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TENORMIN
Overview
What is TENORMIN?
TENORMIN (atenolol), a synthetic, beta-selective (cardioselective) adrenoreceptor blocking agent, may be chemically described as benzeneacetamide, 4 -[2'-hydroxy-3'-[(1- methylethyl) amino] propoxy]-. The molecular and structural formulas are:
Atenolol (free base) has a molecular weight of 266. It is a relatively polar hydrophilic compound with a water solubility of 26.5 mg/mL at 37°C and a log partition coefficient (octanol/water) of 0.23. It is freely soluble in 1N HCl (300 mg/mL at 25°C) and less soluble in chloroform (3 mg/mL at 25°C).
TENORMIN is available as 25, 50 and 100 mg tablets for oral administration.
Inactive Ingredients: Magnesium stearate, microcrystalline cellulose, povidone, sodium starch glycolate.
What does TENORMIN look like?
What are the available doses of TENORMIN?
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How should I use TENORMIN?
Hypertension
TENORMIN is indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure lowers the risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including atenolol.
Control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. Many patients will require more than 1 drug to achieve blood pressure goals. For specific advice on goals and management, see published guidelines, such as those of the National High Blood Pressure Education Program’s Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC).
Numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. The largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly.
Elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmHg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. Relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal.
Some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (eg, on angina, heart failure, or diabetic kidney disease). These considerations may guide selection of therapy.
TENORMIN may be administered with other antihypertensive agents.
Angina Pectoris Due to Coronary Atherosclerosis
Acute Myocardial Infarction
The initial dose of TENORMIN is 50 mg given as one tablet a day either alone or added to diuretic therapy. The full effect of this dose will usually be seen within one to two weeks. If an optimal response is not achieved, the dosage should be increased to TENORMIN 100 mg given as one tablet a day. Increasing the dosage beyond 100 mg a day is unlikely to produce any further benefit.
TENORMIN may be used alone or concomitantly with other antihypertensive agents including thiazide-type diuretics, hydralazine, prazosin, and alpha-methyldopa.
What interacts with TENORMIN?
TENORMIN is contraindicated in sinus bradycardia, heart block greater than first degree, cardiogenic shock, and overt cardiac failure. (See .)
TENORMIN is contraindicated in those patients with a history of hypersensitivity to the atenolol or any of the drug product’s components.
What are the warnings of TENORMIN?
Cardiac Failure
Sympathetic stimulation is necessary in supporting circulatory function in congestive heart failure, and beta blockade carries the potential hazard of further depressing myocardial contractility and precipitating more severe failure.
In patients with acute myocardial infarction, cardiac failure which is not promptly and effectively controlled by 80 mg of intravenous furosemide or equivalent therapy is a contraindication to beta-blocker treatment.
In Patients Without a History of Cardiac Failure
Continued depression of the myocardium with beta-blocking agents over a period of time can, in some cases, lead to cardiac failure. At the first sign or symptom of impending cardiac failure, patients should be treated appropriately according to currently recommended guidelines, and the response observed closely. If cardiac failure continues despite adequate treatment, TENORMIN should be withdrawn. (See )
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Concomitant Use of Calcium Channel Blockers
Bradycardia and heart block can occur and the left ventricular end diastolic pressure can rise when beta-blockers are administered with verapamil or diltiazem. Patients with pre-existing conduction abnormalities or left ventricular dysfunction are particularly susceptible. (See .)
Bronchospastic Diseases
PATIENTS WITH BRONCHOSPASTIC DISEASE SHOULD, IN GENERAL, NOT RECEIVE BETA BLOCKERS. Because of its relative beta selectivity, however, TENORMIN may be used with caution in patients with bronchospastic disease who do not respond to, or cannot tolerate, other antihypertensive treatment. Since beta selectivity is not absolute, the lowest possible dose of TENORMIN should be used with therapy initiated at 50 mg and a beta-stimulating agent (bronchodilator) should be made available. If dosage must be increased, dividing the dose should be considered in order to achieve lower peak blood levels.
Major Surgery
Chronically administered beta-blocking therapy should not be routinely withdrawn prior to major surgery, however the impaired ability of the heart to respond to reflex adrenergic stimuli may augment the risks of general anesthesia and surgical procedures.
Diabetes and Hypoglycemia
TENORMIN should be used with caution in diabetic patients if a beta-blocking agent is required. Beta blockers may mask tachycardia occurring with hypoglycemia, but other manifestations such as dizziness and sweating may not be significantly affected. At recommended doses TENORMIN does not potentiate insulin-induced hypoglycemia and, unlike nonselective beta blockers, does not delay recovery of blood glucose to normal levels.
Thyrotoxicosis
Beta-adrenergic blockade may mask certain clinical signs (eg, tachycardia) of hyperthyroidism. Abrupt withdrawal of beta blockade might precipitate a thyroid storm; therefore, patients suspected of developing thyrotoxicosis from whom TENORMIN therapy is to be withdrawn should be monitored closely. (See .)
Untreated Pheochromocytoma
TENORMIN should not be given to patients with untreated pheochromocytoma.
Pregnancy and Fetal Injury
Atenolol can cause fetal harm when administered to a pregnant woman. Atenolol crosses the placental barrier and appears in cord blood. Administration of atenolol, starting in the second trimester of pregnancy, has been associated with the birth of infants that are small for gestational age. No studies have been performed on the use of atenolol in the first trimester and the possibility of fetal injury cannot be excluded. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to the fetus.
Neonates born to mothers who are receiving TENORMIN at parturition or breast-feeding may be at risk for hypoglycemia and bradycardia. Caution should be exercised when TENORMIN is administered during pregnancy or to a woman who is breast-feeding. (See .)
Atenolol has been shown to produce a dose-related increase in embryo/fetal resorptions in rats at doses equal to or greater than 50 mg/kg/day or 25 or more times the maximum recommended human antihypertensive dose. Although similar effects were not seen in rabbits, the compound was not evaluated in rabbits at doses above 25 mg/kg/day or 12.5 times the maximum recommended human antihypertensive dose.
What are the precautions of TENORMIN?
General
Patients already on a beta blocker must be evaluated carefully before TENORMIN is administered. Initial and subsequent TENORMIN dosages can be adjusted downward depending on clinical observations including pulse and blood pressure. TENORMIN may aggravate peripheral arterial circulatory disorders.
Impaired Renal Function
The drug should be used with caution in patients with impaired renal function. (See .)
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Drug Interactions
Catecholamine-depleting drugs (eg, reserpine) may have an additive effect when given with beta-blocking agents. Patients treated with TENORMIN plus a catecholamine depletor should therefore be closely observed for evidence of hypotension and/or marked bradycardia which may produce vertigo, syncope, or postural hypotension.
Calcium channel blockers may also have an additive effect when given with TENORMIN (See ).
Disopyramide is a Type I antiarrhythmic drug with potent negative inotropic and chronotropic effects. Disopyramide has been associated with severe bradycardia, asystole and heart failure when administered with beta blockers.
Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with beta blockers.
Beta blockers may exacerbate the rebound hypertension which can follow the withdrawal of clonidine. If the two drugs are coadministered, the beta blocker should be withdrawn several days before the gradual withdrawal of clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta blockers should be delayed for several days after clonidine administration has stopped.
Concomitant use of prostaglandin synthase inhibiting drugs, eg, indomethacin, may decrease the hypotensive effects of beta blockers.
Information on concurrent usage of atenolol and aspirin is limited. Data from several studies, ie, TIMI-II, ISIS-2, currently do not suggest any clinical interaction between aspirin and beta blockers in the acute myocardial infarction setting.
While taking beta blockers, patients with a history of anaphylactic reaction to a variety of allergens may have a more severe reaction on repeated challenge, either accidental, diagnostic or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat the allergic reaction.
Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia.
Carcinogenesis, Mutagenesis, Impairment of Fertility
Two long-term (maximum dosing duration of 18 or 24 months) rat studies and one long-term (maximum dosing duration of 18 months) mouse study, each employing dose levels as high as 300 mg/kg/day or 150 times the maximum recommended human antihypertensive dose, did not indicate a carcinogenic potential of atenolol. A third (24 month) rat study, employing doses of 500 and 1,500 mg/kg/day (250 and 750 times the maximum recommended human antihypertensive dose) resulted in increased incidences of benign adrenal medullary tumors in males and females, mammary fibroadenomas in females, and anterior pituitary adenomas and thyroid parafollicular cell carcinomas in males. No evidence of a mutagenic potential of atenolol was uncovered in the dominant lethal test (mouse), cytogenetics test (Chinese hamster) or Ames test ().
Fertility of male or female rats (evaluated at dose levels as high as 200 mg/kg/day or 100 times the maximum recommended human dose) was unaffected by atenolol administration.
Animal Toxicology
Chronic studies employing oral atenolol performed in animals have revealed the occurrence of vacuolation of epithelial cells of Brunner's glands in the duodenum of both male and female dogs at all tested dose levels of atenolol (starting at 15 mg/kg/day or 7.5 times the maximum recommended human antihypertensive dose) and increased incidence of atrial degeneration of hearts of male rats at 300 but not 150 mg atenolol/kg/day (150 and 75 times the maximum recommended human antihypertensive dose, respectively).
Usage in Pregnancy
See .
Nursing Mothers
Atenolol is excreted in human breast milk at a ratio of 1.5 to 6.8 when compared to the concentration in plasma. Caution should be exercised when TENORMIN is administered to a nursing woman. Clinically significant bradycardia has been reported in breast-fed infants. Premature infants, or infants with impaired renal function, may be more likely to develop adverse effects.
Neonates born to mothers who are receiving TENORMIN at parturition or breast-feeding may be at risk for hypoglycemia and bradycardia. Caution should be exercised when TENORMIN is administered during pregnancy or to a woman who is breast-feeding (See ).
Pediatric Use
Safety and effectiveness in pediatric patients have not been established.
Geriatric Use
Hypertension and Angina Pectoris Due to Coronary Atherosclerosis:
Clinical studies of TENORMIN did not include sufficient number of patients aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
Acute Myocardial Infarction:
Of the 8,037 patients with suspected acute myocardial infarction randomized to TENORMIN in the ISIS-1 trial (See ), 33% (2,644) were 65 years of age and older. It was not possible to identify significant differences in efficacy and safety between older and younger patients; however, elderly patients with systolic blood pressure < 120 mmHg seemed less likely to benefit (See ).
In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. Evaluation of patients with hypertension or myocardial infarction should always include assessment of renal function.
What are the side effects of TENORMIN?
Most adverse effects have been mild and transient.
The frequency estimates in the following table were derived from controlled studies in hypertensive patients in which adverse reactions were either volunteered by the patient (US studies) or elicited, eg, by checklist (foreign studies). The reported frequency of elicited adverse effects was higher for both TENORMIN and placebo-treated patients than when these reactions were volunteered. Where frequency of adverse effects of TENORMIN and placebo is similar, causal relationship to TENORMIN is uncertain.
| CARDIOVASCULAR | ||||
| Bradycardia | 3 | 0 | 3 | 0 |
| Cold Extremities | 0 | 0.5 | 12 | 5 |
| Postural Hypotension | 2 | 1 | 4 | 5 |
| Leg Pain | 0 | 0.5 | 3 | 1 |
| CENTRAL NERVOUS SYSTEM/ | NEUROMUSCULAR | |||
| Dizziness | 4 | 1 | 13 | 6 |
| Vertigo | 2 | 0.5 | 2 | 0.2 |
| Light-headedness | 1 | 0 | 3 | 0.7 |
| Tiredness | 0.6 | 0.5 | 26 | 13 |
| Fatigue | 3 | 1 | 6 | 5 |
| Lethargy | 1 | 0 | 3 | 0.7 |
| Drowsiness | 0.6 | 0 | 2 | 0.5 |
| Depression | 0.6 | 0.5 | 12 | 9 |
| Dreaming | 0 | 0 | 3 | 1 |
| GASTROINTESTINAL | ||||
| Diarrhea | 2 | 0 | 3 | 2 |
| Nausea | 4 | 1 | 3 | 1 |
| RESPIRATORY (see ) | ||||
| Wheeziness | 0 | 0 | 3 | 3 |
| Dyspnea | 0.6 | 1 | 6 | 4 |
Acute Myocardial Infarction
In a series of investigations in the treatment of acute myocardial infarction, bradycardia and hypotension occurred more commonly, as expected for any beta blocker, in atenolol-treated patients than in control patients. However, these usually responded to atropine and/or to withholding further dosage of atenolol. The incidence of heart failure was not increased by atenolol. Inotropic agents were infrequently used. The reported frequency of these and other events occurring during these investigations is given in the following table.
In a study of 477 patients, the following adverse events were reported during either intravenous and/or oral atenolol administration:
In the subsequent International Study of Infarct Survival (ISIS-1) including over 16,000 patients of whom 8,037 were randomized to receive TENORMIN treatment, the dosage of intravenous and subsequent oral TENORMIN was either discontinued or reduced for the following reasons:
During postmarketing experience with TENORMIN, the following have been reported in temporal relationship to the use of the drug: elevated liver enzymes and/or bilirubin, hallucinations, headache, impotence, Peyronie's disease, postural hypotension which may be associated with syncope, psoriasiform rash or exacerbation of psoriasis, psychoses, purpura, reversible alopecia, thrombocytopenia, visual disturbance, sick sinus syndrome, and dry mouth. TENORMIN, like other beta blockers, has been associated with the development of antinuclear antibodies (ANA), lupus syndrome, and Raynaud’s phenomenon.
| Bradycardia | 43 | (18%) | 24 | (10%) |
| Hypotension | 60 | (25%) | 34 | (15%) |
| Bronchospasm | 3 | (1.2%) | 2 | (0.9%) |
| Heart Failure | 46 | (19%) | 56 | (24%) |
| Heart Block | 11 | (4.5%) | 10 | (4.3%) |
| BBB + Major | 16 | (6.6%) | 28 | (12%) |
| 28 | (11.5%) | 45 | (19%) | |
| Atrial Fibrillation | 12 | (5%) | 29 | (11%) |
| Atrial Flutter | 4 | (1.6%) | 7 | (3%) |
| 39 | (16%) | 52 | (22%) | |
| Cardiac Reinfarction | 0 | (0%) | 6 | (2.6%) |
| Total Cardiac Arrests | 4 | (1.6%) | 16 | (6.9%) |
| 4 | (1.6%) | 12 | (5.1%) | |
| Deaths | 7 | (2.9%) | 16 | (6.9%) |
| Cardiogenic Shock | 1 | (0.4%) | 4 | (1.7%) |
| 0 | (0%) | 2 | (0.9%) | |
| 0 | (0%) | 2 | (0.9%) | |
| Renal Failure | 1 | (0.4%) | 0 | (0%) |
| Pulmonary Emboli | 3 | (1.2%) | 0 | (0%) |
| Reasons for Reduced Dosage | ||||
| Hypotension/Bradycardia | 105 | (1.3%) | 1168 | (14.5%) |
| Cardiogenic Shock | 4 | (.04%) | 35 | (.44%) |
| Reinfarction | 0 | (0%) | 5 | (.06%) |
| Cardiac Arrest | 5 | (.06%) | 28 | (.34%) |
| Heart Block (> first degree) | 5 | (.06%) | 143 | (1.7%) |
| Cardiac Failure | 1 | (.01%) | 233 | (2.9%) |
| Arrhythmias | 3 | (.04%) | 22 | (.27%) |
| Bronchospasm | 1 | (.01%) | 50 | (.62%) |
What should I look out for while using TENORMIN?
TENORMIN is contraindicated in sinus bradycardia, heart block greater than first degree, cardiogenic shock, and overt cardiac failure. (See .)
TENORMIN is contraindicated in those patients with a history of hypersensitivity to the atenolol or any of the drug product’s components.
What might happen if I take too much TENORMIN?
Overdosage with TENORMIN has been reported with patients surviving acute doses as high as 5 g. One death was reported in a man who may have taken as much as 10 g acutely.
The predominant symptoms reported following TENORMIN overdose are lethargy, disorder of respiratory drive, wheezing, sinus pause and bradycardia. Additionally, common effects associated with overdosage of any beta-adrenergic blocking agent and which might also be expected in TENORMIN overdose are congestive heart failure, hypotension, bronchospasm and/or hypoglycemia.
Treatment of overdose should be directed to the removal of any unabsorbed drug by induced emesis, gastric lavage, or administration of activated charcoal. TENORMIN can be removed from the general circulation by hemodialysis. Other treatment modalities should be employed at the physician's discretion and may include:
BRADYCARDIA: Atropine intravenously. If there is no response to vagal blockade, give isoproterenol cautiously. In refractory cases, a transvenous cardiac pacemaker may be indicated.
HEART BLOCK (SECOND OR THIRD DEGREE): Isoproterenol or transvenous cardiac pacemaker.
CARDIAC FAILURE: Digitalize the patient and administer a diuretic. Glucagon has been reported to be useful.
HYPOTENSION: Vasopressors such as dopamine or norepinephrine (levarterenol). Monitor blood pressure continuously.
BRONCHOSPASM: A beta stimulant such as isoproterenol or terbutaline and/or aminophylline.
HYPOGLYCEMIA: Intravenous glucose.
Based on the severity of symptoms, management may require intensive support care and facilities for applying cardiac and respiratory support.
How should I store and handle TENORMIN?
Store at 20° to 25°C (68° to 77°F); excursions permitted from 15° to 30°C (59° to 86°F). [See USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Protect from light and moisture.Product: 68151-3727NDC: 68151-3727-1 1 mL in a SYRINGE, PLASTIC Product: 68151-3727NDC: 68151-3727-1 1 mL in a SYRINGE, PLASTIC
Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
In man, absorption of an oral dose is rapid and consistent but incomplete. Approximately 50% of an oral dose is absorbed from the gastrointestinal tract, the remainder being excreted unchanged in the feces. Peak blood levels are reached between two (2) and four (4) hours after ingestion. Unlike propranolol or metoprolol, but like nadolol, TENORMIN undergoes little or no metabolism by the liver, and the absorbed portion is eliminated primarily by renal excretion. Over 85% of an intravenous dose is excreted in urine within 24 hours compared with approximately 50% for an oral dose. TENORMIN also differs from propranolol in that only a small amount (6%-16%) is bound to proteins in the plasma. This kinetic profile results in relatively consistent plasma drug levels with about a fourfold interpatient variation.
The elimination half-life of oral TENORMIN is approximately 6 to 7 hours, and there is no alteration of the kinetic profile of the drug by chronic administration. Following intravenous administration, peak plasma levels are reached within 5 minutes. Declines from peak levels are rapid (5- to 10-fold) during the first 7 hours; thereafter, plasma levels decay with a half-life similar to that of orally administered drug. Following oral doses of 50 mg or 100 mg, both beta-blocking and antihypertensive effects persist for at least 24 hours. When renal function is impaired, elimination of TENORMIN is closely related to the glomerular filtration rate; significant accumulation occurs when the creatinine clearance falls below 35 mL/min/1.73m. (See .)
Non-Clinical Toxicology
TENORMIN is contraindicated in sinus bradycardia, heart block greater than first degree, cardiogenic shock, and overt cardiac failure. (See .)TENORMIN is contraindicated in those patients with a history of hypersensitivity to the atenolol or any of the drug product’s components.
Catecholamine-depleting drugs (eg, reserpine) may have an additive effect when given with beta-blocking agents. Patients treated with TENORMIN plus a catecholamine depletor should therefore be closely observed for evidence of hypotension and/or marked bradycardia which may produce vertigo, syncope, or postural hypotension.
Calcium channel blockers may also have an additive effect when given with TENORMIN (See ).
Disopyramide is a Type I antiarrhythmic drug with potent negative inotropic and chronotropic effects. Disopyramide has been associated with severe bradycardia, asystole and heart failure when administered with beta blockers.
Amiodarone is an antiarrhythmic agent with negative chronotropic properties that may be additive to those seen with beta blockers.
Beta blockers may exacerbate the rebound hypertension which can follow the withdrawal of clonidine. If the two drugs are coadministered, the beta blocker should be withdrawn several days before the gradual withdrawal of clonidine. If replacing clonidine by beta-blocker therapy, the introduction of beta blockers should be delayed for several days after clonidine administration has stopped.
Concomitant use of prostaglandin synthase inhibiting drugs, eg, indomethacin, may decrease the hypotensive effects of beta blockers.
Information on concurrent usage of atenolol and aspirin is limited. Data from several studies, ie, TIMI-II, ISIS-2, currently do not suggest any clinical interaction between aspirin and beta blockers in the acute myocardial infarction setting.
While taking beta blockers, patients with a history of anaphylactic reaction to a variety of allergens may have a more severe reaction on repeated challenge, either accidental, diagnostic or therapeutic. Such patients may be unresponsive to the usual doses of epinephrine used to treat the allergic reaction.
Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia.
Patients already on a beta blocker must be evaluated carefully before TENORMIN is administered. Initial and subsequent TENORMIN dosages can be adjusted downward depending on clinical observations including pulse and blood pressure. TENORMIN may aggravate peripheral arterial circulatory disorders.
In addition, a variety of adverse effects have been reported with other beta-adrenergic blocking agents, and may be considered potential adverse effects of TENORMIN.
Hematologic:
Allergic:
Central Nervous System:
Gastrointestinal:
Other:
Miscellaneous:
The oculomucocutaneous syndrome associated with the beta blocker practolol has not been reported with TENORMIN. Furthermore, a number of patients who had previously demonstrated established practolol reactions were transferred to TENORMIN therapy with subsequent resolution or quiescence of the reaction.
Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
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