Carvedilol Information
Carvedilol ()
Carvedilol () Dosage And Administration
Carvedilol () should be taken with food to slow the rate of absorption and reduce the incidence of orthostatic effects.
Carvedilol () Dosage Forms And Strengths
The white, oval shaped, biconvex film-coated tablets are available in the following strengths: 3.125 mg– engraved with on one side and 175 on the other side, 6.25 mg–engraved with on one side and 176 on the other side, 12.5 mg–engraved with on one side and 177 on the other side, and 25 mg–engraved with on one side and 178 on the other side.
Carvedilol () Contraindications
Carvedilol () is contraindicated in the following conditions:
Carvedilol () Warnings And Precautions
Patients with coronary artery disease, who are being treated with Carvedilol () , should be advised against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction and ventricular arrhythmias have been reported in angina patients following the abrupt discontinuation of therapy with β-blockers. The last 2 complications may occur with or without preceding exacerbation of the angina pectoris. As with other β-blockers, when discontinuation of Carvedilol () is planned, the patients should be carefully observed and advised to limit physical activity to a minimum. Carvedilol () should be discontinued over 1 to 2 weeks whenever possible. If the angina worsens or acute coronary insufficiency develops, it is recommended that Carvedilol () be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue therapy with Carvedilol () abruptly even in patients treated only for hypertension or heart failure.
Postural hypotension occurred in 1.8% and syncope in 0.1% of hypertensive patients, primarily following the initial dose or at the time of dose increase and was a cause for discontinuation of therapy in 1% of patients.
In the CAPRICORN study of survivors of an acute myocardial infarction, hypotension or postural hypotension occurred in 20.2% of patients receiving Carvedilol () compared to 12.6% of placebo patients. Syncope was reported in 3.9% and 1.9% of patients, respectively. These events were a cause for discontinuation of therapy in 2.5% of patients receiving Carvedilol () , compared to 0.2% of placebo patients.
Starting with a low dose, administration with food, and gradual up-titration should decrease the likelihood of syncope or excessive hypotension. During initiation of therapy, the patient should be cautioned to avoid situations such as driving or hazardous tasks, where injury could result should syncope occur.
Patients with bronchospastic disease (e.g., chronic bronchitis and emphysema) should, in general, not receive β-blockers. Carvedilol () may be used with caution, however, in patients who do not respond to, or cannot tolerate, other antihypertensive agents. It is prudent, if Carvedilol () is used, to use the smallest effective dose, so that inhibition of endogenous or exogenous β-agonists is minimized.
In clinical trials, patients with bronchospastic disease were enrolled if they did not require oral or inhaled medication to treat their bronchospastic disease. In such patients, it is recommended that Carvedilol () be used with caution. The dosing recommendations should be followed closely and the dose should be lowered if any evidence of bronchospasm is observed during up-titration.
In general, β-blockers may mask some of the manifestations of hypoglycemia, particularly tachycardia. Nonselective β-blockers may potentiate insulin-induced hypoglycemia and delay recovery of serum glucose levels. Patients subject to spontaneous hypoglycemia, or diabetic patients receiving insulin or oral hypoglycemic agents, should be cautioned about these possibilities.
Studied designed to examine the effects of Carvedilol () on glycemic control in patients with diabetes and heart failure have not been conducted.
Carvedilol () Adverse Reactions
Carvedilol () has been evaluated for safety in patients with left ventricular dysfunction following myocardial infarction and in hypertensive patients. The observed adverse event profile was consistent with the pharmacology of the drug and the health status of the patients in the clinical trials. Adverse events reported for each of these patient populations are provided below. Excluded are adverse events considered too general to be informative, and those not reasonably associated with the use of the drug because they were associated with the condition being treated or are very common in the treated population. Rates of adverse events were generally similar across demographic subsets (men and women, elderly and non-elderly, blacks and non-blacks).
Left Ventricular Dysfunction Following Myocardial Infarction
Carvedilol () has been evaluated for safety in survivors of an acute myocardial infarction with left ventricular dysfunction in the CAPRICORN trial which involved 969 patients who received Carvedilol () and 980 who received placebo. Approximately 75% of the patients received Carvedilol () for at least 6 months and 53% received Carvedilol () for at least 12 months. Patients were treated for an average of 12.9 months and 12.8 months with Carvedilol () and placebo, respectively.
The following adverse events were reported with a frequency of >1% but ≤3% and more frequently with Carvedilol () : Flu syndrome, cerebrovascular accident, peripheral vascular disorder, hypotonia, depression, gastrointestinal pain, arthritis, and gout. The overall rates of discontinuations due to adverse events were similar in both groups of patients. In this database, the only cause of discontinuation >1%, and occurring more often on Carvedilol () was hypotension (1.5% on Carvedilol () , 0.2% on placebo).
Hypertension
Carvedilol () has been evaluated for safety in hypertension in more than 2,193 patients in US clinical trials and in 2,976 patients in international clinical trials. Approximately 36% of the total treated population received Carvedilol () for at least 6 months. Most adverse events reported during therapy with Carvedilol () were of mild to moderate severity. In US controlled clinical trials directly comparing Carvedilol () in doses up to 50 mg (n = 1,142) to placebo (n = 462), 4.9% of patients receiving Carvedilol () discontinued for adverse events versus 5.2% of placebo patients. Although there was no overall difference in discontinuation rates, discontinuations were more common in the Carvedilol () group for postural hypotension (1% versus 0). The overall incidence of adverse events in US placebo-controlled trials increased with increasing dose of Carvedilol () . For individual adverse events this could only be distinguished for dizziness, which increased in frequency from 2% to 5% as total daily dose increased from 6.25 mg to 50 mg.
Table 1 shows adverse events in US placebo-controlled clinical trials for hypertension that occurred with an incidence of >1% regardless of causality, and that were more frequent in drug-treated patients than placebo-treated patients.
Dyspnea and fatigue were also reported in these studies, but the rates were equal or greater in patients who received placebo.
The following adverse events not described above were reported as possibly or probably related to Carvedilol () in worldwide open or controlled trials with Carvedilol () in patients with hypertension.
Incidence >0.1% to ≤1%
Cardiovascular:
Central and Peripheral Nervous System:
Psychiatric:
Reproductive, male:
Skin and Appendages:
Special Senses:
Urinary System:
Autonomic Nervous System:
Metabolic and Nutritional:
Hematologic:
The following events were reported in ≤0.1% of patients and are potentially important: Complete AV block, bundle branch block, myocardial ischemia, cerebrovascular disorder, convulsions, migraine, neuralgia, paresis, anaphylactoid reaction, alopecia, exfoliative dermatitis, amnesia, GI hemorrhage, bronchospasm, pulmonary edema, decreased hearing, respiratory alkalosis, increased BUN, decreased HDL, pancytopenia, and atypical lymphocytes.
Reversible elevations in serum transaminases (ALT or AST) have been observed during treatment with Carvedilol () . Rates of transaminase elevations (2- to 3-times the upper limit of normal) observed during controlled clinical trials have generally been similar between patients treated with Carvedilol () and those treated with placebo. However, transaminase elevations, confirmed by rechallenge, have been observed with Carvedilol () . In a long-term, placebo-controlled trial in severe heart failure, patients treated with Carvedilol () had lower values for hepatic transaminases than patients treated with placebo, possibly because improvements in cardiac function induced by Carvedilol () led to less hepatic congestion and/or improved hepatic blood flow.
Carvedilol () has not been associated with clinically significant changes in serum potassium, total triglycerides, total cholesterol, HDL cholesterol, uric acid, blood urea nitrogen, or creatinine. No clinically relevant changes were noted in fasting serum glucose in hypertensive patients.
The following adverse reactions have been identified during post-approval use of Carvedilol () . Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
Reports of aplastic anemia and severe skin reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis, and erythema multiforme) have been rare and received only when Carvedilol () was administered concomitantly with other medications associated with such reactions. Urinary incontinence in women (which resolved upon discontinuation of the medication) and interstitial pneumonitis have been reported rarely.
Carvedilol () Drug Interactions
Patients taking both agents with β-blocking properties and a drug that can deplete catecholamines (e.g., reserpine and monoamine oxidase inhibitors) should be observed closely for signs of hypotension and/or severe bradycardia.
Concomitant administration of clonidine with agents with β-blocking properties may potentiate blood-pressure- and heart-rate-lowering effects. When concomitant treatment with agents with β-blocking properties and clonidine is to be terminated, the β-blocking agent should be discontinued first. Clonidine therapy can then be discontinued several days later by gradually decreasing the dosage.
Carvedilol () Use In Specific Populations
Effectiveness of Carvedilol () in patients younger than 18 years of age has not been established.
In a double-blind trial, 161 children (mean age 6 years, range 2 months to 17 years; 45% less than 2 years old) with chronic heart failure [NYHA class II-IV, left ventricular ejection fraction
Of the 975 myocardial infarction patients randomized to Carvedilol () in the CAPRICORN trial, 48% (468) were 65 years of age or older, and 11% (111) were 75 years of age or older.
Of the 2,065 hypertensive patients in US clinical trials of efficacy or safety who were treated with Carvedilol () , 21% (436) were 65 years of age or older. Of 3,722 patients receiving Carvedilol () in hypertension clinical trials conducted worldwide, 24% were 65 years of age or older.
With the exception of dizziness in hypertensive patients (incidence 8.8% in the elderly versus 6% in younger patients), no overall differences in the safety or effectiveness (see Figure 2) were observed between the older subjects and younger subjects in each of these populations. Similarly, other reported clinical experience has not identified differences in responses between the elderly and younger subjects, but greater sensitivity of some older individuals cannot be ruled out.
Carvedilol () Overdosage
Overdosage may cause severe hypotension, bradycardia, cardiac insufficiency, cardiogenic shock, and cardiac arrest. Respiratory problems, bronchospasms, vomiting, lapses of consciousness, and generalized seizures may also occur.
The patient should be placed in a supine position and, where necessary, kept under observation and treated under intensive-care conditions. Gastric lavage or pharmacologically induced emesis may be used shortly after ingestion. The following agents may be administered:
If peripheral vasodilation dominates, it may be necessary to administer adrenaline or noradrenaline with continuous monitoring of circulatory conditions. For therapy-resistant bradycardia, pacemaker therapy should be performed. For bronchospasm, β-sympathomimetics (as aerosol or IV) or aminophylline IV should be given. In the event of seizures, slow IV injection of diazepam or clonazepam is recommended.
NOTE: In the event of severe intoxication where there are symptoms of shock, treatment with antidotes must be continued for a sufficiently long period of time consistent with the 7- to 10-hour half-life of Carvedilol () .
Cases of overdosage with Carvedilol () alone or in combination with other drugs have been reported. Quantities ingested in some cases exceeded 1,000 milligrams. Symptoms experienced included low blood pressure and heart rate. Standard supportive treatment was provided and individuals recovered.
Carvedilol () Description
Carvedilol () is a nonselective β-adrenergic blocking agent with α-blocking activity. It is (±)-1-(Carbazol-4-yloxy)-3-[[2-(o-methoxyphenoxy)ethyl]amino]-2-propanol. Carvedilol () is a racemic mixture with the following structure:
Carvedilol () is a white, oval shaped, biconvex film-coated tablet containing 3.125 mg, 6.25 mg, 12.5 mg, or 25 mg of Carvedilol () . Inactive ingredients consist of colloidal silicon dioxide, crospovidone, hypromellose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, sodium citrate, sucrose, and titanium dioxide.
Carvedilol () is a white to off-white powder with a molecular weight of 406.5 and a molecular formula of CHNO. It is freely soluble in dimethylsulfoxide; soluble in methylene chloride and methanol; sparingly soluble in 95% ethanol and isopropanol; slightly soluble in ethyl ether; and practically insoluble in water, gastric fluid (simulated, TS, pH 1.1), and intestinal fluid (simulated, TS without pancreatin, pH 7.5).
Carvedilol () Clinical Pharmacology
Left Ventricular Dysfunction Following Myocardial Infarction
The basis for the beneficial effects of Carvedilol () in patients with left ventricular dysfunction following an acute myocardial infarction is not established.
Hypertension
The mechanism by which β-blockade produces an antihypertensive effect has not been established.
β-adrenoreceptor blocking activity has been demonstrated in animal and human studies showing that Carvedilol () (1) reduces cardiac output in normal subjects; (2) reduces exercise- and/or isoproterenol-induced tachycardia; and (3) reduces reflex orthostatic tachycardia. Significant β-adrenoreceptor blocking effect is usually seen within 1 hour of drug administration.
α-adrenoreceptor blocking activity has been demonstrated in human and animal studies, showing that Carvedilol () (1) attenuates the pressor effects of phenylephrine; (2) causes vasodilation; and (3) reduces peripheral vascular resistance. These effects contribute to the reduction of blood pressure and usually are seen within 30 minutes of drug administration.
Due to the α-receptor blocking activity of Carvedilol () , blood pressure is lowered more in the standing than in the supine position, and symptoms of postural hypotension (1.8%), including rare instances of syncope, can occur. Following oral administration, when postural hypotension has occurred, it has been transient and is uncommon when Carvedilol () is administered with food at the recommended starting dose and titration increments are closely followed.
In hypertensive patients with normal renal function, therapeutic doses of Carvedilol () decreased renal vascular resistance with no change in glomerular filtration rate or renal plasma flow. Changes in excretion of sodium, potassium, uric acid, and phosphorus in hypertensive patients with normal renal function were similar after Carvedilol () and placebo.
Carvedilol () has little effect on plasma catecholamines, plasma aldosterone, or electrolyte levels, but it does significantly reduce plasma renin activity when given for at least 4 weeks. It also increases levels of atrial natriuretic peptide.
Carvedilol () is rapidly and extensively absorbed following oral administration, with absolute bioavailability of approximately 25% to 35% due to a significant degree of first-pass metabolism. Following oral administration, the apparent mean terminal elimination half-life of Carvedilol () generally ranges from 7 to 10 hours. Plasma concentrations achieved are proportional to the oral dose administered. When administered with food, the rate of absorption is slowed, as evidenced by a delay in the time to reach peak plasma levels, with no significant difference in extent of bioavailability. Taking Carvedilol () with food should minimize the risk of orthostatic hypotension.
Carvedilol () is extensively metabolized. Following oral administration of radiolabelled Carvedilol () to healthy volunteers, Carvedilol () accounted for only about 7% of the total radioactivity in plasma as measured by area under the curve (AUC). Less than 2% of the dose was excreted unchanged in the urine. Carvedilol () is metabolized primarily by aromatic ring oxidation and glucuronidation. The oxidative metabolites are further metabolized by conjugation via glucuronidation and sulfation. The metabolites of Carvedilol () are excreted primarily via the bile into the feces. Demethylation and hydroxylation at the phenol ring produce three active metabolites with β-receptor blocking activity. Based on preclinical studies, the 4'-hydroxyphenyl metabolite is approximately 13 times more potent than Carvedilol () for β-blockade.
Compared to Carvedilol () , the three active metabolites exhibit weak vasodilating activity. Plasma concentrations of the active metabolites are about one-tenth of those observed for Carvedilol () and have pharmacokinetics similar to the parent.
Carvedilol () undergoes stereoselective first-pass metabolism with plasma levels of R(+)-Carvedilol () approximately 2 to 3 times higher than S(-)-Carvedilol () following oral administration in healthy subjects. The mean apparent terminal elimination half-lives for R(+)-Carvedilol () range from 5 to 9 hours compared with 7 to 11 hours for the S(-)-enantiomer.
The primary P450 enzymes responsible for the metabolism of both R(+) and S(-)-Carvedilol () in human liver microsomes were CYP2D6 and CYP2C9 and to a lesser extent CYP3A4, 2C19, 1A2, and 2E1. CYP2D6 is thought to be the major enzyme in the 4’- and 5’-hydroxylation of Carvedilol () , with a potential contribution from 3A4. CYP2C9 is thought to be of primary importance in the O-methylation pathway of S(-)-Carvedilol () .
Carvedilol () is subject to the effects of genetic polymorphism with poor metabolizers of debrisoquin (a marker for cytochrome P450 2D6) exhibiting 2- to 3-fold higher plasma concentrations of R(+)-Carvedilol () compared to extensive metabolizers. In contrast, plasma levels of S(-)-Carvedilol () are increased only about 20% to 25% in poor metabolizers, indicating this enantiomer is metabolized to a lesser extent by cytochrome P450 2D6 than R(+)-Carvedilol () . The pharmacokinetics of Carvedilol () do not appear to be different in poor metabolizers of S-mephenytoin (patients deficient in cytochrome P450 2C19).
Carvedilol () is more than 98% bound to plasma proteins, primarily with albumin. The plasma-protein binding is independent of concentration over the therapeutic range. Carvedilol () is a basic, lipophilic compound with a steady-state volume of distribution of approximately 115 L, indicating substantial distribution into extravascular tissues. Plasma clearance ranges from 500 to 700 mL/min.
Geriatric
Plasma levels of Carvedilol () average about 50% higher in the elderly compared to young subjects.
Hepatic Impairment
Compared to healthy subjects, patients with severe liver impairment (cirrhosis) exhibit a 4- to 7-fold increase in Carvedilol () levels. Carvedilol () is contraindicated in patients with severe liver impairment.
Renal Impairment
Although Carvedilol () is metabolized primarily by the liver, plasma concentrations of Carvedilol () have been reported to be increased in patients with renal impairment. Based on mean AUC data, approximately 40% to 50% higher plasma concentrations of Carvedilol () were observed in hypertensive patients with moderate to severe renal impairment compared to a control group of hypertensive patients with normal renal function. However, the ranges of AUC values were similar for both groups. Changes in mean peak plasma levels were less pronounced, approximately 12% to 26% higher in patients with impaired renal function.
Consistent with its high degree of plasma protein-binding, Carvedilol () does not appear to be cleared significantly by hemodialysis.
Since Carvedilol () undergoes substantial oxidative metabolism, the metabolism and pharmacokinetics of Carvedilol () may be affected by induction or inhibition of cytochrome P450 enzymes.
Rifampin
In a pharmacokinetic study conducted in 8 healthy male subjects, rifampin (600 mg daily for 12 days) decreased the AUC and C of Carvedilol () by about 70%.
Cimetidine
In a pharmacokinetic study conducted in 10 healthy male subjects, cimetidine (1000 mg/day) increased the steady-state AUC of Carvedilol () by 30% with no change in C.
Glyburide
In 12 healthy subjects, combined administration of Carvedilol () (25 mg once daily) and a single dose of glyburide did not result in a clinically relevant pharmacokinetic interaction for either compound.
Hydrochlorothiazide
A single oral dose of Carvedilol () 25 mg did not alter the pharmacokinetics of a single oral dose of hydrochlorothiazide 25 mg in 12 patients with hypertension. Likewise, hydrochlorothiazide had no effect on the pharmacokinetics of Carvedilol () .
Digoxin
Following concomitant administration of Carvedilol () (25 mg once daily) and digoxin (0.25 mg once daily) for 14 days, steady-state AUC and trough concentrations of digoxin were increased by 14% and 16%, respectively, in 12 hypertensive patients.
Torsemide
In a study of 12 healthy subjects, combined oral administration of Carvedilol () 25 mg once daily and torsemide 5 mg once daily for 5 days did not result in any significant differences in their pharmacokinetics compared with administration of the drugs alone.
Warfarin
Carvedilol () (12.5 mg twice daily) did not have an effect on the steady-state prothrombin time ratios and did not alter the pharmacokinetics of R(+)- and S(-)-warfarin following concomitant administration with warfarin in 9 healthy volunteers.
Carvedilol () Clinical Studies
CAPRICORN was a double-blind study comparing Carvedilol () and placebo in 1,959 patients with a recent myocardial infarction (within 21 days) and left ventricular ejection fraction of ≤40%, with (47%) or without symptoms of heart failure. Patients given Carvedilol () received 6.25 mg twice daily, titrated as tolerated to 25 mg twice daily. Patients had to have a systolic blood pressure >90 mm Hg, a sitting heart rate >60 beats/minute, and no contraindication to β-blocker use. Treatment of the index infarction included aspirin (85%), IV or oral β-blockers (37%), nitrates (73%), heparin (64%), thrombolytics (40%), and acute angioplasty (12%). Background treatment included ACE inhibitors or angiotensin receptor blockers (97%), anticoagulants (20%), lipid-lowering agents (23%), and diuretics (34%). Baseline population characteristics included an average age of 63 years, 74% male, 95% Caucasian, mean blood pressure 121/74 mm Hg, 22% with diabetes, and 54% with a history of hypertension. Mean dosage achieved of Carvedilol () was 20 mg twice daily; mean duration of follow-up was 15 months.
All-cause mortality was 15% in the placebo group and 12% in the Carvedilol () group, indicating a 23% risk reduction in patients treated with Carvedilol () (95% CI 2-40%, p = 0.03), as shown in Figure 1. The effects on mortality in various subgroups are shown in Figure 2. Nearly all deaths were cardiovascular (which were reduced by 25% by Carvedilol () ), and most of these deaths were sudden or related to pump failure (both types of death were reduced by Carvedilol () ). Another study endpoint, total mortality and all-cause hospitalization, did not show a significant improvement.
There was also a significant 40% reduction in fatal or non-fatal myocardial infarction observed in the group treated with Carvedilol () (95% CI 11% to 60%, p = 0.01). A similar reduction in the risk of myocardial infarction was also observed in a meta-analysis of placebo-controlled trials of Carvedilol () in heart failure.
Carvedilol () was studied in 2 placebo-controlled trials that utilized twice-daily dosing, at total daily doses of 12.5 to 50 mg. In these and other studies, the starting dose did not exceed 12.5 mg. At 50 mg/day, Carvedilol () reduced sitting trough (12–hour) blood pressure by about 9/5.5 mm Hg; at 25 mg/day the effect was about 7.5/3.5 mm Hg. Comparisons of trough to peak blood pressure showed a trough to peak ratio for blood pressure response of about 65%. Heart rate fell by about 7.5 beats/minute at 50 mg/day. In general, as is true for other β-blockers, responses were smaller in black than non black patients. There were no age- or gender-related differences in response.
The peak antihypertensive effect occurred 1 to 2 hours after a dose. The dose-related blood pressure response was accompanied by a dose-related increase in adverse effects.
Carvedilol () How Supplied/storage And Handling
Carvedilol () tablets are available as follows:
3.125 mg – Each white, oval shaped, biconvex, film-coated tablet engraved with on one side and 175 on the other side contains 3.125 mg of Carvedilol () . Tablets are supplied in bottles of 100 (NDC 0228-2175-11) with a child-resistant closure.
6.25 mg – Each white, oval shaped, biconvex, film-coated tablet engraved with on one side and 176 on the other side contains 6.25 mg of Carvedilol () . Tablets are supplied in bottles of 100 (NDC 0228-2176-11) with a child-resistant closure.
12.5 mg – Each white, oval shaped, biconvex, film-coated tablet engraved with on one side and 177 on the other side contains 12.5 mg of Carvedilol () . Tablets are supplied in bottles of 100 (NDC 0228-2177-11) with a child-resistant closure.
25 mg – Each white, oval shaped, biconvex, film-coated tablet engraved with on one side and 178 on the other side contains 25 mg of Carvedilol () . Tablets are supplied in bottles of 100 (NDC 0228-2178-11) with a child-resistant closure.
Store below 30°C (86°F). Protect from moisture.Dispense in a tight, light-resistant container.
Carvedilol () Patient Counseling Information
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PHARMACIST-DETACH HERE AND GIVE INSTRUCTIONS TO PATIENT
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PATIENT INFORMATION — Rx Only
Carvedilol () TABLETS
Read the Patient Information that comes with Carvedilol () before you start taking it and each time you get a refill. There may be new information. This information does not take the place of talking with your doctor about your medical condition or your treatment. If you have any questions about Carvedilol () , ask your doctor or pharmacist.
WHAT IS Carvedilol () ?
Carvedilol () is a prescription medicine that belongs to a group of medicines called “beta-blockers”. Carvedilol () is used, often with other medicines, for the following conditions:
Carvedilol () is not approved for use in children under 18 years of age.
WHO SHOULD NOT TAKE Carvedilol () ?
Do not take Carvedilol () if you:
WHAT SHOULD I TELL MY DOCTOR BEFORE TAKING Carvedilol () ?
Tell your doctor about all of your medical conditions, including if you:
Keep a list of all the medicines you take. Show this list to your doctor and pharmacist before you start a new medicine.
HOW SHOULD I TAKE Carvedilol () ?
It is important for you to take your medicine every day as directed by your doctor. If you stop taking Carvedilol () suddenly, you could have chest pain and/or a heart attack. If your doctor decides that you should stop taking Carvedilol () , your doctor may slowly lower your dose over a period of time before stopping it completely.
WHAT SHOULD I AVOID WHILE TAKING Carvedilol () ?
Carvedilol () can cause you to feel dizzy, tired, or faint. Do not drive a car, use machinery, or do anything that needs you to be alert if you have these symptoms.
WHAT ARE POSSIBLE SIDE EFFECTS OF Carvedilol () ?
Other side effects of Carvedilol () include shortness of breath, weight gain, diarrhea, and fewer tears or dry eyes that become bothersome if you wear contact lenses.
Call your doctor if you have any side effects that bother you or don’t go away.
How should I store Carvedilol () ?
GENERAL INFORMATION ABOUT Carvedilol ()
Medicines are sometimes prescribed for conditions other than those described in patient information leaflets. Do not use Carvedilol () for a condition for which it was not prescribed. Do not give Carvedilol () to other people, even if they have the same symptoms you have. It may harm them.
This leaflet summarizes the most important information about Carvedilol () . If you would like more information, talk with your doctor. You can ask your doctor or pharmacist for information about Carvedilol () that is written for healthcare professionals. You can also find out more about Carvedilol () by calling 1-800-432-8534. This call is free.
WHAT ARE THE INGREDIENTS IN Carvedilol () ?
Active Ingredient: Carvedilol ()
Inactive Ingredients: Colloidal silicon dioxide, crospovidone, hypromellose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, sodium citrate, sucrose, and titanium dioxide
Carvedilol () tablets come in the following strengths: 3.125 mg, 6.25 mg, 12.5 mg, 25 mg
Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
Manufactured by:Shasun Chemicals & Drugs Limited. Unit 11R.S. No.: 32, 33 & 34, PIMS Road,Periyakalapet, Pondicherry – 605014. IndiaFor: Actavis Elizabeth LLC200 Elmora Avenue, Elizabeth, NJ 07207 USA
50427PM40-9054Revised: August 2008
