Quinidine-induced ventricular flutter and fibrillation without digitalis therapy

Koster, Rudolph W.; Wellens, Hein J.J.

doi:10.1016/0002-9149(76)90471-9

Cited by 138 publications

(24 citation statements)

References 25 publications

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“…In this study we show that persistent AF reduced the likelihood of patients developing TdP when administered QT-prolonging drugs. This is surprising given the frequent short-long-short cycles in AF, but is in accord with previous reports indicating heightened risk after conversion of AF (23). There are a number of lines of evidence that suggest dysregulation of the QT interval in AF.…”

Section: Discussionsupporting

confidence: 77%

“…Virtually all of these drugs block the rapid component of the cardiac-delayed rectifier (I Kr ) as a major mechanism of action, and marked QT prolongation and pause-dependent TdP are the major class toxicities. Clinical anecdotes have long suggested that TdP, when it occurs in this setting, develops after conversion of rhythm to SR and rarely when the underlying rhythm remains AF (23,24). To test these anecdotes, we have previously infused the potent I Kr blocker dofetilide in 9 patients before and immediately after cardioversion of AF, and showed that although there was little QT prolongation during AF, some patients displayed striking QT prolongation (and 1 had TdP) in the post-cardioversion challenge (25).…”

Section: Discussionmentioning

confidence: 99%

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Persistent Atrial Fibrillation Is Associated With Reduced Risk of Torsades de Pointes in Patients With Drug-Induced Long QT Syndrome

Darbar

Kimbrough

Jawaid

et al. 2008

Journal of the American College of Cardiology

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Persistent Atrial Fibrillation Is Associated With Reduced Risk of Torsades de Pointes in Patients With Drug-Induced Long QT Syndrome

Darbar

Kimbrough

Jawaid

et al. 2008

Journal of the American College of Cardiology

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“…AVT was found to be induced mainly by quinidinel [8][9][10][11][12][13] and by other antiarrhythmic and cardiac drugs such as procainamide,"l 1" disopyramide,'5' 18 lidocainell and prenylamine. "1 Occasionally, other drugs such as phenothiazines,'7 as well as hypokalemia,4 7 hypomagnesemia, ' 18 electrical ventricular stimulation,19 congenital QT prolongation syndrome,20 or acute central nervous system damage2' may precipitate AVT.…”

mentioning

confidence: 99%

Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients.

Keren¹,

Tzivoni²,

Gavish³

et al. 1981

Circulation

231

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“…Interestingly, data provided in 1977 by the Boston Collaborative Drug Surveillance Program (Cohen et at, 1977) showed a substantially lower incidence of adverse effects in patients treated with combined digitalis and quinidine than in patients treated with quinidine alone. However, that report as well as others (Davies et al, 1965;Koster and Wellens, 1976) revealed that in the majority of patients with apparently quinidine-induced ventricular dysrhythmias, digitalis had also been prescribed, suggesting a possible interaction between the two drugs (Aronson, 1978). In 1977, two reports provided preliminary evidence for an interaction between digoxin and quinidine (Ejvinsson, 1977;Kaufmann, 1978) and in the following year three groups independently reported that quinidine increases the serum/plasma digoxin concentration (Doering and Konig, 1978;Ejvinsson, 1978;Leahey et aI., 1978).…”

mentioning

confidence: 53%

The Quinidine-Digoxin Interaction in Perspective

Fichtl

Doering

1983

Clinical Pharmacokinetics

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The administration of quinidine to patients receiving digoxin maintenance therapy results in a marked increase in the serum/plasma digoxin concentration. With over 90% of patients being affected the incidence of this drug interaction is rather high. The change in serum digoxin concentration is proportional to the dose of quinidine. At usual therapeutic doses of quinidine, the serum digoxin concentration tends to double on the average, although there is pronounced individual variation, the reported increase ranging from 25 to over 300%. The serum digoxin concentration begins to rise within 24 hours after starting quinidine and a new steady-state level is established in about 3 to 6 days. It remains elevated for as long as quinidine is co-administered. Quinidine increases the serum digoxin concentration in anuric patients also; in these patients it may take a week or more until a new steady-state is established.The sustained elevation of serum digoxin concentration during quinidine co-administration is undoubtedly due to a decrease in total body clearance of digoxin. Quinidine decreases both renal and extrarenal clearance of digoxin. Obviously quinidine inter/eres with renal tubular excretion of digoxin since it affects neither the glomerular filtration rate nor protein binding of digoxin. The mechanism by which quinidine decreases extrarenal clearance of digoxin remains to be elucidated.Conflicting results have been reported with regard to the influence of quinidine on the elimination half-life (t'l,) and volume of distribution of digoxin. At least in the relevant patient group, i.e. in cardiac patients on long term treatment with combined digoxin and quinidine, the digoxin t", is apparently increased, but both no change and a substantial decrease in volume of distribution during q~inidine ,co-administration has been reported. Direct measurements of digoxin tissue levels in vivo seem to favour the latter finding. However, specific binding of digoxin in vitro is unaffected by quinidine at concentrations thought to be in the therapeutic range. Whether quinidine interferes with nonspecific binding of digoxin remains to be determined.The clinical effect on the heart of the increased serum digoxin concentration in the quinidine-digoxin interaction is still controversial. However, the evidence available at present strongly suggests that the increase results at least partially in an increased cardiac effect. Likewise, data provided recently by the Boston Drug Surveillance Program and several case reports indicate an increased digoxin toxicity during quinidine administration. Based on our present knowledge of this drug interaction, only tentative therapeutic recommendations can be given.

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Quinidine-induced ventricular flutter and fibrillation without digitalis therapy

Cited by 138 publications

References 25 publications

Persistent Atrial Fibrillation Is Associated With Reduced Risk of Torsades de Pointes in Patients With Drug-Induced Long QT Syndrome

Persistent Atrial Fibrillation Is Associated With Reduced Risk of Torsades de Pointes in Patients With Drug-Induced Long QT Syndrome

Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients.

The Quinidine-Digoxin Interaction in Perspective

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