The Five Biggest Contradictions in Fitness
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The Five Biggest Contradictions in Fitness

It’s no secret that when people contradict themselves, it has the effect of making the flaws in their actions or statements seem glaringly obvious. But what about when WE ourselves get caught contradicting ourselves by someone else?

By: Nick Tumminello Added: January 6th, 2014
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Thread: Altace?

  1. #1
    "COUNT CRACKULA" Bam Bam's Avatar
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    Altace?

    i visited the site but cant access teh warnings

    can anyone tell me if this eats muscle tissue cause i am on this stuff
    Blocka Blocka

    I am AMINAL

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  3. #2
    Wannabebig Member
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    I don't know why it would.

  4. #3
    "COUNT CRACKULA" Bam Bam's Avatar
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    cause some bp meds do
    Blocka Blocka

    I am AMINAL

  5. #4
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    Bam- I would be interested to know what you have heard/read about how BP meds cause catabolism to muscle tissue.

  6. #5
    Banned ogarchamplin's Avatar
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    WARNINGS.) Use of ALTACE in combination with thiazide diuretics gives a blood pressure lowering effect
    greater than that seen with either agent alone.
    In single-dose studies, doses of 5–20 mg of ALTACE lowered blood pressure within 1–2 hours, with peak
    reductions achieved 3–6 hours after dosing. The antihypertensive effect of a single dose persisted for 24
    hours. In longer term (4–12 weeks) controlled studies, once-daily doses of 2.5–10 mg were similar in their
    effect, lowering supine or standing systolic and diastolic blood pressures 24 hours after dosing by about 6/4
    mm Hg more than placebo. In comparisons of peak vs. trough effect, the trough effect represented about
    50–60% of the peak response. In a titration study comparing divided (bid) vs. qd treatment, the divided regimen
    was superior, indicating that for some patients the antihypertensive effect with once-daily dosing is not
    adequately maintained. (See DOSAGE AND ADMINISTRATION.)
    In most trials, the antihypertensive effect of ALTACE increased during the first several weeks of repeated
    measurements. The antihypertensive effect of ALTACE has been shown to continue during long-term therapy
    for at least 2 years. Abrupt withdrawal of ALTACE has not resulted in a rapid increase in blood pressure.
    ALTACE has been compared with other ACE inhibitors, beta-blockers, and thiazide diuretics. It was approximately
    as effective as other ACE inhibitors and as atenolol. In both caucasians and blacks, hydrochlorothiazide
    (25 or 50 mg) was significantly more effective than ramipril.
    Except for thiazides, no formal interaction studies of ramipril with other antihypertensive agents have been
    carried out. Limited experience in controlled and uncontrolled trials combining ramipril with a calcium channel
    blocker, a loop diuretic, or triple therapy (beta-blocker, vasodilator, and a diuretic) indicate no unusual drugdrug
    interactions. Other ACE inhibitors have had less than additive effects with beta adrenergic blockers, presumably
    because both drugs lower blood pressure by inhibiting parts of the renin-angiotensin system.
    ALTACE was less effective in blacks than in caucasians. The effectiveness of ALTACE was not influenced
    by age, sex, or weight.
    In a baseline controlled study of 10 patients with mild essential hypertension, blood pressure reduction
    was accompanied by a 15% increase in renal blood flow. In healthy volunteers, glomerular filtration rate
    was unchanged.
    Heart Failure Post Myocardial Infarction
    ALTACE was studied in the Acute Infarction Ramipril Efficacy (AIRE) trial. This was a multinational (mainly
    European) 161-center, 2006-patient, double-blind, randomized, parallel-group study comparing ALTACE to
    placebo in stable patients, 2–9 days after an acute myocardial infarction (MI), who had shown clinical signs
    of congestive heart failure (CHF) at any time after the MI. Patients in severe (NYHA class IV) heart failure,
    patients with unstable angina, patients with heart failure of congenital or valvular etiology, and patients with
    contraindications to ACE inhibitors were all excluded. The majority of patients had received thrombolytic therapy
    at the time of the index infarction, and the average time between infarction and initiation of treatment
    was 5 days.
    Patients randomized to ramipril treatment were given an initial dose of 2.5 mg twice daily. If the initial regimen
    caused undue hypotension, the dose was reduced to 1.25 mg, but in either event doses were titrated
    upward (as tolerated) to a target regimen (achieved in 77% of patients randomized to ramipril) of 5 mg twice
    daily. Patients were then followed for an average of 15 months (range 6–46).
    The use of ALTACE was associated with a 27% reduction (p=0.002), in the risk of death from any cause;
    about 90% of the deaths that occurred were cardiovascular, mainly sudden death. The risks of progression to
    severe heart failure and of CHF-related hospitalization were also reduced, by 23% (p=0.017) and 26%
    (p=0.011), respectively. The benefits of ALTACE therapy were seen in both genders, and they were not
    affected by the exact timing of the initiation of therapy, but older patients may have had a greater benefit than
    those under 65. The benefits were seen in patients on, and not on, various concomitant medications; at the
    time of randomization these included aspirin (about 80% of patients), diuretics (about 60%), organic nitrates
    (about 55%), beta-blockers (about 20%), calcium channel blockers (about 15%), and digoxin (about 12%).
    INDICATIONS AND USAGE
    Reduction in Risk of Myocardial Infarction, Stroke, and Death from Cardiovascular Causes
    Altace is indicated in patients 55 years or older at high risk of developing a major cardiovascular event
    because of a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes that is accompanied
    by at least one other cardiovascular risk factor (hypertension, elevated total cholesterol levels, low
    HDL levels, cigarette smoking, or documented microalbuminuria), to reduce the risk of myocardial infarction,
    stroke, or death from cardiovascular causes. Altace can be used in addition to other needed treatment (such
    as antihypertensive, antiplatelet or lipid-lowering therapy).
    Hypertension
    ALTACE is indicated for the treatment of hypertension. It may be used alone or in combination with thiazide
    diuretics.
    In using ALTACE, 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 ALTACE does not have a similar
    risk. (See WARNINGS.)
    In considering use of ALTACE, it should be noted that in controlled trials ACE inhibitors have an effect on
    blood pressure that is less in black patients than in non-blacks. In addition, ACE inhibitors (for which adequate
    data are available) cause a higher rate of angioedema in black than in non-black patients. (See WARNINGS,
    Angioedema.)
    Heart Failure Post Myocardial Infarction
    Ramipril is indicated in stable patients who have demonstrated clinical signs of congestive heart failure
    within the first few days after sustaining acute myocardial infarction. Administration of ramipril to such
    patients has been shown to decrease the risk of death (principally cardiovascular death) and to decrease the
    risks of failure-related hospitalization and progression to severe/resistant heart failure. (See CLINICAL PHARMACOLOGY,
    Heart Failure Post Myocardial Infarction for details and limitations of the survival trial.)
    CONTRAINDICATIONS
    ALTACE is contraindicated in patients who are hypersensitive to this product or any other angiotensin
    converting enzyme inhibitor (e.g., a patient who has experienced angioedema during therapy with any
    other ACE inhibitor).
    WARNINGS
    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 ALTACE) may be
    subject to a variety of adverse reactions, some of them serious.
    Head and Neck Angioedema
    Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of
    angioedema while receiving an ACE inhibitor. (See also CONTRAINDICATIONS.)
    Angioedema of the face, extremities, lips, tongue, glottis, and larynx has been reported in patients treated
    with angiotensin converting enzyme inhibitors. Angioedema associated with laryngeal edema can be
    fatal. If laryngeal stridor or angioedema of the face, tongue, or glottis occurs, treatment with ALTACE
    should be discontinued and appropriate therapy instituted immediately. Where there is involvement of
    the tongue, glottis, or larynx, likely to cause airway obstruction, appropriate therapy, e.g., subcutaneous
    epinephrine solution 1:1,000 (0.3 ml to 0.5 ml) should be promptly administered. (See
    ADVERSE REACTIONS.)
    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.
    In a large U.S. postmarketing study, angioedema (defined as reports of angio, face, larynx, tongue, or
    throat edema) was reported in 3/1523 (0.20%) of black patients and in 8/8680 (0.09%) of white patients.
    These rates were not different statistically.
    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 were avoided when ACE inhibitors were temporarily withheld, but they reappeared
    upon inadvertent rechallenge.
    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.
    Hypotension
    ALTACE can cause symptomatic hypotension, after either the initial dose or a later dose when the dosage
    has been increased. Like other ACE inhibitors, ramipril has been only rarely associated with hypotension in
    uncomplicated hypertensive patients. Symptomatic hypotension is most likely to occur in patients who have
    been volume- and/or salt-depleted as a result of prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea,
    or vomiting. Volume and/or salt depletion should be corrected before initiating therapy with ALTACE.
    were 55 years or older and considered at high risk of developing a major cardiovascular event because of a history
    of coronary artery disease, stroke, peripheral vascular disease, or diabetes that was accompanied by at
    least one other cardiovascular risk factor (hypertension, elevated total cholesterol levels, low HDL levels, cigarette
    smoking, or documented microalbuminuria). Patients were either normotensive or under treatment with
    other antihypertensive agents. Patients were excluded if they had clinical heart failure or were known to have
    a low ejection fraction (<0.40). This study was designed to examine the long-term (mean of five years) effects
    of ALTACE (10 mg orally once a day) on the combined endpoint of myocardial infarction, stroke or death from
    cardiovascular causes.
    The HOPE study results showed that ALTACE (10 mg/day) significantly reduced the rate of myocardial infarction,
    stroke or death from cardiovascular causes (651/4645 vs. 826/4652, relative risk 0.78), as well as the rates
    of the 3 components of the combined endpoint.
    Altace Placebo Relative Risk
    Outcome (N=4645) (N=4652) (95% CI)
    no. (%) P value
    Combined End-point
    (MI, stroke, or 651 (14.0%) 826 (17.8%) 0.78 (0.70–0.86), P=0.0001
    death from CV cause)
    Component End-point
    Death from 282 (6.1%) 377 (8.1%) 0.74 (0.64–0.87), P=0.0002
    Cardiovascular Causes
    Myocardial infarction 459 (9.9%) 570 (12.3%) 0.80 (0.70–0.90), P=0.0003
    Stroke 156 (3.4%) 226 (4.9%) 0.68 (0.56–0.84), P=0.0002
    Overall Mortality
    (Death from any Cause) 482 (10.4%) 569 (12.2%) 0.84 (0.75–0.95), P=0.005
    This effect was evident after about one year of treatment.
    Figure 1: Kaplan-Meier Estimates of the composite outcome of MI, Stroke, or Death from CV causes in the
    Ramipril Group and the Placebo Group. The relative risk of the composite outcomes in the Ramipril Group as
    compared with the Placebo Group was 0.78% (95% confidence interval, 0.70–0.86).
    Ramipril was effective in different demographic subgroups, (i.e., gender, age), subgroups defined by underlying
    disease (e.g., cardiovascular disease, hypertension), and subgroups defined by concomitant medication.
    There were insufficient data to determine whether or not ramipril was equally effective in ethnic subgroups.
    This study was designed with a prespecified substudy in diabetics with at least one other cardiovascular risk
    factor. Effects of ramipril on the combined endpoint and its components were similar in diabetics (n=3,577) to
    those in the overall study population.
    Altace Placebo Relative
    Outcome (N=1808) (N=1769) Risk Reduction
    no. (%) (95% CI)
    Combined End-point
    (MI, stroke, or 277 (15.3%) 351 (19.8%) 0.25 (0.12–0.36), P=0.0004
    death from CV cause)
    Component End-point
    Death from 112 (6.2%) 172 (9.7%) 0.37 (0.21–0.51), P=0.0001
    Cardiovascular Causes
    Myocardial infarction 185 (10.2%) 229 (12.9%) 0.22 (0.06–0.36), P=0.01
    Stroke 76 (4.2%) 108 (6.1%) 0.33 (0.10–0.50), P=0.007
    Figure 2. The Beneficial Effect of Treatment with Ramipril on the Composite Outcome of Myocardial
    Infarction, Stroke, or Death from Cardiovascular Causes Overall and in Various Subgroups. Cerebrovascular disease
    was defined as stroke or transient ischemic attacks. The size of each symbol is proportional to the number
    of patients in each group. The dashed line indicates overall relative risk.
    The benefits of Altace were observed among patients who were taking aspirin or other anti-platelet agents,
    beta-blockers, and lipid-lowering agents as well as diuretics and calcium channel blockers.
    Hypertension
    Administration of ALTACE to patients with mild to moderate hypertension results in a reduction of both
    supine and standing blood pressure to about the same extent with no compensatory tachycardia. Symptomatic
    postural hypotension is infrequent, although it can occur in patients who are salt- and/or volume-depleted. (See
    Prescribing Information as of February 2003.
    ALTACE® Capsules
    (ramipril)
    USE IN PREGNANCY
    When used in pregnancy during the second and third trimesters, ACE inhibitors can cause injury
    and even death to the developing fetus. When pregnancy is detected, ALTACE® should be discontinued
    as soon as possible. See WARNINGS: Fetal/neonatal morbidity and mortality.
    DESCRIPTION
    Ramipril is a 2-aza-bicyclo [3.3.0]-octane-3-carboxylic acid derivative. It is a white, crystalline substance soluble
    in polar organic solvents and buffered aqueous solutions. Ramipril melts between 105°C and 112°C.
    The CAS Registry Number is 87333-19-5. Ramipril’s chemical name is (2S,3aS,6aS)-1[(S)-N-[(S)-1-Carboxy-3-
    phenylpropyl] alanyl] octahydrocyclopenta [b]pyrrole-2-carboxylic acid, 1-ethyl ester; its structural formula is:
    Its empiric formula is C23H32N2O5, and its molecular weight is 416.5.
    Ramiprilat, the diacid metabolite of ramipril, is a non-sulfhydryl angiotensin converting enzyme inhibitor.
    Ramipril is converted to ramiprilat by hepatic cleavage of the ester group.
    ALTACE (ramipril) is supplied as hard shell capsules for oral administration containing 1.25 mg, 2.5 mg, 5 mg,
    and 10 mg of ramipril. The inactive ingredients present are pregelatinized starch NF, gelatin, and titanium dioxide.
    The 1.25 mg capsule shell contains yellow iron oxide, the 2.5 mg capsule shell contains D&C yellow #10
    and FD&C red #40, the 5 mg capsule shell contains FD&C blue #1 and FD&C red #40, and the 10 mg capsule
    shell contains FD&C blue #1.
    CLINICAL PHARMACOLOGY
    Mechanism of Action
    Ramipril and ramiprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and animals. ACE is
    a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance,
    angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE
    results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased
    aldosterone secretion. The latter decrease may result in a small increase of serum potassium. In hypertensive
    patients with normal renal function treated with ALTACE alone for up to 56 weeks, approximately 4% of
    patients during the trial had an abnormally high serum potassium and an increase from baseline greater than
    0.75 mEq/L, and none of the patients had an abnormally low potassium and a decrease from baseline greater
    than 0.75 mEq/L. In the same study, approximately 2% of patients treated with ALTACE and hydrochlorothiazide
    for up to 56 weeks had abnormally high potassium values and an increase from baseline of 0.75 mEq/L
    or greater, and approximately 2% had abnormally low values and decreases from baseline of 0.75 mEq/L or
    greater. (See PRECAUTIONS.) Removal of angiotensin II negative feedback on renin secretion leads to
    increased plasma renin activity.
    The effect of ramipril on hypertension appears to result at least in part from inhibition of both tissue and circulating
    ACE activity, thereby reducing angiotensin II formation in tissue and plasma.
    ACE is identical to kininase, an enzyme that degrades bradykinin. Whether increased levels of bradykinin, a
    potent vasodepressor peptide, play a role in the therapeutic effects of ALTACE remains to be elucidated.
    While the mechanism through which ALTACE lowers blood pressure is believed to be primarily suppression of
    the renin-angiotensin-aldosterone system, ALTACE has an antihypertensive effect even in patients with low-renin
    hypertension. Although ALTACE was antihypertensive in all races studied, black hypertensive patients (usually a
    low-renin hypertensive population) had a smaller average response to monotherapy than non-black patients.
    Pharmacokinetics and Metabolism
    Following oral administration of ALTACE, peak plasma concentrations of ramipril are reached within one
    hour. The extent of absorption is at least 50–60% and is not significantly influenced by the presence of food in
    the GI tract, although the rate of absorption is reduced.
    In a trial in which subjects received ALTACE capsules or the contents of identical capsules dissolved in
    water, dissolved in apple juice, or suspended in apple sauce, serum ramiprilat levels were essentially unrelated
    to the use or nonuse of the concomitant liquid or food.
    Cleavage of the ester group (primarily in the liver) converts ramipril to its active diacid metabolite, ramiprilat.
    Peak plasma concentrations of ramiprilat are reached 2–4 hours after drug intake. The serum protein binding of
    ramipril is about 73% and that of ramiprilat about 56%; in vitro, these percentages are independent of concentration
    over the range of 0.01 to 10µg/ml.
    Ramipril is almost completely metabolized to ramiprilat, which has about 6 times the ACE inhibitory activity
    of ramipril, and to the diketopiperazine ester, the diketopiperazine acid, and the glucuronides of ramipril and
    ramiprilat, all of which are inactive. After oral administration of ramipril, about 60% of the parent drug and its
    metabolites is eliminated in the urine, and about 40% is found in the feces. Drug recovered in the feces may
    represent both biliary excretion of metabolites and/or unabsorbed drug, however the proportion of a dose eliminated
    by the bile has not been determined. Less than 2% of the administered dose is recovered in urine as
    unchanged ramipril.
    Blood concentrations of ramipril and ramiprilat increase with increased dose, but are not strictly dose-proportional.
    The 24-hour AUC for ramiprilat, however, is dose-proportional over the 2.5–20 mg dose range. The
    absolute bioavailabilities of ramipril and ramiprilat were 28% and 44%, respectively, when 5 mg of oral ramipril
    was compared with the same dose of ramipril given intravenously.
    Plasma concentrations of ramiprilat decline in a triphasic manner (initial rapid decline, apparent elimination
    phase, terminal elimination phase). The initial rapid decline, which represents distribution of the drug into a
    large peripheral compartment and subsequent binding to both plasma and tissue ACE, has a half-life of 2–4
    hours. Because of its potent binding to ACE and slow dissociation from the enzyme, ramiprilat shows two elimination
    phases. The apparent elimination phase corresponds to the clearance of free ramiprilat and has a halflife
    of 9–18 hours. The terminal elimination phase has a prolonged half-life (>50 hours) and probably represents
    the binding/dissociation kinetics of the ramiprilat/ACE complex. It does not contribute to the accumulation of
    the drug. After multiple daily doses of ramipril 5–10 mg, the half-life of ramiprilat concentrations within the therapeutic
    range was 13–17 hours.
    After once-daily dosing, steady-state plasma concentrations of ramiprilat are reached by the fourth dose.
    Steady-state concentrations of ramiprilat are somewhat higher than those seen after the first dose of ALTACE,
    especially at low doses (2.5 mg), but the difference is clinically insignificant.
    In patients with creatinine clearance less than 40 ml/min/1.73m2, peak levels of ramiprilat are approximately
    doubled, and trough levels may be as much as quintupled. In multiple-dose regimens, the total exposure to
    ramiprilat (AUC) in these patients is 3–4 times as large as it is in patients with normal renal function who receive
    similar doses.
    The urinary excretion of ramipril, ramiprilat, and their metabolites is reduced in patients with impaired
    renal function. Compared to normal subjects, patients with creatinine clearance less than 40 ml/min/1.73m2
    had higher peak and trough ramiprilat levels and slightly longer times to peak concentrations. (See DOSAGE
    AND ADMINISTRATION.)
    In patients with impaired liver function, the metabolism of ramipril to ramiprilat appears to be slowed, possibly
    because of diminished activity of hepatic esterases, and plasma ramipril levels in these patients are
    increased about 3-fold. Peak concentrations of ramiprilat in these patients, however, are not different from
    those seen in subjects with normal hepatic function, and the effect of a given dose on plasma ACE activity does
    not vary with hepatic function.
    Pharmacodynamics
    Single doses of ramipril of 2.5–20 mg produce approximately 60–80% inhibition of ACE activity 4 hours after
    dosing with approximately 40–60% inhibition after 24 hours. Multiple oral doses of ramipril of 2.0 mg or more
    cause plasma ACE activity to fall by more than 90% 4 hours after dosing, with over 80% inhibition of ACE activity
    remaining 24 hours after dosing. The more prolonged effect of even small multiple doses presumably
    reflects saturation of ACE binding sites by ramiprilat and relatively slow release from those sites.
    Pharmacodynamics and Clinical Effects
    Reduction in Risk of Myocardial Infarction, Stroke, and Death from Cardiovascular Causes
    The Heart Outcomes Prevention Evaluation study (HOPE study) was a large, multi-center, randomized, placebo
    controlled, 2x2 factorial design, double-blind study conducted in 9,541 patients (4,645 on ALTACE) who
    ALTACE® Capsules
    (ramipril)
    CI 6173-3
    CH2
    CH2
    C
    NH
    C
    C
    O
    N
    H
    H
    H
    COOH
    H H H3C C H5C2O
    O
    P=0.0001
    0.20
    0.15
    0.10
    0.05
    0.00
    0 500 1000 1500
    Placebo
    Ramipril
    Proportion of Patients
    Days of Follow-up
    ALTACE® Capsules
    (ramipril)
    CI 6173-3
    In patients with 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, ALTACE therapy should be started under close medical supervision;
    they should be followed closely for the first 2 weeks of treatment and whenever the dose of ramipril or diuretic
    is increased.
    If hypotension occurs, the patient should be placed in a supine position and, if necessary, treated with intravenous
    infusion of physiological saline. ALTACE treatment usually can be continued following restoration of
    blood pressure and volume.
    Hepatic Failure
    Rarely, ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice and progresses
    to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome is not understood.
    Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should
    discontinue the ACE inhibitor and receive appropriate medical follow-up.
    Neutropenia/Agranulocytosis
    As with other ACE inhibitors, rarely, a mild – in isolated cases severe – reduction in the red blood cell count
    and hemoglobin content, white blood cell or platelet count may develop. In isolated cases, agranulocytosis,
    pancytopenia, and bone marrow depression may occur. Hematological reactions to ACE inhibitors are more
    likely to occur in patients with collagen vascular disease (e.g. systemic lupus erythematosus, scleroderma) and
    renal impairment. Monitoring of white blood cell counts should be considered in patients with collagen-vascular
    disease, especially if the disease is associated with impaired renal function.
    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 ALTACE 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 intraamniotic environment.
    If oligohydramnios is observed, ALTACE 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 transfusion or dialysis may be required as means of reversing hypotension and/or
    substituting for disordered renal function. ALTACE which crosses the placenta can be removed from the
    neonatal circulation by these means, but limited experience has not shown that such removal is central to the
    treatment of these infants.
    No teratogenic effects of ALTACE were seen in studies of pregnant rats, rabbits, and cynomolgus monkeys.
    On a body surface area basis, the doses used were up to approximately 400 times (in rats and monkeys) and
    2 times (in rabbits) the recommended human dose.
    PRECAUTIONS
    Impaired Renal Function: As a consequence of inhibiting the renin-angiotensin-aldosterone system,
    changes in renal function may be anticipated in susceptible individuals. In patients with severe congestive heart
    failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment
    with angiotensin converting enzyme inhibitors, including ALTACE, may be associated with oliguria and/or progressive
    azotemia and (rarely) with acute renal failure and/or death.
    In hypertensive patients with unilateral or bilateral renal artery stenosis, increases in blood urea nitrogen and
    serum creatinine may occur. Experience with another angiotensin converting enzyme inhibitor suggests that
    these increases are usually reversible upon discontinuation of ALTACE and/or diuretic therapy. In such patients
    renal function should be monitored during the first few weeks of therapy. Some hypertensive patients with no
    apparent pre-existing renal vascular disease have developed increases in blood urea nitrogen and serum creatinine,
    usually minor and transient, especially when ALTACE has been given concomitantly with a diuretic. This
    is more likely to occur in patients with pre-existing renal impairment. Dosage reduction of ALTACE and/or discontinuation
    of the diuretic may be required.
    Evaluation of the hypertensive patient should always include assessment of renal function. (See
    DOSAGE AND ADMINISTRATION.)
    Hyperkalemia: In clinical trials, hyperkalemia (serum potassium greater than 5.7 mEq/L) occurred in approximately
    1% of hypertensive patients receiving ALTACE (ramipril). In most cases, these were isolated values,
    which resolved despite continued therapy. None of these patients was discontinued from the trials because of
    hyperkalemia. Risk factors for the development of hyperkalemia include renal insufficiency, diabetes mellitus,
    and the concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing
    salt substitutes, which should be used cautiously, if at all, with ALTACE. (See Drug Interactions.)
    Cough: Presumably due to the inhibition of the degradation of endogenous bradykinin, persistent nonproductive
    cough has been reported with all ACE inhibitors, always resolving after discontinuation of therapy. ACE
    inhibitor-induced cough should be considered in the differential diagnosis of cough.
    Impaired Liver Function: Since ramipril is primarily metabolized by hepatic esterases to its active moiety,
    ramiprilat, patients with impaired liver function could develop markedly elevated plasma levels of ramipril. No
    formal pharmacokinetic studies have been carried out in hypertensive patients with impaired liver function.
    However, since the renin-angiotensin system may be activated in patients with severe liver cirrhosis and/or
    ascites, particular caution should be exercised in treating these patients.
    Surgery/Anesthesia: In patients undergoing surgery or during anesthesia with agents that produce hypotension,
    ramipril may block angiotensin II formation that would otherwise occur secondary to compensatory renin
    release. Hypotension that occurs as a result of this mechanism can be corrected by volume expansion.
    Information for Patients
    Pregnancy: Female patients of childbearing age should be told about the consequences of second- and
    third-trimester exposure to ACE inhibitors, and they should also be told that these consequences do not appear
    to have resulted from intrauterine ACE inhibitor exposure that has been limited to the first trimester. These
    patients should be asked to report pregnancies to their physicians as soon as possible.
    Angioedema: Angioedema, including laryngeal edema, can occur with treatment with ACE inhibitors, especially
    following the first dose. Patients should be so advised and told to report immediately any signs or symptoms
    suggesting angioedema (swelling of face, eyes, lips, or tongue, or difficulty in breathing) and to take no
    more drug until they have consulted with the prescribing physician.
    Symptomatic Hypotension: Patients should be cautioned that lightheadedness can occur, especially during
    the first days of therapy, and it should be reported. Patients should be told that if syncope occurs, ALTACE
    should be discontinued until the physician has been consulted.
    All patients should be cautioned that inadequate fluid intake or excessive perspiration, diarrhea, or vomiting
    can lead to an excessive fall in blood pressure, with the same consequences of lightheadedness and possible
    syncope.
    Hyperkalemia: Patients should be told not to use salt substitutes containing potassium without consulting
    their physician.
    Neutropenia: Patients should be told to promptly report any indication of infection (e.g., sore throat, fever),
    which could be a sign of neutropenia.
    Drug Interactions
    With nonsteroidal anti-inflammatory agents: Rarely, concomitant treatment with ACE inhibitors and nonsteroidal
    anti-inflammatory agents have been associated with worsening of renal failure and an increase in
    serum potassium.
    With diuretics: Patients on diuretics, especially those in whom diuretic therapy was recently instituted, may
    occasionally experience an excessive reduction of blood pressure after initiation of therapy with ALTACE. The
    possibility of hypotensive effects with ALTACE can be minimized by either discontinuing the diuretic or increasing
    the salt intake prior to initiation of treatment with ALTACE. If this is not possible, the starting dose should
    be reduced. (See DOSAGE AND ADMINISTRATION.)
    With potassium supplements and potassium-sparing diuretics: ALTACE can attenuate potassium loss
    caused by thiazide diuretics. Potassium-sparing diuretics (spironolactone, amiloride, triamterene, and others) or
    potassium supplements can increase the risk of hyperkalemia. Therefore, if concomitant use of such agents is
    indicated, they should be given with caution, and the patient’s serum potassium should be monitored frequently.
    With lithium: Increased serum lithium levels and symptoms of lithium toxicity have been reported in
    patients receiving ACE inhibitors during therapy with lithium. These drugs should be coadministered with caution,
    and frequent monitoring of serum lithium levels is recommended. If a diuretic is also used, the risk of lithium
    toxicity may be increased.
    With Oral Hypoglycemic Agents or Insulin: Rarely, hypoglycemia has been reported during concomitant
    therapy. Upon initiation of ALTACE or with an increase in dose, such patients should be closely monitored for
    symptoms of hypoglycemic reactions with dosage adjustment of concomitant oral hypoglycemic agents or
    insulin therapy as necessary.
    Other: Neither ALTACE nor its metabolites have been found to interact with food, digoxin, antacid,
    furosemide, cimetidine, indomethacin, and simvastatin. The combination of ALTACE and propranolol showed
    no adverse effects on dynamic parameters (blood pressure and heart rate). The co-administration of ALTACE
    and warfarin did not adversely affect the anticoagulant effects of the latter drug. Additionally, co-administration
    of ALTACE with phenprocoumon did not affect minimum phenprocoumon levels or interfere with the subjects’
    state of anti-coagulation.
    Carcinogenesis, Mutagenesis, Impairment of Fertility
    No evidence of a tumorigenic effect was found when ramipril was given by gavage to rats for up to 24 months
    at doses of up to 500 mg/kg/day or to mice for up to 18 months at doses of up to 1000 mg/kg/day. (For either
    species, these doses are about 200 times the maximum recommended human dose when compared on the
    basis of body surface area.) No mutagenic activity was detected in the Ames test in bacteria, the micronucleus
    test in mice, unscheduled DNA synthesis in a human cell line, or a forward gene-mutation assay in a Chinese
    hamster ovary cell line. Several metabolites and degradation products of ramipril were also negative in the Ames
    test. A study in rats with dosages as great as 500 mg/kg/day did not produce adverse effects on fertility.
    Pregnancy
    Pregnancy Categories C (first trimester) and D (second and third trimesters). See WARNINGS:
    Fetal/Neonatal Morbidity and Mortality.
    Nursing Mothers
    Ingestion of single 10 mg oral dose of ALTACE resulted in undetectable amounts of ramipril and its metabolites
    in breast milk. However, because multiple doses may produce low milk concentrations that are not predictable
    from single doses, women receiving ALTACE should not breast feed.
    Geriatric Use
    Of the total number of patients who received ramipril in US clinical studies of ALTACE 11.0% were 65 and
    over while 0.2% were 75 and over. No overall differences in effectiveness or safety were observed between
    these patients and younger patients, and other reported clinical experience has not identified differences in
    responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot
    be ruled out.
    One pharmacokinetic study conducted in hospitalized elderly patients indicated that peak ramiprilat levels
    and area under the plasma concentration time curve (AUC) for ramiprilat are higher in older patients.
    Pediatric Use
    Safety and effectiveness in pediatric patients have not been established.
    ADVERSE REACTIONS
    Hypertension
    ALTACE has been evaluated for safety in over 4,000 patients with hypertension; of these, 1,230 patients
    were studied in US controlled trials, and 1,107 were studied in foreign controlled trials. Almost 700 of these
    patients were treated for at least one year. The overall incidence of reported adverse events was similar in
    ALTACE and placebo patients. The most frequent clinical side effects (possibly or probably related to study
    drug) reported by patients receiving ALTACE in US placebo-controlled trials were: headache (5.4%), “dizziness”
    (2.2%) and fatigue or asthenia (2.0%), but only the last was more common in ALTACE patients than in
    patients given placebo. Generally, the side effects were mild and transient, and there was no relation to total
    dosage within the range of 1.25 to 20 mg. Discontinuation of therapy because of a side effect was required in
    approximately 3% of US patients treated with ALTACE. The most common reasons for discontinuation were:
    cough (1.0%), “dizziness” (0.5%), and impotence (0.4%).
    Of observed side effects considered possibly or probably related to study drug that occurred in US placebocontrolled
    trials in more than 1% of patients treated with ALTACE, only asthenia (fatigue) was more common
    on Altace than placebo (2% vs. 1%).
    PATIENTS IN US PLACEBO CONTROLLED STUDIES
    ALTACE Placebo
    (n=651) (n=286)
    n % n %
    Asthenia (Fatigue) 13 2 2 1
    In placebo-controlled trials, there was also an excess of upper respiratory infection and flu syndrome in the
    ramipril group, not attributed at that time to ramipril. As these studies were carried out before the relationship
    of cough to ACE inhibitors was recognized, some of these events may represent ramipril-induced cough. In a
    later 1-year study, increased cough was seen in almost 12% of ramipril patients, with about 4% of patients
    requiring discontinuation of treatment.
    Heart Failure Post Myocardial Infarction
    Adverse reactions (except laboratory abnormalities) considered possibly/probably related to study drug that
    occurred in more than one percent of patients and more frequently on ramipril are shown below. The incidences
    represent the experiences from the AIRE study. The follow-up time was between 6 and 46 months for
    this study.
    Percentage of Patients with Adverse Events Possibly/ Probably Related to Study Drug
    Placebo-Controlled (AIRE) Mortality Study
    Adverse Event Ramipril Placebo
    (n=1004) (n=982)
    Hypotension 11 5
    Cough Increased 8 4
    Dizziness 4 3
    Angina Pectoris 3 2
    Nausea 2 1
    Postural Hypotension 2 1
    Syncope 2 1
    Vomiting 2 0.5
    Vertigo 2 0.7
    Abnormal Kidney Function 1 0.5
    Diarrhea 1 0.4
    HOPE Study:
    Safety data in the HOPE trial were collected as reasons for discontinuation or temporary interruption of treatment.
    The incidence of cough was similar to that seen in the AIRE trial. The rate of angioedema was the same
    as in previous clinical trials (see WARNINGS).
    RAMIPRIL PLACEBO
    (N=4645) (N=4652)
    % %
    Discontinuation at any time 34 32
    Permanent discontinuation 29 28
    Reasons for stopping Cough 7 2
    Hypotension or Dizziness 1.9 1.5
    Angioedema 0.3 0.1
    Other adverse experiences reported in controlled clinical trials (in less than 1% of ramipril patients), or rarer events
    seen in postmarketing experience, include the following (in some, a causal relationship to drug use is uncertain):
    Body As a Whole: Anaphylactoid reactions. (See WARNINGS.)
    Cardiovascular: Angina/chest pain, arrhythmias including bradycardia or tachycardia, cardiac arrest, congestive
    heart failure, symptomatic hypotension (reported in 0.5% of patients in US trials) (See WARNINGS and
    PRECAUTIONS), syncope, palpitations, transient ischemia attack, and myocardial infarction or cerebrovascular
    accident possibly due to excessive hypotension.
    Hematologic: Pancytopenia, hemolytic anemia and thrombocytopenia.
    Renal: Some hypertensive patients with no apparent pre-existing renal disease have developed minor, usually
    transient, increases in blood urea nitrogen and serum creatinine when taking ALTACE, particularly when
    ALTACE was given concomitantly with a diuretic. (See WARNINGS.) Acute renal failure.
    Angioneurotic Edema: Angioneurotic edema has been reported in 0.3% of patients in US clinical trials.
    (See WARNINGS.)
    Gastrointestinal: Pancreatitis, abdominal pain (sometimes with enzyme changes suggesting pancreatitis),
    anorexia, constipation, diarrhea, dry mouth, dyspepsia, dysphagia, gastroenteritis, hepatitis, increased salivation
    and taste disturbance.
    Dermatologic: Apparent hypersensitivity reactions (manifested by urticaria, pruritus, or rash, with or without
    fever), photosensitivity, purpura, oncholysis, pemphigus, pemphigoid, erythema multiforme, toxic epidermal
    necrolysis, and Stevens-Johnson syndrome.
    Neurologic and Psychiatric: Anxiety, amnesia, convulsions, depression, hearing loss, insomnia, nervousness,
    neuralgia, neuropathy, paresthesia, somnolence, tinnitus, tremor, vertigo, and vision disturbances.
    Miscellaneous: As with other ACE inhibitors, a symptom complex has been reported which may include a
    positive ANA, an elevated erythrocyte sedimentation rate, arthralgia/arthritis, myalgia, fever, vasculitis,
    eosinophilia, photosensitivity, rash and other dermatologic manifestations. Additionally, as with other ACE
    inhibitors, eosinophilic pneumonitis has been reported.
    Fetal/Neonatal Morbidity and Mortality. See WARNINGS: Fetal/Neonatal Morbidity and Mortality.
    Other: arthralgia, arthritis, dyspnea, edema, epistaxis, hypoglycemia (see PRECAUTIONS, Drug
    Interactions), impotence, increased sweating, malaise, myalgia, and weight gain.
    Clinical Laboratory Test Findings:
    Creatinine and Blood Urea Nitrogen: Increases in creatinine levels occurred in 1.2% of patients receiving
    ALTACE alone, and in 1.5% of patients receiving ALTACE and a diuretic. Increases in blood urea nitrogen levels
    occurred in 0.5% of patients receiving ALTACE alone and in 3% of patients receiving ALTACE with a diuretic.
    None of these increases required discontinuation of treatment. Increases in these laboratory values are
    more likely to occur in patients with renal insufficiency or those pretreated with a diuretic and, based on experience
    with other ACE inhibitors, would be expected to be especially likely in patients with renal artery stenosis.
    (See WARNINGS and PRECAUTIONS.) Since ramipril decreases aldosterone secretion, elevation of serum
    potassium can occur. Potassium supplements and potassium-sparing diuretics should be given with caution,
    and the patient’s serum potassium should be monitored frequently. (See WARNINGS and PRECAUTIONS.)
    Hemoglobin and Hematocrit: Decreases in hemoglobin or hematocrit (a low value and a decrease of 5 g/dl
    or 5% respectively) were rare, occurring in 0.4% of patients receiving ALTACE alone and in 1.5% of patients
    receiving ALTACE plus a diuretic. No US patients discontinued treatment because of decreases in hemoglobin
    or hematocrit.
    Other (causal relationships unknown): Clinically important changes in standard laboratory tests were
    rarely associated with ALTACE administration. Elevations of liver enzymes, serum bilirubin, uric acid, and blood
    glucose have been reported, as have cases of hyponatremia and scattered incidents of leukopenia, eosinophilia,
    and proteinuria. In US trials, less than 0.2% of patients discontinued treatment for laboratory abnormalities;
    all of these were cases of proteinuria or abnormal liver-function tests.
    OVERDOSAGE
    Single oral doses in rats and mice of 10–11 g/kg resulted in significant lethality. In dogs, oral doses as high
    as 1 g/kg induced only mild gastrointestinal distress. Limited data on human overdosage are available. The most
    likely clinical manifestations would be symptoms attributable to hypotension.
    Laboratory determinations of serum levels of ramipril and its metabolites are not widely available, and such
    determinations have, in any event, no established role in the management of ramipril overdose.
    No data are available to suggest physiological maneuvers (e.g., maneuvers to change the pH of the urine)
    that might accelerate elimination of ramipril and its metabolites. Similarly, it is not known which, if any, of these
    substances can be usefully removed from the body by hemodialysis.
    Angiotensin II could presumably serve as a specific antagonist-antidote in the setting of ramipril overdose,
    but angiotensin II is essentially unavailable outside of scattered research facilities. Because the hypotensive
    effect of ramipril is achieved through vasodilation and effective hypovolemia, it is reasonable to treat ramipril
    overdose by infusion of normal saline solution.
    DOSAGE AND ADMINISTRATION
    Blood pressure decreases associated with any dose of ALTACE depend, in part, on the presence or absence
    of volume depletion (e.g., past and current diuretic use) or the presence or absence of renal artery stenosis. If
    such circumstances are suspected to be present, the initial starting dose should be 1.25 mg once daily.
    Reduction in Risk of Myocardial Infarction, Stroke, and Death from Cardiovascular Causes
    ALTACE should be given at an initial dose of 2.5 mg, once a day for 1 week, 5 mg, once a day for the next
    3 weeks, and then increased as tolerated, to a maintenance dose of 10 mg, once a day. If the patient is hypertensive
    or recently post myocardial infarction, it can also be given as a divided dose.
    Hypertension
    The recommended initial dose for patients not receiving a diuretic is 2.5 mg once a day. Dosage should be
    adjusted according to the blood pressure response. The usual maintenance dosage range is 2.5 to 20 mg per
    day administered as a single dose or in two equally divided doses. In some patients treated once daily, the antihypertensive
    effect may diminish toward the end of the dosing interval. In such patients, an increase in dosage
    or twice daily administration should be considered. If blood pressure is not controlled with ALTACE alone, a
    diuretic can be added.
    Heart Failure Post Myocardial Infarction
    For the treatment of post-infarction patients who have shown signs of congestive failure, the recommended
    starting dose of ALTACE is 2.5 mg twice daily (5 mg per day). A patient who becomes hypotensive at this dose
    may be switched to 1.25 mg twice daily, and after one week at the starting dose, patients should then be titrated
    (if tolerated) toward a target dose of 5 mg twice daily, with dosage increases being about 3 weeks apart.
    After the initial dose of ALTACE, the patient should be observed under medical supervision for at least two
    hours and until blood pressure has stabilized for at least an additional hour. (See WARNINGS and PRECAUTIONS,
    Drug Interactions.) If possible, the dose of any concomitant diuretic should be reduced which may
    diminish the likelihood of hypotension. The appearance of hypotension after the initial dose of ALTACE does not
    preclude subsequent careful dose titration with the drug, following effective management of the hypotension.
    The ALTACE Capsule is usually swallowed whole. The ALTACE Capsule can also be opened and the contents
    sprinkled on a small amount (about 4 oz.) of apple sauce or mixed in 4 oz. (120 ml) of water or apple juice.
    To be sure that ramipril is not lost when such a mixture is used, the mixture should be consumed in its entirety.
    The described mixtures can be pre-prepared and stored for up to 24 hours at room temperature or up to 48
    hours under refrigeration.
    Concomitant administration of ALTACE with potassium supplements, potassium salt substitutes, or potassium-
    sparing diuretics can lead to increases of serum potassium. (See PRECAUTIONS.)
    In patients who are currently being treated with a diuretic, symptomatic hypotension occasionally can occur
    following the initial dose of ALTACE. To reduce the likelihood of hypotension, the diuretic should, if possible,
    be discontinued two to three days prior to beginning therapy with ALTACE. (See WARNINGS.) Then, if blood
    pressure is not controlled with ALTACE alone, diuretic therapy should be resumed.
    If the diuretic cannot be discontinued, an initial dose of 1.25 mg ALTACE should be used to avoid excess
    hypotension.
    Dosage Adjustment in Renal Impairment
    In patients with creatinine clearance <40 ml/min/1.73m2 (serum creatinine approximately >2.5 mg/dl) doses
    only 25% of those normally used should be expected to induce full therapeutic levels of ramiprilat. (See CLINICAL
    PHARMACOLOGY.)
    Hypertension: For patients with hypertension and renal impairment, the recommended initial dose is 1.25
    mg ALTACE once daily. Dosage may be titrated upward until blood pressure is controlled or to a maximum total
    daily dose of 5 mg.
    Heart Failure Post Myocardial Infarction: For patients with heart failure and renal impairment, the recommended
    initial dose is 1.25 mg ALTACE once daily. The dose may be increased to 1.25 mg b.i.d. and up to a
    maximum dose of 2.5 mg b.i.d. depending upon clinical response and tolerability.
    HOW SUPPLIED
    ALTACE is available in potencies of 1.25 mg, 2.5 mg, 5 mg, and 10 mg in hard gelatin capsules.
    ALTACE 1.25 mg capsules are supplied as yellow, hard gelatin capsules in bottles of 100 (NDC 61570-110-
    01), and Unit Dose packs of 100 (NDC 61570-110-56).
    ALTACE 2.5 mg capsules are supplied as orange, hard gelatin capsules in bottles of 100 (NDC 61570-111-
    01), 500 (NDC 61570-111-05), 1000 (NDC 61570-111-10) and Unit Dose packs of 100 (NDC 61570-111-56), and
    Bulk pack of 5000’s (NDC 61570-111-50).
    ALTACE 5 mg capsules are supplied as red, hard gelatin capsules in bottles of 100 (NDC 61570-112-01), 500
    (NDC 61570-112-05), 1000 (NDC 61570-112-10) and Unit Dose packs of 100 (NDC 61570-112-56), and Bulk
    pack of 5000’s (NDC 61570-112-50).
    ALTACE 10 mg capsules are supplied as Process Blue, hard gelatin capsules in bottles of 100 (NDC 61570-
    120-01), 500 (NDC 61570-120-05), 1000 (NDC 61570-120-10).
    Dispense in well-closed container with safety closure.
    Store at controlled room temperature (59° to 86°F).
    Rx only.
    Distributed by: Monarch Pharmaceuticals, Inc., Bristol, TN 37620
    Manufactured by: Aventis Pharmaceuticals Inc., Kansas City, MO 64137
    Prescribing Information as of February 2003. CI 6173-3

  7. #6
    King Nothing ericg's Avatar
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    That has to be the longest post in the history of wbb - kudos to those who actually read through the entire thing.
    Current Stats --------------- Training Goals: Improve athletic conditioning.
    Squat - 305lbs - 1/23/06 ----- 335
    Deadlift - 415lbs - 2/4/06 ---- 435
    Bench - 90s*7 ----------------- 100s*5
    Weight - 208 ------------------ 190
    Height - 5'10"

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    WBBB|"Many of life's failures are people who did not realize how close they were to success when they gave up" - Thomas Edison

  8. #7
    Banned ogarchamplin's Avatar
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    sorry i was trying to do Bam Bam a favor

  9. #8
    "COUNT CRACKULA" Bam Bam's Avatar
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    ok i got a no out of that for eating muscle b ut maybe a yes on making me infertal?
    Blocka Blocka

    I am AMINAL

  10. #9
    King Nothing ericg's Avatar
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    That sucks from - probably a good thing for the society though :evillaugh
    Current Stats --------------- Training Goals: Improve athletic conditioning.
    Squat - 305lbs - 1/23/06 ----- 335
    Deadlift - 415lbs - 2/4/06 ---- 435
    Bench - 90s*7 ----------------- 100s*5
    Weight - 208 ------------------ 190
    Height - 5'10"

    My Journal|My Routine|My FitDay
    WBBB|"Many of life's failures are people who did not realize how close they were to success when they gave up" - Thomas Edison

  11. #10
    Bulking Sith Knight Stephen Riddington's Avatar
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    Quote Originally Posted by ericg
    That has to be the longest post in the history of wbb - kudos to those who actually read through the entire thing.
    :withstupi
    You tried your best and you failed miserably. The lesson is 'never try'-Homer Simpson
    My brother always said that drowning in beer would be like heaven. Well, my brother's not here and I have two soakers... This sucks!!!-Bob McKenzie
    Hockey is murder on ice-Jim Murray
    Give a guy a gun, he thinks he's Superman. Give him two and he thinks he's God.-Superintendent Pang (Hard Boiled)

  12. #11
    "COUNT CRACKULA" Bam Bam's Avatar
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    so can someone put this medical stuff in lehmans terms for me


    also altace is kinda steep for a monthly prescript
    Blocka Blocka

    I am AMINAL

  13. #12
    King Nothing ericg's Avatar
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    I looked through it and didnt find anything about muscle loss. Course I would want a second opinion if I were you.
    Current Stats --------------- Training Goals: Improve athletic conditioning.
    Squat - 305lbs - 1/23/06 ----- 335
    Deadlift - 415lbs - 2/4/06 ---- 435
    Bench - 90s*7 ----------------- 100s*5
    Weight - 208 ------------------ 190
    Height - 5'10"

    My Journal|My Routine|My FitDay
    WBBB|"Many of life's failures are people who did not realize how close they were to success when they gave up" - Thomas Edison

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