Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1509
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LANOXIN (Tablet)
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General: Recommended dosages of digoxin may require considerable
modification because of individual sensitivity of the patient to the
drug, the presence of associated conditions, or the use of concurrent
medications. In selecting a dose of digoxin, the following factors
must be considered:<br/>Serum Digoxin Concentrations: In general, the dose of digoxin used should be determined
on clinical grounds. However, measurement of serum digoxin concentrations
can be helpful to the clinician in determining the adequacy of digoxin
therapy and in assigning certain probabilities to the likelihood of
digoxin intoxication. About two-thirds of adults considered adequately
digitalized (without evidence of toxicity) have serum digoxin concentrations
ranging from 0.8 to 2.0 ng/mL. However, digoxin may produce clinical
benefits even at serum concentrations below this range. About two-thirds
of adult patients with clinical toxicity have serum digoxin concentrations
greater than 2.0 ng/mL. However, since one-third of patients
with clinical toxicity have concentrations less than 2.0 ng/mL,
values below 2.0 ng/mL do not rule out the possibility that a
certain sign or symptom is related to digoxin therapy. Rarely, there
are patients who are unable to tolerate digoxin at serum concentrations
below 0.8 ng/mL. Consequently, the serum concentration of digoxin
should always be interpreted in the overall clinical context, and
an isolated measurement should not be used alone as the basis for
increasing or decreasing the dose of the drug. To allow adequate time for equilibration of digoxin between serum
and tissue, sampling of serum concentrations should be done just before
the next scheduled dose of the drug. If this is not possible, sampling
should be done at least 6 to 8 hours after the last dose, regardless
of the route of administration or the formulation used. On a once-daily
dosing schedule, the concentration of digoxin will be 10% to 25% lower
when sampled at 24 versus 8 hours, depending upon the patient's
renal function. On a twice-daily dosing schedule, there will be only
minor differences in serum digoxin concentrations whether sampling
is done at 8 or 12 hours after a dose. If a discrepancy exists between the reported serum concentration
and the observed clinical response, the clinician should consider
the following possibilities:<br/>Heart Failure:<br/>Adults: Digitalization may be accomplished by either of
two general approaches that vary in dosage and frequency of administration,
but reach the same endpoint in terms of total amount of digoxin accumulated
in the body.<br/>Infants and Children: In general, divided daily dosing is recommended
for infants and young children (under age 10). In the newborn
period, renal clearance of digoxin is diminished and suitable dosage
adjustments must be observed. This is especially pronounced in the
premature infant. Beyond the immediate newborn period, children generally
require proportionally larger doses than adults on the basis of body
weight or body surface area. Children over 10 years of age require
adult dosages in proportion to their body weight. Some researchers
have suggested that infants and young children tolerate slightly higher
serum concentrations than do adults. Daily
maintenance doses for each age group are given in Table 6 and
should provide therapeutic effects with minimum risk of toxicity in
most patients with heart failure and normal sinus rhythm. These recommendations
assume the presence of normal renal function: In children with renal disease, digoxin must
be carefully titrated based upon clinical response. It cannot be overemphasized that both
the adult and pediatric dosage guidelines provided are based upon
average patient response and substantial individual variation can
be expected. Accordingly, ultimate dosage selection must be based
upon clinical assessment of the patient. Atrial Fibrillation: Peak digoxin body stores larger than the 8 to
12 mcg/kg required for most patients with heart failure and normal
sinus rhythm have been used for control of ventricular rate in patients
with atrial fibrillation. Doses of digoxin used for the treatment
of chronic atrial fibrillation should be titrated to the minimum dose
that achieves the desired ventricular rate control without causing
undesirable side effects. Data are not available to establish the
appropriate resting or exercise target rates that should be achieved.<br/>Dosage Adjustment When Changing
Preparations: The difference in bioavailability between LANOXIN
Injection or LANOXICAPS and LANOXIN Elixir Pediatric or LANOXIN Tablets
must be considered when changing patients from one dosage form to
another. Doses of 100 mcg (0.1 mg)
and 200 mcg (0.2 mg) of LANOXICAPS are approximately equivalent
to 125-mcg (0.125-mg) and 250-mcg (0.25-mg) doses of LANOXIN Tablets
and Elixir Pediatric, respectively (see Table 1 in CLINICAL PHARMACOLOGY:
Pharmacokinetics).
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LANOXIN (digoxin)
is one of the cardiac (or digitalis) glycosides, a closely related
group of drugs having in common specific effects on the myocardium.These drugs are found in a number of plants.
Digoxin is extracted from the leaves of Digitalis lanata. The term���digitalis���is
used to designate the whole group of glycosides. The glycosides are
composed of two portions: a sugar and a cardenolide (hence���glycosides���). Digoxin is described chemically as (3��,5��,12��)-3-[(O-2,6-dideoxy-��-D-ribo-hexopyranosyl-(1���4)-O-2,6-dideoxy-��-D-ribo-hexopyranosyl-(1���4)-2,6-dideoxy-��-D-ribo-hexopyranosyl)oxy]-12,14-dihydroxy-card-20(22)-enolide. Its molecular
formula is CHO, its molecular
weight is 780.95, and its structural formula is: Digoxin exists as odorless white crystals
that melt with decomposition above 230��C. The drug is practically
insoluble in water and in ether; slightly soluble in diluted (50%)
alcohol and in chloroform; and freely soluble in pyridine. LANOXIN is supplied as 125-mcg (0.125-mg) or 250-mcg
(0.25-mg) tablets for oral administration. Each tablet contains the
labeled amount of digoxin USP and the following inactive ingredients:
corn and potato starches, lactose, and magnesium stearate. In addition,
the dyes used in the 125-mcg (0.125-mg) tablets are D&C Yellow
No. 10 and FD&C Yellow No. 6.
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Digitalis glycosides are contraindicated in patients
with ventricular fibrillation or in patients with a known hypersensitivity
to digoxin. A hypersensitivity reaction to other digitalis preparations
usually constitutes a contraindication to digoxin.
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LANOXIN (digoxin) Tablets, Scored 125 mcg (0.125 mg):
Bottles of 100 with child-resistant cap (NDC 0173-0242-55) and 1000
(NDC 0173-0242-75); unit dose pack of 100 (NDC 0173-0242-56). Imprinted
with LANOXIN and Y3B (yellow). Store at 25��C (77��F); excursions permitted
to 15 to 30��C (59 to 86��F) [see USP Controlled Room Temperature]
in a dry place and protect from light. LANOXIN (digoxin) Tablets, Scored 250 mcg (0.25 mg):
Bottles of 100 with child-resistant cap (NDC 0173-0249-55), 1000 (NDC
0173-0249-75), and 5000 (NDC 0173-0249-80); unit dose pack of 100
(NDC 0173-0249-56). Imprinted with LANOXIN and X3A (white). Store at 25��C (77��F);
excursions permitted to 15 to 30��C (59 to 86��F) [see USP
Controlled Room Temperature] in a dry place. Manufactured for GlaxoSmithKline Research Triangle Park, NC 27709 by DSM Pharmaceuticals, Inc. Greenville, NC
27834 or GlaxoSmithKline Research Triangle Park, NC 27709 ��2006,
GlaxoSmithKline. All rights reserved. November
2006RL-2258
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Use in Patients with Impaired
Renal Function: Digoxin is primarily excreted by the kidneys; therefore,
patients with impaired renal function require smaller than usual maintenance
doses of digoxin (see DOSAGE AND ADMINISTRATION). Because of the prolonged
elimination half-life, a longer period of time is required to achieve
an initial or new steady-state serum concentration in patients with
renal impairment than in patients with normal renal function. If appropriate
care is not taken to reduce the dose of digoxin, such patients are
at high risk for toxicity, and toxic effects will last longer in such
patients than in patients with normal renal function.<br/>Use in Patients with Electrolyte
Disorders: In patients with hypokalemia or hypomagnesemia,
toxicity may occur despite serum digoxin concentrations below 2.0 ng/mL,
because potassium or magnesium depletion sensitizes the myocardium
to digoxin. Therefore, it is desirable to maintain normal serum potassium
and magnesium concentrations in patients being treated with digoxin.
Deficiencies of these electrolytes may result from malnutrition, diarrhea,
or prolonged vomiting, as well as the use of the following drugs or
procedures: diuretics, amphotericin B, corticosteroids, antacids,
dialysis, and mechanical suction of gastrointestinal secretions. Hypercalcemia from any cause predisposes the patient
to digitalis toxicity. Calcium, particularly when administered rapidly
by the intravenous route, may produce serious arrhythmias in digitalized
patients. On the other hand, hypocalcemia can nullify the effects
of digoxin in humans; thus, digoxin may be ineffective until serum
calcium is restored to normal. These interactions are related to the
fact that digoxin affects contractility and excitability of the heart
in a manner similar to that of calcium.<br/>Use in Thyroid Disorders and
Hypermetabolic States: Hypothyroidism may reduce the requirements for digoxin.
Heart failure and/or atrial arrhythmias resulting from hypermetabolic
or hyperdynamic states (e.g., hyperthyroidism, hypoxia, or arteriovenous
shunt) are best treated by addressing the underlying condition. Atrial
arrhythmias associated with hypermetabolic states are particularly
resistant to digoxin treatment. Care must be taken to avoid toxicity
if digoxin is used.<br/>Use in Patients with Acute
Myocardial Infarction: Digoxin should be used with caution in patients
with acute myocardial infarction. The use of inotropic drugs in some
patients in this setting may result in undesirable increases in myocardial
oxygen demand and ischemia.<br/>Use During Electrical Cardioversion: It may be desirable to reduce the dose of digoxin
for 1 to 2 days prior to electrical cardioversion of atrial fibrillation
to avoid the induction of ventricular arrhythmias, but physicians
must consider the consequences of increasing the ventricular response
if digoxin is withdrawn. If digitalis toxicity is suspected, elective
cardioversion should be delayed. If it is not prudent to delay cardioversion,
the lowest possible energy level should be selected to avoid provoking
ventricular arrhythmias.<br/>Laboratory Test Monitoring: Patients receiving digoxin should have their serum
electrolytes and renal function (serum creatinine concentrations)
assessed periodically; the frequency of assessments will depend on
the clinical setting. For discussion of serum digoxin concentrations,
see DOSAGE AND ADMINISTRATION section.<br/>Drug Interactions: Potassium-depleting diuretics are a major contributing factor to digitalis
toxicity. Calcium, particularly
if administered rapidly by the intravenous route, may produce serious
arrhythmias in digitalized patients. Quinidine, verapamil, amiodarone, propafenone, indomethacin, itraconazole, alprazolam, and spironolactone raise the serum digoxin
concentration due to a reduction in clearance and/or in volume of
distribution of the drug, with the implication that digitalis intoxication
may result. Erythromycin and clarithromycin (and possibly other macrolide antibiotics) and tetracycline may increase digoxin absorption
in patients who inactivate digoxin by bacterial metabolism in the
lower intestine, so that digitalis intoxicationmay result (see CLINICAL
PHARMACOLOGY: Absorption). Propantheline and diphenoxylate, by decreasing
gut motility, may increase digoxin absorption. Antacids, kaolin-pectin, sulfasalazine, neomycin,
cholestyramine, certain anticancer
drugs, and metoclopramide may interfere with intestinal
digoxin absorption, resulting in unexpectedly low serum concentrations. Rifampin may decrease serum digoxin
concentration, especially in patients with renal dysfunction, by increasing
the non-renal clearance of digoxin. There have been inconsistent reports
regarding the effects of other drugs [e.g., quinine, penicillamine] on serum digoxin concentration. Thyroid administration to a digitalized,
hypothyroid patient may increase the dose requirement of digoxin.
Concomitant use of digoxin and sympathomimetics increases the risk of cardiac arrhythmias. Succinylcholine may cause a sudden extrusion of potassium
from muscle cells, and may thereby cause arrhythmias in digitalized
patients. Although beta-adrenergic blockers or calcium channel blockers
and digoxin may be useful in combination to control atrial fibrillation,
their additive effects on AV node conduction can result in advanced
or complete heart block. Due to the considerable
variability of these interactions, the dosage of digoxin should be
individualized when patients receive these medications concurrently.
Furthermore, caution should be exercised when combining digoxin with
any drug that may cause a significant deterioration in renal function,
sincea decline in glomerular filtration or tubular secretion may
impair the excretion of digoxin.<br/>Drug/Laboratory Test Interactions: The use of therapeutic doses of digoxin may cause
prolongation of the PR interval and depression of the ST segment on
the electrocardiogram. Digoxin may produce false positive ST-T changes
on the electrocardiogram during exercise testing. These electrophysiologic
effects reflect an expected effect of the drug and are not indicative
of toxicity.<br/>Carcinogenesis, Mutagenesis,
Impairment of Fertility: There have been no long-term studies performed in
animals to evaluate carcinogenic potential, nor have studies been
conducted to assess the mutagenic potential of digoxin or its potential
to affect fertility.<br/>Pregnancy:<br/>Teratogenic Effects: Pregnancy
Category C. Animal reproduction studies have not been conducted
with digoxin. It is also not known whether digoxin can cause fetal
harm when administered to a pregnant woman or can affect reproductive
capacity. Digoxin should be given to a pregnant woman only if clearly
needed.<br/>Nursing Mothers: Studies have shown that digoxin concentrations in
the mother's serum and milk are similar. However, the estimated
exposure of a nursing infant to digoxin via breast feeding will be
far below the usual infant maintenance dose. Therefore, this amount
should have no pharmacologic effect upon the infant. Nevertheless,
caution should be exercised when digoxin is administered to anursing
woman.<br/>Pediatric Use: Newborn infants display considerable variability
in their tolerance to digoxin. Premature and immature infants are
particularly sensitive to the effects of digoxin, and the dosage of
the drug must not only be reduced but must be individualized according
to their degree of maturity. Digitalis glycosides can cause poisoning
in children due to accidental ingestion.<br/>Geriatric Use: The majority of clinical experience gained with
digoxin has been in the elderly population. This experience has not
identified differences in response or adverse effects between the
elderly and younger patients. However, this drug is known to be substantially
excreted by the kidney, and the risk of toxic reactions to this drug
may be greater in patients with impaired renal function. Because elderly
patients are more likely to have decreased renal function, care should
be taken in dose selection, which should be based on renal function,
and it may be useful to monitor renal function (see DOSAGE AND ADMINISTRATION).
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Treatment of Adverse Reactions
Produced by Overdosage: Digoxin should
be temporarily discontinued until the adverse reaction resolves. Every
effort should also be made to correct factors that may contribute
to the adverse reaction (such as electrolyte disturbances or concurrent
medications). Once the adverse reaction has resolved, therapy with
digoxin may be reinstituted, following a careful reassessment of dose. Withdrawal of digoxin may be all that is required
to treat the adverse reaction. However, when the primary manifestation
of digoxin overdosage is a cardiac arrhythmia, additional therapy
may be needed. If the rhythm disturbance
is a symptomatic bradyarrhythmia or heart block, consideration should
be given to the reversal of toxicity with DIGIBIND' [Digoxin
Immune Fab (Ovine)] (see Massive Digitalis Overdosage subsection),
the use of atropine, or the insertion of a temporary cardiac pacemaker.
However, asymptomatic bradycardia or heart block related to digoxin
may require only temporary withdrawal of the drug and cardiac monitoring
of the patient. If the rhythm disturbance
is a ventricular arrhythmia, consideration should be given to the
correction of electrolyte disorders, particularly if hypokalemia (see
Administration of Potassium subsection) or hypomagnesemia is present.
DIGIBIND is a specific antidote for digoxin and may be used to reverse
potentially life-threatening ventricular arrhythmias due to digoxin
overdosage.<br/>Administration of Potassium: Everyeffort should be made to maintain the serum potassium concentration
between 4.0 and 5.5 mmol/L. Potassium is usually administered
orally, but when correction of the arrhythmia is urgent and the serum
potassium concentration is low, potassium may be administered cautiously
by the intravenous route. The electrocardiogram should be monitored
for any evidence of potassium toxicity (e.g., peaking of T waves)
and to observe the effect on the arrhythmia. Potassium salts may be
dangerous in patients who manifest bradycardia or heart block due
to digoxin (unless primarily related to supraventricular tachycardia)
and in the setting of massive digitalis overdosage (see Massive Digitalis
Overdosage subsection).<br/>Massive Digitalis Overdosage: Manifestations
of life-threatening toxicity include ventricular tachycardia or ventricular
fibrillation, or progressive bradyarrhythmias, or heart block. The
administration of more than 10 mg of digoxin in a previously
healthy adult, or more than 4 mg in a previously healthy child,
or a steady-state serum concentration greater than 10 ng/mL often
results in cardiac arrest. DIGIBIND should
be used to reverse the toxic effects of ingestion of a massive overdose.
The decision to administer DIGIBIND to a patient who has ingested
a massive dose of digoxin but who has not yet manifested life-threatening
toxicity should depend on the likelihood that life-threatening toxicity
will occur (see above). Patients with massive
digitalis ingestion should receive large doses of activated charcoal
to prevent absorption and bind digoxin in the gut during enteroenteric
recirculation. Emesis or gastric lavage may be indicated especially
if ingestion has occurred within 30 minutes of the patient's
presentation at the hospital. Emesis should not be induced in patients
who are obtunded. If a patient presents more than 2 hours after
ingestion or already has toxic manifestations, it may be unsafe to
induce vomiting or attempt passage of a gastric tube, because such
maneuvers may induce an acute vagal episode that can worsen digitalis-related
arrhythmias. Severe digitalis intoxication
can cause a massive shift of potassium from inside to outside the
cell, leading to life-threatening hyperkalemia. The administration
of potassium supplements in the setting of massive intoxication may
be hazardous and should be avoided. Hyperkalemia caused by massive
digitalis toxicity is best treated with DIGIBIND; initial treatment
with glucose and insulin may also be required if hyperkalemia itself
is acutely life-threatening.
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digoxin
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LANOXIN (Tablet)
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In general, the adverse reactions of digoxin are
dose-dependent and occur at doses higher than those needed to achieve
a therapeutic effect. Hence, adverse reactions are less common when
digoxin is used within the recommended dose range or therapeutic serum
concentration range and when there is careful attention to concurrent
medications and conditions. Because some
patients may be particularly susceptible to side effects with digoxin,
the dosage of the drug should always be selected carefully and adjusted
as the clinical condition of the patient warrants. In the past, when
high doses of digoxin were used and little attention was paid to clinical
status or concurrent medications, adverse reactions to digoxin were
more frequent andsevere. Cardiac adverse reactions accounted for
about one-half, gastrointestinal disturbances for about one-fourth,
and CNS and other toxicity for about one-fourth of these adverse reactions.
However, available evidence suggests that the incidence and severity
of digoxin toxicity has decreased substantially in recent years. In
recent controlled clinical trials, in patients with predominantly
mild to moderate heart failure, the incidence of adverse experiences
was comparable in patients taking digoxin and inthose taking placebo.
In a large mortality trial, the incidence of hospitalization for suspected
digoxin toxicity was 2% in patients taking LANOXIN compared to 0.9%
in patients taking placebo. In this trial, the most common manifestations
of digoxin toxicity included gastrointestinal and cardiac disturbances;
CNS manifestations were less common.<br/>Adults:<br/>Cardiac: Therapeutic doses of digoxin may cause heart block
in patients with pre-existing sinoatrial or AV conduction disorders;
heart block can be avoided by adjusting the dose of digoxin. Prophylactic
use of a cardiac pacemaker may be considered if the risk of heart
block is considered unacceptable. High doses of digoxin may produce
a variety of rhythm disturbances, such as first-degree, second-degree
(Wenckebach), or third-degree heart block (including asystole); atrial
tachycardia with block; AV dissociation; accelerated junctional (nodal)
rhythm; unifocal or multiform ventricular premature contractions (especially
bigeminy or trigeminy); ventricular tachycardia; and ventricular fibrillation.
Digoxin produces PR prolongation and ST segment depression which shouldnot by themselves be considered digoxin toxicity. Cardiac toxicity
can also occur at therapeutic doses in patients who have conditions
which may alter their sensitivity to digoxin (see WARNINGS and PRECAUTIONS).<br/>Gastrointestinal: Digoxin may
cause anorexia, nausea, vomiting, and diarrhea. Rarely, the use of
digoxin has been associated with abdominal pain, intestinal ischemia,
and hemorrhagic necrosis of the intestines.<br/>CNS: Digoxin
can produce visual disturbances (blurred or yellow vision), headache,
weakness, dizziness, apathy, confusion, and mental disturbances (such
as anxiety, depression, delirium, and hallucination).<br/>Other: Gynecomastia
has been occasionally observed following the prolonged use of digoxin.
Thrombocytopenia and maculopapular rash and other skin reactions have
been rarely observed. Table 4 summarizes
the incidence of those adverse experiences listed above for patients
treated with LANOXIN Tablets or placebo from two randomized, double-blind,
placebo-controlled withdrawal trials. Patients in these trials were
also receiving diuretics with or without angiotensin-converting enzyme
inhibitors. These patients had been stable on digoxin, and were randomized
to digoxin or placebo. The results shown in Table 4 reflect the experience
in patients following dosage titration with the use of serum digoxin
concentrations and careful follow-up. These adverse experiences are
consistent with results from a large, placebo-controlled mortality
trial (DIG trial) wherein over half the patients were not receiving
digoxin prior to enrollment.<br/>Infants and Children: The side effects
of digoxin in infants and children differ from those seen in adults
in several respects. Although digoxin may produce anorexia, nausea,
vomiting, diarrhea, and CNS disturbances in young patients, these
are rarely the initial symptoms of overdosage. Rather, the earliest
and most frequent manifestation of excessive dosing with digoxin in
infants and children is the appearance of cardiac arrhythmias, including
sinus bradycardia. In children, the use of digoxin may produce any
arrhythmia. The most common are conduction disturbances or supraventricular
tachyarrhythmias, such as atrial tachycardia (with or without block)
and junctional (nodal) tachycardia. Ventricular arrhythmias are less
common. Sinus bradycardia may be a sign of impending digoxin intoxication,
especially in infants, even in the absence of first-degree heart block.
Any arrhythmia or alteration in cardiac conduction that develops in
a child taking digoxin should be assumed to be caused by digoxin,
until further evaluationproves otherwise.
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Sinus Node Disease and AV
Block: Because digoxin
slows sinoatrial and AV conduction, the drug commonly prolongs the
PR interval. The drug may cause severe sinus bradycardia or sinoatrial
block in patients with pre-existing sinus node disease and may cause
advanced or complete heart block in patients with pre-existing incomplete
AV block. In such patients consideration should be given to the insertion
of a pacemaker before treatment with digoxin.<br/>Accessory AV Pathway (Wolff-Parkinson-White
Syndrome): After intravenous
digoxin therapy, some patients with paroxysmal atrial fibrillation
or flutter and a coexisting accessory AV pathway have developed increased
antegrade conduction across the accessory pathway bypassing the AV
node, leading to a very rapid ventricular response or ventricular
fibrillation. Unless conduction down the accessory pathway has been
blocked (either pharmacologically or by surgery), digoxin should not
be used in such patients. The treatment of paroxysmal supraventricular
tachycardia in such patients is usually direct-current cardioversion.<br/>Use in Patients with Preserved
Left Ventricular Systolic Function: Patients with
certain disorders involving heart failure associated with preserved
left ventricular ejection fraction may be particularly susceptible
to toxicity of the drug. Such disorders include restrictive cardiomyopathy,
constrictive pericarditis, amyloid heart disease, and acute cor pulmonale.
Patients with idiopathic hypertrophic subaortic stenosis may have
worsening of the outflow obstruction due to the inotropic effects
of digoxin.
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Heart Failure: LANOXIN is indicated for the treatment of mild to
moderate heart failure. LANOXIN increases left ventricular ejection
fraction and improves heart failure symptoms as evidenced by exercise
capacity and heart failure-related hospitalizations and emergency
care, while having no effect on mortality. Where possible, LANOXIN
should be used with a diuretic and an angiotensin-converting enzyme
inhibitor, but an optimal order for starting these three drugs cannot
be specified.<br/>Atrial Fibrillation: LANOXIN is indicated for the control of ventricular
response rate in patients with chronic atrial fibrillation.
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LANOXIN
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