Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1395
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MAVIK (Tablet)
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Hypertension: The recommended
initial dosage of MAVIK for patients not receiving a diuretic is 1 mg
once daily in non-black patients and 2 mg in black patients. Dosage
should be adjusted according to the blood pressure response. Generally,
dosage adjustments should be made at intervals of at least 1 week.
Most patients have required dosages of 2 to 4 mg once daily. There
is little clinical experience with doses above 8 mg. Patients inadequately treated
with once-daily dosing at 4 mg may be treated with twice-daily dosing.
If blood pressure is not adequately controlled with MAVIK monotherapy,
a diuretic may be added. In patients who are currently being treated with a diuretic, symptomatic
hypotension occasionally can occur following the initial dose of MAVIK.
To reduce the likelihood of hypotension, the diuretic should, if
possible, be discontinued two to three days prior to beginning therapy
with MAVIK. (See WARNINGS.)
Then, if blood pressure is not controlled with MAVIK alone, diuretic
therapy should be resumed. If the diuretic cannot be discontinued,
an initial dose of 0.5 mg MAVIK should be used with careful medical
supervision for several hours until blood pressure has stabilized.
The dosage should subsequently be titrated (as described above) to
the optimal response. (See WARNINGS, PRECAUTIONS, and DRUG INTERACTIONS.) Concomitant administration
of MAVIK with potassium supplements, potassium salt substitutes, or
potassium sparing diuretics can lead to increases of serum potassium.
(See PRECAUTIONS.)<br/>Heart Failure Post Myocardial Infarction or Left-Ventricular
Dysfunction Post Myocardial Infarction: The recommended
starting dose is 1 mg, once daily. Following the initial dose, all
patients should be titrated (as tolerated) toward a target dose of
4 mg, once daily. If a 4 mg dose is not tolerated, patients
can continue therapy with the greatest tolerated dose.<br/>Dosage Adjustment in Renal Impairment or Hepatic Cirrhosis: For patients with
a creatinine clearance<30 mL/min. or with hepatic cirrhosis,
the recommended starting dose, based on clinical and pharmacokinetic
data, is 0.5 mg daily. Patients should subsequently have their dosage
titrated (as described above) to the optimal response.
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Mechanism of Action: Trandolapril is
deesterified to the diacid metabolite, trandolaprilat, which is approximately
eight times more active as an inhibitor of ACE activity. ACE is a
peptidyl dipeptidase that catalyzes the conversion of angiotensin
I to the vasoconstrictor, angiotensin II. Angiotensin II is a potent
peripheral vasoconstrictor that also stimulates secretion of aldosterone
by the adrenal cortex and provides negative feedback for renin secretion.
The effect of trandolapril in hypertension appears to result primarily
from the inhibition of circulating and tissue ACE activity thereby
reducing angiotensin II formation, decreasing vasoconstriction, decreasing
aldosterone secretion, and increasing plasma renin. Decreased aldosterone
secretion leads to diuresis, natriuresis, and a small increase of
serum potassium. Incontrolled clinical trials, treatment with MAVIK
alone resulted in mean increases in potassium of 0.1 mEq/L. (See PRECAUTIONS.) ACE is identical to kininase II, an enzyme that degrades bradykinin,
a potent peptide vasodilator; whether increased levels of bradykinin
play a role in the therapeutic effect of trandolapril remains to be
elucidated. While
the principal mechanism of antihypertensive effect is thought to be
through the renin-angiotensin-aldosterone system, trandolapril exerts
antihypertensive actions even in patients with low-renin hypertension.
MAVIK was an effective antihypertensive in all races studied. Both
black patients (usually a predominantly low-renin group) and non-black
patients responded to 2 to 4 mg of MAVIK.<br/>Pharmacokinetics and Metabolism:<br/>Pharmacokinetics: Trandolapril's
ACE-inhibiting activity is primarily due to its diacid metabolite,
trandolaprilat. Cleavage of the ester group of trandolapril, primarily
in the liver, is responsible for conversion. Absolute bioavailability
after oral administration of trandolapril is about 10% as trandolapril
and 70% as trandolaprilat. After oral trandolapril under fasting
conditions, peak trandolapril levels occur at about one hour and peak
trandolaprilat levels occur between 4 and 10 hours. In healthy subjects,
the mean elimination half-life of trandolapril is less than one hour
(0.68���0.76 hours). At steady state, the mean effective half-life
of trandolaprilat is 22.5 hours (17.1���28.5 hours). Like
all ACE inhibitors, trandolaprilat also has a prolonged terminal elimination
phase, involving a small fraction of administered drug, probably representing
binding to plasma and tissue ACE. During multiple dosing of trandolapril,
there is no significant accumulation of trandolaprilat. Food slows
absorption of trandolapril, but does not affect AUC or Cof trandolaprilat or Cof trandolapril.<br/>Metabolism and Excretion: After oral
administration of trandolapril, about 33% of parent drug and metabolites
are recovered in urine, mostly as trandolaprilat, with about 66% in
feces. The extent of the absorbed dose which is biliary excreted
has not been determined. Plasma concentrations (Cand
AUC of trandolapril and Cof trandolaprilat) are dose
proportional over the 1-4 mg range, but the AUC of trandolaprilat
is somewhat less than dose proportional. In addition to trandolaprilat,
at least 7 other metabolites have been found, principally glucuronides
or deesterification products. Serum protein binding of trandolapril is about 80%, and is independent
of concentration. Binding of trandolaprilat is concentration-dependent,
varying from 65% at 1000 ng/mL to 94% at 0.1 ng/mL, indicating saturation
of binding with increasing concentration. The volume of distribution of trandolapril is about 18 liters. Total
plasma clearances of trandolapril and trandolaprilat after approximately2 mg IV doses are about 52 liters/hour and 7 liters/hour respectively.
Renal clearance of trandolaprilat varies from 1-4 liters/hour,
depending on dose.<br/>Special Populations:<br/>Pediatric: Trandolapril
pharmacokinetics have not been evaluated in patients<18
years of age.<br/>Geriatric and Gender: Trandolapril
pharmacokinetics have been investigated in the elderly (>65
years) and in both genders. The plasma concentration of trandolapril
is increased in elderly hypertensive patients, but the plasma concentration
of trandolaprilat and inhibition of ACE activity are similar in elderly
and young hypertensive patients. The pharmacokinetics of trandolapril
and trandolaprilat and inhibition of ACE activity are similar in male
and female elderly hypertensive patients.<br/>Race: Pharmacokinetic
differences have not been evaluated in different races.<br/>Renal Insufficiency: Compared
to normal subjects, the plasma concentrations of trandolapril and
trandolaprilat are approximately 2-fold greater and renal clearance
is reduced by about 85% in patients with creatinine clearance below
30 ml/min and in patients on hemodialysis. Dosage adjustment is recommended
in renally impairedpatients. (See DOSAGE
AND ADMINISTRATION .)<br/>Hepatic Insufficiency: Following
oral administration in patients with mild to moderate alcoholic cirrhosis,
plasma concentrations of trandolapril and trandolaprilat were, respectively,
9-fold and 2-fold greater than in normal subjects, but inhibition
of ACE activity was not affected. Lower doses should be considered
in patients with hepatic insufficiency. (See DOSAGE AND ADMINISTRATION.)<br/>Drug Interactions: Trandolapril
did not affect the plasma concentration (pre-dose and 2 hours post-dose)
of oral digoxin (0.25 mg). Coadministration of trandolapril and cimetidine
led to an increase of about 44% in Cfor trandolapril,
but no difference in the pharmacokinetics of trandolaprilat or in
ACE inhibition. Coadministration of trandolapril and furosemide led
to an increase of about 25% in the renal clearance of trandolaprilat,
but no effect was seen on the pharmacokinetics of furosemide or trandolaprilat
or on ACE inhibition.<br/>Pharmacodynamics and Clinical Effects: A single 2-mg dose
of MAVIK produces 70 to 85% inhibition of plasma ACE activity at 4
hours with about 10% decline at 24 hours and about half the effect
manifest at 8 days. Maximum ACE inhibition is achieved with a plasma
trandolaprilat concentration of 2 ng/mL. ACE inhibition is a
function of trandolaprilat concentration, not trandolapril concentration.
The effect of trandolapril on exogenous angiotensin I was not measured.<br/>Hypertension: Four placebo-controlled
dose response studies were conducted using once-daily oral dosing
of MAVIK in doses from 0.25 to 16 mg per day in 827 black and non-black
patients with mild to moderate hypertension. The minimal effective
once-daily dose was 1 mg in non-black patients and 2 mg in black patients.
Further decreases in trough supine diastolic blood pressure were
obtained in non-black patients with higher doses, and no further response
was seen with doses above 4 mg (up to 16 mg). The antihypertensive
effect diminished somewhat at the end of the dosing interval, but
trough/peak ratios are well above 50% for all effective doses. There
was a slightly greater effect on the diastolic pressure, but no difference
on systolic pressure with b.i.d. dosing. During chronic therapy,
the maximum reduction in blood pressure with any dose is achieved
within one week. Following 6 weeks of monotherapy in placebo-controlled
trials in patients with mild to moderate hypertension, once-daily
doses of 2 to 4 mg lowered supine or standing systolic/diastolic blood
pressure 24 hours after dosing by an average 7-10/4-5 mmHg below placebo
responses in non-black patients. Once-daily doses of 2 to 4 mg
lowered blood pressure 4-6/3-4 mmHg in black patients. Trough to
peak ratios for effective doses ranged from 0.5 to 0.9. There wereno differences in response between men and women, but responses were
somewhat greater in patients under 60 than in patients over 60 years
old. Abrupt withdrawal of MAVIK has not been associated with a rapid
increase in blood pressure. Administration of MAVIK to patients with mild to moderate hypertension
results in a reduction of supine, sitting and standing blood pressure
to about the same extent without compensatory tachycardia. Symptomatic hypotension
is infrequent, although it can occur in patients who are salt- and/or
volume-depleted. (See WARNINGS.) Use of MAVIK in combination with thiazide diuretics gives a blood
pressure lowering effect greater than that seen with either agent
alone, and the additional effect of trandolapril is similar to the
effect of monotherapy.<br/>Heart Failure Post Myocardial Infarction or Left Ventricular
Dysfunction Post Myocardial Infarction: The Trandolapril
Cardiac Evaluation (TRACE) Trial was a Danish, 27-center, double-blind,
placebo controlled, parallel-group study of the effect of trandolapril
on all-cause mortality in stable patients with echocardiographic evidence
of left ventricular dysfunction 3 to 7 days after a myocardial infarction.
Subjects with residual ischemia or overt heart failure were included.
Patients tolerant of a test dose of1 mg trandolapril were randomized
to placebo (n=873) or trandolapril (n=876) and followed for 24 months.
Among patients randomized to trandolapril, who began treatment on
1 mg, 62% were successfully titrated to a target dose of 4 mg once
daily over a period of weeks. The use of trandolapril was associated
with a 16% reduction in the risk of all-cause mortality (p=0.042),
largely cardiovascular mortality. Trandolapril was also associated
with a 20% reduction in the risk of progression of heart failure (p=0.047),
defined by a time-to-first-event analysis of death attributed to heart
failure, hospitalization for heart failure, or requirement for open-label
ACE inhibitor for the treatment of heart failure. There was no significant
effect of treatment on other end-points: subsequent hospitalization,
incidence of recurrent myocardial infarction, exercise tolerance,
ventricular function, ventricular dimensions, or NYHA class. The population in TRACE
was entirely Caucasian and had less usage than would be typical in
a U.S. population of other post-infarction interventions: 42% thrombolysis,
16% beta-adrenergic blockade, and 6.7% PTCA or CABG during the entire
period of follow-up. Blood pressure control, especially in the placebo
group, was poor: 47 to 53% of patients randomized to placebo and
32 to 40% of patients randomized to trandolapril had blood pressures>140/95 at 90-day follow-up visits.
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MAVIK is contraindicated
in patients who are hypersensitive to this product and in patients
with a history of angioedema related to previous treatment with an
ACE inhibitor.
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MAVIK (trandolapril tablets)
are supplied as follows: 1 mg tablet - Salmon colored, round shaped, scored, compressed tablets,
with Abbott���A���logo on one side and Abbo-Code identification letters FT on the other
side. NDC 0074-2278-13 - bottles of 100 NDC 0074-2278-11 - unit
dose packs of 100 2 mg
tablet - Yellow colored, round shaped, compressed tablets, with Abbott���A���logo on one side
and Abbo-Code identification letters FX on the other side. NDC 0074-2279-13
- bottles of 100 NDC 0074-2279-11 - unit dose packs of 100 4 mg tablet - Rose colored, round
shaped, compressed tablets, with Abbott���A���logo on one side and Abbo-Code identification
letters FZ on the other side. NDC 0074-2280-13 - bottles of 100
NDC 0074-2280-11 - unit dose packs of 100 Dispense in well-closed container with safety closure.<br/>Storage: Store at controlled
room temperature: 20-25��C (68-77��F) see USP.
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No data are available with
respect to overdosage in humans. The oral LDof trandolaprilin mice was 4875 mg/Kg in males and 3990 mg/Kg in females. In rats,
an oral dose of 5000 mg/Kg caused low mortality (1 male out of 5;
0 females). In dogs, an oral dose of 1000 mg/Kg did not cause mortality
and abnormal clinical signs were not observed. In humans the most
likely clinical manifestation would be symptoms attributable to severe
hypotension. Laboratory
determinations of serum levels of trandolapril and its metabolites
are not widely available, and such determinations have, in any event,
no established role in the management of trandolapril overdose. No
data are available to suggest that physiological maneuvers (e.g.,
maneuvers to change the pH of the urine) might accelerate elimination
of trandolapril and its metabolites. Trandolaprilat is removed by
hemodialysis. Angiotensin II could presumably serve as a specific
antagonist antidote in the setting of trandolapril overdose, but angiotensin
II is essentially unavailable outside of scattered research facilities.
Because the hypotensive effect of trandolapril is achieved through
vasodilation and effective hypovolemia, it is reasonable to treat
trandolapril overdose by infusion of normal saline solution.
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Trandolapril
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MAVIK (Tablet)
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The safety experience in
U.S. placebo-controlled trials included 1069 hypertensive patients,
of whom 832 received MAVIK. Nearly 200 hypertensive patients received
MAVIK for over one year in open-label trials. In controlled trials,
withdrawals for adverse events were 2.1% on placebo and 1.4% on MAVIK.
Adverse events considered at least possibly related to treatment
occurring in 1% of MAVIK-treated patients and more common on MAVIK
than placebo, pooled for all doses, are shown below, together with
the frequency of discontinuation of treatment because of these events. Headache and fatigue were
all seen in more than 1% of MAVIK-treated patients but were more frequently
seen on placebo. Adverse events were not usually persistent or difficult
to manage.<br/>Left Ventricular Dysfunction Post Myocardial Infarction: Adverse reactions
related to MAVIK occurring at a rate greater than that observed in
placebo-treated patients with left ventricular dysfunction, are shown
below. The incidences represent the experiences from the TRACE study.
The follow-up time was between 24 and 50 months for this study. Clinical adverse
experiences possibly or probably related or of uncertain relationship
to therapy occurring in 0.3% to 1.0% (except as noted) of the patients
treated with MAVIK (with or without concomitant calcium ion antagonist
or diuretic) in controlled or uncontrolled trials (N=1134) and less
frequent, clinically significant events seen in clinical trials or
post-marketing experience include (listed by body system):<br/>General Body Function: Chest pain,
malaise, fever.<br/>Cardiovascular: AV first
degree block, bradycardia, edema, flushing, hypotension, palpitations.<br/>Central Nervous System: Drowsiness,
insomnia, paresthesia, vertigo.<br/>Dermatologic: Pruritus,
rash, pemphigus, alopecia, sweating.<br/>Eye, Ear, Nose, Throat: Epistaxis,
throat inflammation, upper respiratory tract infection.<br/>Emotional, Mental, Sexual States: Anxiety,
impotence, decreased libido.<br/>Gastrointestinal: Abdominal
distention, abdominal pain/cramps, constipation, dyspepsia, diarrhea,
vomiting, nausea, dry mouth, pancreatitis.<br/>Hemopoietic: Agranulocytosis,
decreased leukocytes, decreased neutrophils.<br/>Metabolism and Endocrine: Increased
creatinine, increased potassium, increased liver enzymes including
SGPT (ALT) and increased SGOT (AST).<br/>Musculoskeletal System: Extremity
pain, muscle cramps, gout.<br/>Pulmonary: Dyspnea,
bronchitis.<br/>Angioedema: Angioedema
has been reported in 4 (0.13%) patients receiving MAVIK in U.S. and
foreign studies. Angioedema associated with laryngeal edema may be
fatal. If angioedema of the face, extremities, lips, tongue, glottis,
and/or larynx occurs, treatment with MAVIK should be discontinued
and appropriate therapy instituted immediately. (See WARNINGS .)<br/>Hypotension: In hypertensive
patients, symptomatic hypotension occurred in 0.6% and near syncope
occurred in 0.2%. Hypotension or syncope was a cause for discontinuation
of therapy in 0.1% of hypertensive patients.<br/>Fetal/Neonatal Morbidity and Mortality: (See WARNINGS - Fetal Neonatal Morbidity and Mortality.)<br/>Cough: (See PRECAUTIONS - Cough.)<br/>Clinical Laboratory Test Findings:<br/>Other: Another
potentially important adverse experience, eosinophilic pneumonitis,
has been attributed to other ACE inhibitors.
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Anaphylactoid and Possibly Related Reactions: Presumably because
angiotensin converting enzyme inhibitors affect the metabolism of
eicosanoids and polypeptides, including endogenous bradykinin, patients
receiving ACE inhibitors, including MAVIK, may be subject to a variety
of adverse reactions, some of them serious.<br/>Anaphylactoid Reactions During Desensitization: Two patients
undergoing desensitizing treatment with hymenoptera venom while receiving
ACE inhibitors sustained life-threatening anaphylactoid reactions.
In the same patients, these reactions did not occur when ACE inhibitors
were temporarily withheld, but they reappeared when the ACE inhibitors
were inadvertently readministered.<br/>Anaphylactoid Reactions During Membrane Exposure: Anaphylactoid
reactions have been reported in patients dialyzed with high-flux membranes
and treated concomitantly with an ACE inhibitor. Anaphylactoid reactions
have also been reported in patients undergoing low-density lipoprotein
apheresis with dextran sulfate absorption.<br/>Head and Neck Angioedema: Angioedema
of the face, extremities, lips, tongue, glottis, and larynx has been
reported in patients treated with ACE inhibitors including MAVIK.
Symptoms suggestive of angioedema or facial edema occurred in 0.13%
of MAVIK-treated patients. Two of the four cases were life-threatening
and resolved without treatment or with medication (corticosteroids).
Angioedema associated with laryngeal edema can be fatal. If laryngeal
stridor or angioedema of the face, tongue or glottis occurs, treatment
with MAVIK should be discontinued immediately, thepatient treated
in accordance with accepted medical care and carefully observed until
the swelling disappears. In instances where swelling is confined
to the face and lips, the condition generally resolves without treatment;
antihistamines may be useful in relieving symptoms. Where there is involvement of the tongue, glottis,
or larynx, likely to cause airway obstruction, emergency therapy,
including but not limited to subcutaneous epinephrine solution 1:1,000
(0.3 to 0.5 mL) should be promptly administered. (See PRECAUTIONS - Information for Patients and ADVERSE REACTIONS.)<br/>Intestinal Angioedema: Intestinal
angioedema has been reported in patients treated with ACE inhibitors.
These patients presented with abdominal pain (with or without nausea
or vomiting); in some cases there was no prior history of facial angioedema
and C-1 esterase levels were normal. The angioedema was diagnosed
by procedures including abdominal CT scan or ultrasound, or at surgery,
and symptoms resolved after stopping the ACE inhibitor. Intestinal
angioedema should be included in the differential diagnosis of patients
on ACE inhibitors presenting with abdominal pain.<br/>Hypotension: MAVIK can
cause symptomatic hypotension. Like other ACE inhibitors, MAVIK has
only rarely been associated with symptomatic hypotension in uncomplicated
hypertensive patients. Symptomatic hypotension is most likely to
occur in patients who have been salt- or volume-depleted as a result
of prolonged treatment with diuretics, dietary salt restriction, dialysis,
diarrhea, or vomiting. Volume and/or salt depletion should be corrected
before initiating treatment with MAVIK. (See PRECAUTIONS - Drug Interactions, and ADVERSE REACTIONS .) In controlled and uncontrolled studies,
hypotension was reported as an adverse event in 0.6% of patients and
led to discontinuations in 0.1% of patients. In patients with concomitant congestive heart failure, with or without
associated renal insufficiency, ACE inhibitor therapy may cause excessive
hypotension, which may be associated with oliguria or azotemia, and
rarely, with acute renal failure and death. In such patients, MAVIK
therapy should be started at the recommended dose under close medical
supervision. These patients should be followed closely during the
first 2 weeks of treatment and, thereafter, whenever the dosage of
MAVIK or diuretic is increased. (See DOSAGE
AND ADMINISTRATION.) Care in avoiding hypotension should
also be taken in patients with ischemic heart disease, aortic stenosis,
or cerebrovascular disease. If symptomatic hypotension occurs, the patient should be placed in
the supine position and, if necessary, normal saline may be administered
intravenously. A transient hypotensive response is not a contraindication
to further doses; however, lower doses of MAVIK or reduced concomitant
diuretic therapy should be considered.<br/>Neutropenia/Agranulocytosis: Another
ACE inhibitor, captopril, has been shown to cause agranulocytosis
and bone marrow depression rarely in patients with uncomplicated hypertension,
but more frequently in patients with renal impairment, especially
if they also have a collagen-vascular disease such as systemic lupus
erythematosus or scleroderma. Available data from clinical trials
of trandolapril are insufficient to show that trandolapril does not
cause agranulocytosis at similar rates. As with other ACE inhibitors,
periodic monitoring of white blood cell counts in patients with collagen-vascular
disease and/or renal disease should be considered.<br/>Hepatic Failure: ACE inhibitors
rarely have been associated with a syndrome of cholestatic jaundice,
fulminant hepatic necrosis, and death. The mechanism of this syndrome
is not understood. Patients receiving ACE inhibitors who develop
jaundice should discontinue the ACE inhibitor and receive appropriate
medical follow-up.<br/>Fetal/Neonatal Morbidity and Mortality: ACE inhibitors
can cause fetal and neonatal morbidity and death when administered
to pregnant women. Several dozen cases have been reported in the
world literature. When pregnancy is detected, ACE inhibitors should
be discontinued as soon as possible. The use of ACE inhibitors during the second and third trimesters
of pregnancy has been associated with fetal and neonatal injury, including
hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible
renal failure, and death. Oligohydramnios has also been reported,
presumably resulting from decreased fetal renal function; oligohydramnios
in this setting has been associated with fetal limb contractures,
craniofacial deformation, and hypoplastic lung development. Prematurity,
intrauterine growth retardation, and patent ductus arteriosus have
also been reported, although it is not clear whether these occurrences
were due to the ACE inhibitor exposure. These adverse effects do not appear to have resulted from intrauterine
ACE-inhibitor exposure that has been limited to the first trimester.
Mothers whose embryos and fetuses are exposed to ACE inhibitors only
during the first trimester should be so informed. Nonetheless, when
patients become pregnant, physicians should make every effort to discontinue
the use of trandolapril as soon as possible. Rarely (probably less often than once in every thousand pregnancies),
no alternative to ACE inhibitors will be found. In these rare cases,
the mothers should be apprised of the potential hazards to their fetuses,
and serial ultrasound examinations should be performed to assess the
intra-amniotic environment. If oligohydramnios is observed, trandolapril should be discontinued
unless it is considered life-saving for the mother. Contraction stress
testing (CST), a non-stress test (NST), or biophysical profiling (BPP)
may be appropriate, depending upon the week of pregnancy. Patients and
physicians should be aware, however, that oligohydramnios may not
appear until after the fetus has sustained irreversible injury. Infants with histories
of in utero exposure
to ACE inhibitors should be closely observed for hypotension, oliguria,
and hyperkalemia. If oliguria occurs, attention should be directed
toward support of blood pressure and renal perfusion. Exchange transfusions
or dialysis may be required as a means of reversing hypotension and/or
substituting for disordered renal function. Doses of 0.8 mg/kg/day (9.4 mg/m/day) in rabbits, 1000
mg/kg/day (7000 mg/m/day) in rats, and 25 mg/kg/day (295
mg/m/day) in cynomolgus monkeys did not produce teratogenic
effects. These doses represent 10 and 3 times (rabbits), 1250 and
2564 times (rats), and 312 and 108 times (monkeys) the maximum projected
human dose of 4 mg based on body-weight and body-surface-area,
respectively assuming a 50 kg woman.
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Hypertension: MAVIK is indicated
for the treatment of hypertension. It may be used alone or in combination
with other antihypertensive medication such as hydrochlorothiazide. In considering the use
of MAVIK, it should be noted that in controlled trials ACE inhibitors
(for which adequate data are available) cause a higher rate of angioedema
in black than in non-black patients. (See WARNINGS���Angioedema.) When using MAVIK, consideration should be given to the fact that
another angiotensin converting enzyme inhibitor, captopril, has caused
agranulocytosis, particularly in patients with renal impairment or
collagen-vascular disease. Available data are insufficient to show
that MAVIK does not have a similar risk. (See WARNINGS .)<br/>Heart Failure Post Myocardial Infarction or Left-Ventricular
Dysfunction Post Myocardial Infarction: MAVIK is indicated
in stable patients who have evidence of left-ventricular systolic
dysfunction (identified by wall motion abnormalities) or who are symptomatic
from congestive heart failure within the first few days after sustaining
acute myocardial infarction. Administration of trandolapril to Caucasian
patients has been shown to decrease the risk of death (principally
cardiovascular death) and to decrease the risk of heart failure-related
hospitalization (see CLINICAL PHARMACOLOGY
- Heart Failure or Left-Ventricular Dysfunction Post Myocardial Infarction for details of the survival trial).
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MAVIK
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