treatment with class I antiarrhythmic drugs, including quinidine, may be considered after the first episode of atrial fibrillation.

Summary Although quinidine, the oldest class I antiarrhythmic drug, has been available for several decades, recent reports have emphasized the possibility of dangerous side effects. Quinidine often successfully maintains sinus rhythm in patients with intermittent atrial fibrillation, suppresses sustained ventricular tachycardia in some patients, and minimally depresses left ventricular function. However, it can cause nonfatal and, occasionally, even fatal proarrhythmic complications. Therefore, it must be administered with caution in appropriately selected patients. FUll

Earn credit on this article. See CME Quiz.

continued 138


NAPROSYN' (NAPROXEN) 5DDmg tablets Briel Summary: Contralndlcations: Patients who have had allergic reactions to NAPROSYN, ANAPROX or ANAPROX OS or in whom aspirin or other NSAIDs induce the syndrome of asthma, rhinitis, and nasal polyps. Because anaphylactic reactions usually occur in patients with a history of such reactions, question patients for asthma, nasal polyps, urticaria, and hypotension associated with NSAIDs before starting therapy. If such symptoms occur, discontinue the drug. Warnings: Senous Gl toxicity such as bleeding, ulceration, and perforation can occur at an~ time, with or without warning

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absence of previous Gl tract symptoms. In clinical trials, symptomatic upper Gl ulcers, gross bleeding or perforation appear to occur in approximately 1% of patients treated for 3-6 months, and in about 2-4% of patients treated for one year Inform patients about the signs and/or symptoms of serious Gl toxicity and what steps to take if they occur. Studies have not identified any subset

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factors known to be associated with peptic ulcer disease, such as

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seem to tolerate ulceration or bleeding less well than others and most spontaneous reports of fatal Gl events are in this population. In considering the use of relatively large doses (within the recommended dosage range), suHicient benefit should be anticipated to oHset the potential increased risk of Gl toxicity. Precautions: DO NOT GIVE NAPROSYN® (NAPROXEN~ CONCOMITANTLY WITH ANAPROX® (NAPROXEN SODIUM OR ANAPROX® OS (NAPROXEN SODIUM) SINCE THEY BO H CIRCULATE IN PLASMA AS THE NAPROXEN ANION. Acute interstitial nephritis with hematuria, proteinuria, and nephrotic syndrome has been reported. Patients with impaired renal function, heart failure, liver dysfunction, patients taking diuretics, and the elderly are at greater risk of overt renal decompensation. If this occurs, discontinue the drug. Use with caution and monitor serum creatinine and/or creatinine clearance in patients with significantly impaired renal function. Use caution m patients with baseline creatinine clearance less than 20 mUminute. Use the lowest effective dose in the elderly or in patients with chronic alcoholic liver disease or cirrhosis. With NSAIDs, borderline elevations of liver tests may occur in up to

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occurred in controlled clinical trials in less than 1% of patients. Severe hepatic reactions, including jaundice and fatal hepatitis, have been reported rarely. If liver disease develops or if systemic manifestations occur (e.g., eosinophilia or rash), discontinue therapy. If steroid dosage is reduced or eliminated during therapy, do so slowly and observe patients closely for adverse effects, including adrenal insufficiency and exacerbation of arthritis symptoms. Determine hemoglobin values periodically for patients with initial values of 10 grams or less who receive long-term therapy. Peripheral edema has been reported. Therefore, use with caution in patients with fluid retention, hypertension or heart failure. The drug's antipyretic and anti-inflammatory activities may reduce fever and inflammation, diminishing the11 diagnostic value. Conduct ophthalmic studies if any change or disturbance in vision occurs. For patients with restricted sodium intake, note that the susftension contains 8 m~/mL of sodium. Information for

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may result in hospitalization and even fatal outcomes. Physicians may wish to discuss with patients the potential risks and likely

~~~e~!iig~sN;:~~it\~enai~~~'i/t~~~;~;~r:lthheo~~hJ~~~su~ea~ fg; an acceptable alternative. Patients should use caution for activities requiring alertness if they experience drowsiness, diuiness, vertigo or depression during therapy. Laboratory Tests: Because serious Gl tract ulceration and bleeding can occur without warn~~~~~~;o~sthf~~~0~n~hf~rci~~~~h~~at~? ~~~tii'n':~~i~;n~~g~~ ;;i~

follow-up. Drug tnteracllons: Use caution when ting concomi-

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probenecid; or methotrexate. Drug/Laboratory Test lnteracllons: The druq may decrease platelet aggregation and prolong bleeding time or mcrease urinary values for 17-ketogenic steroids. Temporarily stop therapy for 72 hours before doing adrenal functron

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genicity. Pregnancy: Category B. Do not use during pregnancy 1

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doses of 2.5-5 mg/kg, with total daily dose not exceeding 15 mg/kg/day, are safe rn children over 2 years of age. Adverse Reactions: In a study, Gl reactions were more frequent and severe in rheumatoid arthritis patients on 1,500 mgiday than in those on 750 mgiday. In studies rn children with juvenile arthritis, rash and prolonged bleeding times were more frequent, Gl and CNS reac-


Gl: The most frequent complaints related to the Gl tract: constipation: heartburn: abdominal pain: nausea: dyspepsia, diarrhea, stomatitis. CNS: headache: drzziness: drowsiness: light-headedness, vertigo. Dermatologic: itching (pruritus): skin eruptions:

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colitis, Gl bleeding and/or perforation, hematemesis, jaundice, melena, peptic ulceration with bleeding and/or perforation, vomitin9.·. Renal: Ql~merular n.ephritis, hematuria, .hyperkalemia, interStitial nephritiS, nephrotiC syndrome, renal d1sease, renal failure, renal papillary necrosis. Hematoloqic: agranulocytosis, eosinophilia, qranulocytopenia, leukopenra, thrombocytopenia. CNS: depressron, dream abnormalities, inability to concentrate, insomnia, malaise, myalgia and muscle weakness. Dermatologic: alopecia, photosensitive dermatitis, skin rashes. Special Senses: hearing impairment. Cardiovascular: congestive heart failure. Respiratory: eosinophilic pneumonitis. General: anaphylactoid reactions, menstrual disorders, pyrexia (chills and fever). Causal Relationship Unknown: Hematologic: aplastic anemia, hemolytic anemia. CNS: aseptic meningitis, cognitive dysfunction. Dermatologic: epidermal necrolysis, erythema multiforme, photosensitivity reactions resembling porphyria cutanea tarda and epidermolysis bullosa, Stevens-Johnson syndrome, urticaria. Gl: non-peptic Gl ulceration, ulcerative stomatitis. Cardiovascular: vasculitis. General: angioneurotic edema, hyperglycemia, hypoglycemia. Overdosage: May have drowsiness, heartburn, indigestion, nausea, vomiting. A few patients have had seizures. Empty stomach and use usual supportive measures. In animals 0.5 g/kg of activated charcoal reduced plasma levels of naproxen. Caullon: Federal law prohibits dispensrng without prescrrption. See package insert for full Prescribing Information. 'Incidence of reported reaction 3%-9%. ~;;:-:-lrSYNTEX-----,1 Where unmarked, incidence less than 3%. L'='='-'·----...J. U.S. patent nos. 3,904,682, 3,996,966 and others. ©1991 Syntex Puerto Rico, Inc. Rev.39 September 1990

I wish to thank Rosanne Avelar for her help in the preparation of this manuscript. Address for correspondence: David M. Salerno, MD, PhD, Division of Cardiology, Hennepin County Medical Center, 70 1 Park Ave S, Minneapolis,

MN 55415.


I. Coplen SE, Antman EM, Berlin JA, et al. Efficacy and safety of quinidine rherapy for maintenance of sinus rhythm after cardioversion: a meta-analysis of randomized control trials. Circulation 1990;82(4):1106-16 [erratum, Circulation 1991;83(2):714] 2. MorganrothJ, GoinJE. Quinidine-related mortality in rhe short-to-medium-term treatment of ventricular arrhythmias: a meta-analysis. Circulation 1991;84(5):1977-83 3. Salerno DM. Quinidine: worse than adverse? (Editorial) Circulation 1991;84(5):2196-8 4. The Cardiac Arrhythmia Suppression Trial (CAST) lnwstigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infurction. N Eng! J Med 1989; 321(6):406-12 5. Wooding-Scott RA, VISCO J, Slaughter RL. Total and unbound concentrations of quinidine and 3-hydroxyquinidine at steady state. Am Heart] 1987;113(2 Pt 1):302-6 6. Garfinkel D, Mamelok RD, Blaschke TF. Altered therapeutic range for quinidine after myocardial infarction and cardiac surgery. Ann Intern Med 1987;107(1):48-50 7. Salerno DM, Gillingham Iq, Berry DA, et al. A comparison of antiarrhythmic drugs for the suppression of ventricular ectopic depolarizations: a meta-analysis. Am Heart J 1990; 120(2):340-53 8. DiMarco JP, Garan H, Ruskin JN. Quinidine for ventricular arrhythmias: value of electrophysiologic testing. Am J Cardiol 1983; 51(1):90-5

9. Swerdlow CD, Yu JO, Jacobson E, et al. Safety and efficacy of intravenous quinidine. Am] Med 1983;75(1):36-42 IO. Borgeat A, Goy JJ, Maendly R, et al. Flecainide versus quinidine for conversion of atrial fibrillation to sinus rhythm. Am J Cardiol 1986; 58(6):496-8 II. Morganroth J, Hunter H. Comparative efficacy and safety of short-acting and sustained release quinidine in rhe treatment of patients wirh ventricular arrhythmias. Am Heart J 1985; 110(6):1176-81 I2. Knobler H, Levij IS, Gavish D, et al. Quinidine-induced hepatitis: a common and reversible hypersensitivity reaction. Arch Intern Med 1986;146(3):526-8 13. Reynolds EW; Vander Ark CR. Quinidine syncope and rhe delayed repolarization syndromes. Mod Concepts Cardiovasc Dis 1976; 45(8): 117-22 I4. Bauman JL, Bauernfeind RA, HoffJV, et al. Torsade de pointes due to quinidine: observations in 31 patients. Am Heart J 1984; 107(3):425-30 I5. Roden DM, Woosley RL, Primm RK. Incidence and clinical features of rhe quinidineassociated long QT syndrome: implications for patient care. Am Heart} 1986;111(6):1088-93 I6. Hager WD, Fenster P, Mayersohn M, et al. Digoxin-quinidine interaction: pharmacokinetic evaluation. N Eng! J Med 1979; 300(22):1238-41 I7. Dinai Y, Sharir M, Naveh N, et al. Bradycardia induced by interaction between quinidine and ophrhalmic timolol. Ann Intern Med 1985; 103(6 Pt 1):890-1 I8. Crawford MH, White DH, O'Rourke RA. Effects of oral quinidine on left ventricular performance in normal subjects and patients wirh congestive cardiomyoparhy. Am J Cardiol 1979;44(4):714-8 I9. Jackman WM, Wang XZ, Friday Iq, et al. Carheter ablation of accessory atrioventricular parhways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Eng! J Med 1991;324(23):1605-11 20. Calkins H, Sousa}, el-Atassi R, et al. Diagnosis and cure of rhe Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test. N Eng!J Med 1991;324(23):1612-8




Quinidine: is it a good drug or a bad drug?

Although quinidine, the oldest class I antiarrhythmic drug, has been available for several decades, recent reports have emphasized the possibility of ...
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