Increased quinidine plasma concentrations during administration of verapamil: A new quinidine-verapamil interaction

Trohman, Richard G.; Estes, Daneil M.; Castellanos, Agustín; Palomo, Andres R.; Myerburg, Robert J.; Kessler, Kenneth M.

doi:10.1016/0002-9149(86)90870-2

Cited by 32 publications

(3 citation statements)

References 4 publications

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“…Plasma Levels : Quinidine levels decrease with phenytoin or nifedipine and increase with verapamil (Trohman et al 1986 ) or diltiazem administration.…”

Section: Quinidinementioning

confidence: 99%

Cardiac Drug Therapy

Khan

2015

Contemporary Cardiology

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“…Plasma Levels : Quinidine levels decrease with phenytoin or nifedipine and increase with verapamil (Trohman et al 1986 ) or diltiazem administration.…”

Section: Quinidinementioning

confidence: 99%

Cardiac Drug Therapy

Khan

2015

Contemporary Cardiology

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“…Verapamil and quinidine may interact to cause excess hypotension, either by combined inhibition of peripheral α-receptors or by an increase in quinidine levels owing to a hepatic interaction between these 2 drugs. 62,63…”

Section: Drug Interactionsmentioning

confidence: 99%

Pharmacologic and Therapeutic Considerations in Hypertension Therapy With Calcium Channel Blockers: Focus on Verapamil

Sica

Prisant

2007

J of Clinical Hypertension

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In the past 2 decades, calcium channel blockers have emerged as important and useful agents for treating hypertension. The safety of this drug class has been vigorously debated for some time, and it has only been in the past few years that such debate has been quieted by favorable outcomes data with these compounds. Calcium channel blockers are a heterogeneous group of compounds as alike as they are dissimilar. Calcium channel blockers can be separated into dihydropyridine and nondihydropyridine subclasses, with representatives of the latter being verapamil and diltiazem. A lengthy treatment experience exists for verapamil, a compound that has progressed from an immediate‐release to a sustained‐release and, more recently, a delayed/sustained‐release formulation designated for administration at bedtime. This latter formulation synchronizes drug delivery with the early morning rise in blood pressure, which is a particularly attractive feature when viewed in the context of the distinctive pharmacokinetic and pharmacodynamic features of verapamil.

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“…In addition, increased concentrations of both quinidine and prazosin occur when given with vera-pamil, perhaps related to inhibition of oxidative metabolism (Hunt et al 1989;Trohman et al 1986). In addition, increased concentrations of both quinidine and prazosin occur when given with vera-pamil, perhaps related to inhibition of oxidative metabolism (Hunt et al 1989;Trohman et al 1986).…”

Section: Other Drug Interactionsmentioning

confidence: 99%

Poisoning Due to Calcium Antagonists

Pearigen

Benowitz

1991

Drug Safety

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The calcium antagonists are a heterogeneous class of drugs which block the inward movement of calcium into cells through 'slow channels' from extracellular sites. By inhibiting phase 0 depolarisation in cardiac pacemaker cells and phase 2 plateau in myocardium, and by depressing calcium ion flux in smooth muscle cells of blood vessels, these agents may exert profound effects on the cardiovascular system, particularly in susceptible individuals or in overdose. Sinus node depression, impaired atrioventricular (AV) conduction, depressed myocardial contractility, and peripheral vasodilatation may result. Pharmacokinetic features of calcium antagonists include rapid and complete absorption from the gastrointestinal tract, with extensive first-pass hepatic metabolism yielding generally low bioavailability. The volume of distribution is generally large and protein binding is high. Elimination is almost entirely by the liver. Impaired renal function does not affect pharmacokinetics. Verapamil is the most potent inhibitor of cardiac conduction and contractility, with diltiazem also showing such effects. Nifedipine is the most potent vasodilator, but only occasionally impairs the sinus node or AV conduction. Significant pharmacodynamic effects are common during combination therapy with calcium antagonists, especially verapamil and beta-blockers. Verapamil may significantly elevate serum digoxin concentrations and may exert additive negative effects on chronotropism and dromotropism when this combination is used. Overdoses of calcium entry blockers are becoming more frequent and reflect an extension of the known pharmacodynamic profile of these agents. Typical features include confusion or lethargy, hypotension, sinus node depression and cardiac conduction defects. Onset of symptoms may be delayed if a sustained release preparation is ingested. Management of calcium antagonist overdose includes gut decontamination with lavage and activated charcoal. All symptomatic patients and patients with a history of ingesting a sustained release preparation should be admitted for ECG monitoring. If bradycardia and/or conduction defects contribute to hypotension, atropine or isoprenaline (isoproterenol) may accelerate the ventricular rate. Transvenous pacing may be required. Depressed myocardial contractility usually responds well to calcium chloride or calcium gluconate administration, but further inotropic support may be required. Peripheral vasodilation should be managed with intravenous fluids and a pressor agent such as dopamine or norepinephrine (noradrenaline).

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Increased quinidine plasma concentrations during administration of verapamil: A new quinidine-verapamil interaction

Cited by 32 publications

References 4 publications

Cardiac Drug Therapy

Cardiac Drug Therapy

Pharmacologic and Therapeutic Considerations in Hypertension Therapy With Calcium Channel Blockers: Focus on Verapamil

Poisoning Due to Calcium Antagonists

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