ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : -56 مورد

Nadolol: Pediatric drug information

Nadolol: Pediatric drug information
2025© UpToDate, Inc. and its affiliates and/or licensors. All Rights Reserved.
For additional information see "Nadolol: Drug information" and "Nadolol: Patient drug information"

For abbreviations, symbols, and age group definitions show table
ALERT: US Boxed Warning
Exacerbation of ischemic heart disease following abrupt withdrawal:

Hypersensitivity to catecholamines has been observed in patients withdrawn from beta-blocker therapy; exacerbation of angina and, in some cases, myocardial infarction have occurred after abrupt discontinuation of such therapy. When discontinuing chronically administered nadolol, particularly in patients with ischemic heart disease, the dosage should be gradually reduced over a period of 1 to 2 weeks and the patient should be carefully monitored. If angina markedly worsens or acute coronary insufficiency develops, nadolol administration should be reinstituted promptly, at least temporarily, and other measures appropriate for the management of unstable angina should be taken. Patients should be warned against interruption or discontinuation of therapy without the physician's advice. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue nadolol therapy abruptly, even in patients treated only for hypertension.

Brand Names: US
  • Corgard [DSC]
Brand Names: Canada
  • APO-Nadolol;
  • MINT-Nadolol
Therapeutic Category
  • Antianginal Agent;
  • Antiarrhythmic Agent, Class II;
  • Antihypertensive Agent;
  • Antimigraine Agent;
  • Beta-Adrenergic Blocker
Dosing: Neonatal
Supraventricular tachycardia, treatment

Supraventricular tachycardia (SVT), treatment: Very limited data available: Term neonates: Oral: Usual dose: 0.5 to 1 mg/kg/day in 1 to 2 divided doses (Ref). Dosing based on a retrospective study of 20 patients with SVT (median age: 30 days [range: 10 to 390 days]) treated with nadolol 0.5 to 2 mg/kg/day (80% of patients responded to 1 mg/kg/day) in 1 to 2 divided doses; 85% of patients were SVT free at 1 year (Ref).

Dosing: Pediatric
Supraventricular tachycardia, treatment

Supraventricular tachycardia (SVT), treatment: Limited data available: Infants, Children, and Adolescents: Oral: Initial: 0.5 to 1 mg/kg/day once daily or in 2 divided doses; increase dose gradually based on clinical response to a maximum of 2.5 mg/kg/day (Ref). Dosing based on a trial of 26 pediatric patients (age range: 3 months to 15 years) which showed SVT was well controlled with a median dose of 1 mg/kg/day (Ref) and a retrospective study of 20 patients with SVT (age range: 10 to 390 days [median age: 30 days]) treated with nadolol 0.5 to 2 mg/kg/day (80% of patients responded to1 mg/kg/day) in 1 to 2 divided doses; 85% of patients were SVT free at 1 year (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Pediatric

There are no pediatric-specific recommendations; based on experience in adult patients, dosing adjustment suggested.

Dosing: Liver Impairment: Pediatric

There are no dosage adjustments provided in the manufacturer's labeling.

Dosing: Adult

(For additional information see "Nadolol: Drug information")

Angina, chronic stable

Angina, chronic stable:

Note: For vasospastic angina, beta-blockers are not recommended; calcium channel blockers and nitrates are preferred. For nonvasospastic angina, titrate beta-blocker to relieve angina or equivalent symptoms (Ref).

Oral: Initial: 40 mg once daily; titrate as needed based on patient response in 40 to 80 mg increments every 3 to 7 days up to 240 mg once daily; usual dose: 40 to 80 mg once daily.

Atrial fibrillation/flutter, maintenance of ventricular rate control

Atrial fibrillation/flutter, maintenance of ventricular rate control (off-label use): Oral: Usual dosage range: 10 to 240 mg once daily; start at the lower end of the usual dosage range and increase gradually as tolerated to achieve ventricular rate control (Ref).

Gastroesophageal variceal hemorrhage prophylaxis in patients with cirrhosis

Gastroesophageal variceal hemorrhage prophylaxis in patients with cirrhosis (off-label use): Note: May use for primary or secondary prophylaxis. Primary prophylaxis is indicated for patients with cirrhosis at high risk of bleeding (identified by medium/large varices, variceal red wale markings on endoscopy, or decompensation with small varices) (Ref).

Oral: Initial: 20 to 40 mg once daily (Ref); adjust every 2 to 3 days to maximal tolerated dose or until heart rate is ~55 to 60 beats per minute (Ref). If systolic BP is <90 mm Hg, reduce dose or discontinue. Some experts recommend a maximum dose of 160 mg/day in patients without ascites and 80 mg/day in patients with ascites (Ref).

Hypertension

Hypertension (alternative agent):

Note: Not recommended in the absence of specific comorbidities (eg, ischemic heart disease, migraine) (Ref).

Oral: Initial: 40 mg once daily; titrate as needed based on patient response in 40 to 80 mg increments up to 320 mg once daily; usual dosage range: 40 to 120 mg once daily (Ref).

Migraine, prevention

Migraine, prevention (off-label use) :

Note: An adequate trial for assessment of effect is considered to be at least 2 to 3 months at a therapeutic dose (Ref).

Oral: Initial: 20 mg once daily; may increase dose based on response and tolerability up to 240 mg/day (Ref).

Supraventricular tachycardia

Supraventricular tachycardia (atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, focal atrial tachycardia) (off-label use): Oral: Initial: 40 mg once daily; titrate as tolerated to a dose that alleviates symptoms up to 320 mg once daily (Ref).

Thyrotoxicosis

Thyrotoxicosis (off-label use):

Note: For control of cardiovascular effects until euthyroidism is established (Ref).

Oral: 40 to 160 mg once daily (Ref).

Ventricular premature beats, symptomatic

Ventricular premature beats, symptomatic (off-label use): Oral: Dosage range: 40 to 320 mg once daily; start at the lower end of the dosage range and titrate based on response and tolerability (Ref).

Ventricular tachycardia, prevention

Ventricular tachycardia, prevention (off-label use):

Note: For catecholaminergic polymorphic ventricular tachycardia and ventricular tachycardia due to congenital long QT syndrome, nadolol is a preferred beta blocker (Ref).

Oral: Dosage range: 40 to 320 mg once daily; start at the lower end of the dosage range and titrate based on response and tolerability (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

Altered kidney function:

CrCl >50 mL/minute/1.73 m2: Administer every 24 hours.

CrCl 31 to 50 mL/minute/1.73 m2: Administer every 24 to 36 hours.

CrCl 10 to 30 mL/minute/1.73 m2: Administer every 24 to 48 hours.

CrCl <10 mL/minute/1.73 m2: Administer every 40 to 60 hours.

Hemodialysis, intermittent (thrice weekly): Administer 3 times per week after hemodialysis (Ref).

Dosing: Liver Impairment: Adult

There are no dosage adjustments provided in the manufacturer’s labeling.

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.

1% to 10%:

Cardiovascular: Bradycardia, cardiac arrhythmia, cardiac conduction disorder, heart failure, hypotension, peripheral vascular insufficiency, Raynaud disease

Nervous system: Dizziness, fatigue

<1%:

Dermatologic: Diaphoresis, pruritus, skin rash, transient alopecia, xeroderma

Endocrine & metabolic: Decreased libido, weight gain

Gastrointestinal: Abdominal distress, anorexia, bloating, constipation, diarrhea, dyspepsia, flatulence, nausea, vomiting, xerostomia

Genitourinary: Erectile dysfunction

Hypersensitivity: Facial edema

Nervous system: Behavioral changes, headache, paresthesia, sedated state, slurred speech

Ophthalmic: Blurred vision, dry eye syndrome

Otic: Tinnitus

Respiratory: Bronchospasm, cough, nasal congestion

Frequency not defined: Cardiovascular: Acute myocardial infarction (after abrupt discontinuation), exacerbation of angina pectoris (after abrupt discontinuation)

Postmarketing:

Cardiovascular: Complete atrioventricular block, first-degree atrioventricular block, thrombosis

Dermatologic: Bullous pemphigoid, psoriasis (Song 2021), purpuric rash

Gastrointestinal: Ischemic colitis

Genitourinary: Peyronie disease

Hematologic & oncologic: Agranulocytosis

Hepatic: Increased liver enzymes

Nervous system: Amnesia, body pain, cognitive dysfunction, depression (including catatonia; reversible), disorientation, emotional lability, hallucination, sleep disturbance

Neuromuscular & skeletal: Laryngospasm

Ophthalmic: Visual disturbance

Respiratory: Pharyngitis, respiratory distress

Miscellaneous: Fever

Contraindications

Bronchial asthma; sinus bradycardia; heart block greater than first degree (except in patients with a functioning artificial pacemaker); cardiogenic shock; uncompensated cardiac failure

Canadian labeling: Additional contraindications (not in US labeling): Hypersensitivity to nadolol or any component of the formulation; cor pulmonale; anesthesia with agents that produce myocardial depression; allergic rhinitis, bronchospasm, or severe chronic obstructive pulmonary disease (COPD)

Warnings/Precautions

Concerns related to adverse events:

• Anaphylactic reactions: Use caution with history of severe anaphylaxis to allergens; patients taking beta-blockers may become more sensitive to repeated challenges. Treatment of anaphylaxis (eg, epinephrine) in patients taking beta-blockers may be ineffective or promote undesirable effects.

Disease-related concerns:

• Bronchospastic disease: In general, patients with bronchospastic disease should not receive beta-blockers; if used at all, should be used cautiously with close monitoring.

• Conduction abnormality: Consider preexisting conditions such as sick sinus syndrome before initiating.

• Diabetes: Use with caution in patients with diabetes mellitus; may potentiate hypoglycemia and/or mask signs and symptoms.

• Heart failure: Use with caution in patients with compensated heart failure and monitor for a worsening of the condition (efficacy of nadolol in HF has not been demonstrated).

• Kidney impairment: Use with caution in patients with kidney impairment; dosage adjustments are required.

• Myasthenia gravis: Use with caution in patients with myasthenia gravis.

• Peripheral vascular disease (PVD) and Raynaud disease: Can precipitate or aggravate symptoms of arterial insufficiency in patients with PVD and Raynaud disease. Use with caution and monitor for progression of arterial obstruction.

• Pheochromocytoma (untreated): Adequate alpha-blockade is required prior to use of any beta-blocker.

• Psoriasis: Beta-blocker use has been associated with induction or exacerbation of psoriasis, but cause and effect have not been firmly established.

• Thyroid disease: May mask signs of hyperthyroidism (eg, tachycardia). If hyperthyroidism is suspected, carefully manage and monitor; abrupt withdrawal may exacerbate symptoms of hyperthyroidism or precipitate thyroid storm.

• Vasospastic angina: Beta-blockers without alpha1-adrenergic receptor blocking activity should be avoided in patients with vasospastic angina since unopposed alpha1-adrenergic receptors mediate coronary vasoconstriction and can worsen anginal symptoms (Mayer 1998).

Special populations:

• Older adults: Bradycardia may be observed more frequently in patients >65 years of age; dosage reductions may be necessary.

Other warnings/precautions:

• Abrupt withdrawal: [US Boxed Warning]: Beta-blocker therapy should not be withdrawn abruptly (particularly in patients with CAD), but gradually tapered to avoid acute tachycardia, hypertension, and/or ischemia. Severe exacerbation of angina, ventricular arrhythmias, and myocardial infarction (MI) have been reported following abrupt withdrawal of beta-blocker therapy. Temporary but prompt resumption of beta-blocker therapy may be indicated with worsening of angina or acute coronary insufficiency.

• Major surgery: Chronic beta-blocker therapy should not be routinely withdrawn prior to major surgery.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Tablet, Oral:

Corgard: 20 mg [DSC] [contains corn starch, fd&c blue #2 (indigotine,indigo carmine)]

Corgard: 20 mg [DSC] [contains fd&c blue #2 (indigotine,indigo carmine)]

Corgard: 40 mg [DSC] [contains corn starch, fd&c blue #2 (indigotine,indigo carmine)]

Corgard: 40 mg [DSC] [contains fd&c blue #2 (indigotine,indigo carmine)]

Corgard: 80 mg [DSC] [scored; contains fd&c blue #2 (indigotine,indigo carmine)]

Generic: 20 mg, 40 mg, 80 mg

Generic Equivalent Available: US

Yes

Pricing: US

Tablets (Nadolol Oral)

20 mg (per each): $0.07 - $4.25

40 mg (per each): $0.12 - $4.01

80 mg (per each): $0.26 - $5.51

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Generic: 40 mg, 80 mg, 160 mg

Extemporaneous Preparations

10 mg/mL oral solution

A 10 mg/mL nadolol oral suspension may be made with tablets in a 1:1 mixture of Ora-Plus and Ora-Sweet. Crush ten 80 mg nadolol tablets in a glass mortar and reduce to a fine powder. Prepare the vehicle by mixing 35 mL of Ora-Plus and 35 mL of Ora-Sweet; stir vigorously. Add a small amount of the vehicle to the powder to make a smooth suspension. Then add remaining vehicle in geometric proportions and mix well. Transfer the mixture to a 4-ounce amber plastic prescription bottle. Rinse mortar with a small quantity of the vehicle sufficient to make a final volume of 80 mL. Label "shake well" and "refrigerate." Stable for 30 days when stored in amber plastic prescription bottles under refrigeration.

Nahata MC, Pai VB. Pediatric Drug Formulations. 6th ed. Cincinnati, OH: Harvey Whitney Books, 2011.
Administration: Pediatric

Oral: May administer without regard to meals.

Administration: Adult

Oral: May be administered without regard to meals.

Storage/Stability

Store at room temperature; avoid excessive heat. Protect from light.

Use

Treatment of hypertension, alone or in combination with other agents (FDA approved in adults); treatment of angina pectoris (FDA approved in adults); has also been used for the treatment of ventricular arrhythmias.

Medication Safety Issues
Sound-alike/look-alike issues:

Corgard may be confused with Cognex, Coreg

International issues:

Nadolol may be confused with Mandol brand name for cefamandole [Belgium, Netherlands, New Zealand, Russia]

Older Adult: High-Risk Medication:

Nadolol is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication in older adults (≥65 years of age). Some disease states of concern include bradycardia, heart block, diabetes, and severe symptomatic aortic stenosis. Use is not recommended as monotherapy for the treatment of uncomplicated hypertension (O’Mahony 2023).

Metabolism/Transport Effects

Substrate of MATE1/2-K, OCT1, OCT2, P-glycoprotein (Major with inhibitors), P-glycoprotein (Minor with inducers); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program

Acetylcholinesterase Inhibitors: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Alfuzosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Alpha2-Agonists: Beta-Blockers may increase rebound hypertensive effects of Alpha2-Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Alpha2-Agonists may increase AV-blocking effects of Beta-Blockers. Sinus node dysfunction may also be enhanced. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Risk D: Consider Therapy Modification

Amifostine: Blood Pressure Lowering Agents may increase hypotensive effects of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider Therapy Modification

Amiodarone: May increase bradycardic effects of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase serum concentration of Beta-Blockers. Risk C: Monitor

Amphetamines: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Antidiabetic Agents: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Antidiabetic Agents. Beta-Blockers (Nonselective) may increase adverse/toxic effects of Antidiabetic Agents. Specifically, beta-blockers may mask the hypoglycemic symptoms of antidiabetic agents. Risk C: Monitor

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may increase hypotensive effects of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor

Arginine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Barbiturates: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Benperidol: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Beta2-Agonists: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Beta2-Agonists. Risk X: Avoid

Bradycardia-Causing Agents: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Brigatinib: May decrease antihypertensive effects of Antihypertensive Agents. Brigatinib may increase bradycardic effects of Antihypertensive Agents. Risk C: Monitor

Brimonidine (Topical): May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Bromperidol: May decrease hypotensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase hypotensive effects of Bromperidol. Risk X: Avoid

Cafedrine: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Cafedrine. Risk C: Monitor

Cannabis: Beta-Blockers may increase adverse/toxic effects of Cannabis. Specifically, the risk of hypoglycemia may be increased. Risk C: Monitor

Ceritinib: Bradycardia-Causing Agents may increase bradycardic effects of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Risk D: Consider Therapy Modification

Cholinergic Agonists: Beta-Blockers may increase adverse/toxic effects of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Risk C: Monitor

Dexmethylphenidate: May decrease therapeutic effects of Antihypertensive Agents. Risk C: Monitor

Diazoxide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Dipyridamole: May increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Disopyramide: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may increase negative inotropic effects of Disopyramide. Risk C: Monitor

DOBUTamine: Beta-Blockers may decrease therapeutic effects of DOBUTamine. Risk C: Monitor

Dronedarone: May increase bradycardic effects of Beta-Blockers. Dronedarone may increase serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in beta-blocker dose. Increase monitoring for clinical response and adverse effects. Risk D: Consider Therapy Modification

DULoxetine: Blood Pressure Lowering Agents may increase hypotensive effects of DULoxetine. Risk C: Monitor

EPHEDrine (Systemic): Beta-Blockers may decrease therapeutic effects of EPHEDrine (Systemic). Risk C: Monitor

EPINEPHrine (Nasal): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Nasal). Risk C: Monitor

EPINEPHrine (Oral Inhalation): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Oral Inhalation). Risk C: Monitor

EPINEPHrine (Systemic): Beta-Blockers (Nonselective) may increase hypertensive effects of EPINEPHrine (Systemic). Risk C: Monitor

Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): Beta-Blockers may increase vasoconstricting effects of Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates). Risk C: Monitor

Etilefrine: Beta-Blockers may decrease therapeutic effects of Etilefrine. Etilefrine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Etofylline: Beta-Blockers may decrease therapeutic effects of Etofylline. Risk X: Avoid

Etrasimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Fexinidazole: Bradycardia-Causing Agents may increase arrhythmogenic effects of Fexinidazole. Risk X: Avoid

Fingolimod: Bradycardia-Causing Agents may increase bradycardic effects of Fingolimod. Management: Consult with the prescriber of any bradycardia-causing agent to see if the agent could be switched to an agent that does not cause bradycardia prior to initiating fingolimod. If combined, perform continuous ECG monitoring after the first fingolimod dose. Risk D: Consider Therapy Modification

Flunarizine: May increase therapeutic effects of Antihypertensive Agents. Risk C: Monitor

Grass Pollen Allergen Extract (5 Grass Extract): Beta-Blockers may increase adverse/toxic effects of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. Management: Consider alternatives to either grass pollen allergen extract (5 grass extract) or beta-blockers in patients with indications for both agents. Canadian product labeling specifically lists this combination as contraindicated. Risk D: Consider Therapy Modification

Green Tea: May decrease serum concentration of Nadolol. Risk C: Monitor

Herbal Products with Blood Pressure Increasing Effects: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Herbal Products with Blood Pressure Lowering Effects: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Hypotension-Associated Agents: Blood Pressure Lowering Agents may increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor

Iloperidone: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Indoramin: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Insulin: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Insulin. Beta-Blockers (Nonselective) may decrease therapeutic effects of Insulin. Risk C: Monitor

Isocarboxazid: May increase antihypertensive effects of Antihypertensive Agents. Risk X: Avoid

Isoproterenol: Beta-Blockers may decrease therapeutic effects of Isoproterenol. Risk C: Monitor

Ivabradine: Bradycardia-Causing Agents may increase bradycardic effects of Ivabradine. Risk C: Monitor

Lacosamide: Bradycardia-Causing Agents may increase AV-blocking effects of Lacosamide. Risk C: Monitor

Landiolol: Bradycardia-Causing Agents may increase bradycardic effects of Landiolol. Risk X: Avoid

Levodopa-Foslevodopa: Blood Pressure Lowering Agents may increase hypotensive effects of Levodopa-Foslevodopa. Risk C: Monitor

Lonafarnib: May increase serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors). Risk C: Monitor

Loop Diuretics: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Lormetazepam: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Lumacaftor and Ivacaftor: May increase serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors or Inducers). Lumacaftor and Ivacaftor may decrease serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors or Inducers). Risk C: Monitor

Mavacamten: Beta-Blockers may increase adverse/toxic effects of Mavacamten. Specifically, negative inotropic effects may be increased. Risk C: Monitor

Metergoline: May decrease antihypertensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase orthostatic hypotensive effects of Metergoline. Risk C: Monitor

Methacholine: Beta-Blockers may increase adverse/toxic effects of Methacholine. Risk C: Monitor

Methylphenidate: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Midodrine: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

Mivacurium: Beta-Blockers may increase therapeutic effects of Mivacurium. Risk C: Monitor

Molsidomine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Naftopidil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Nicergoline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Nicorandil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

NIFEdipine (Topical): May increase adverse/toxic effects of Beta-Blockers. Risk C: Monitor

NIFEdipine: May increase hypotensive effects of Beta-Blockers. NIFEdipine may increase negative inotropic effects of Beta-Blockers. Risk C: Monitor

Nitrendipine: May increase therapeutic effects of Beta-Blockers. Risk C: Monitor

Nitroprusside: Blood Pressure Lowering Agents may increase hypotensive effects of Nitroprusside. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Beta-Blockers. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Beta-Blockers. Risk C: Monitor

Obinutuzumab: May increase hypotensive effects of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider Therapy Modification

Opipramol: Beta-Blockers may increase serum concentration of Opipramol. Opipramol may increase serum concentration of Beta-Blockers. Risk C: Monitor

Ozanimod: May increase bradycardic effects of Bradycardia-Causing Agents. Risk C: Monitor

P-glycoprotein/ABCB1 Inhibitors: May increase serum concentration of Nadolol. Risk C: Monitor

Pentoxifylline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Perazine: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Pholcodine: Blood Pressure Lowering Agents may increase hypotensive effects of Pholcodine. Risk C: Monitor

Phosphodiesterase 5 Inhibitors: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Ponesimod: Bradycardia-Causing Agents may increase bradycardic effects of Ponesimod. Management: Avoid coadministration of ponesimod with drugs that may cause bradycardia when possible. If combined, monitor heart rate closely and consider obtaining a cardiology consult. Do not initiate ponesimod in patients on beta-blockers if HR is less than 55 bpm. Risk D: Consider Therapy Modification

Prazosin: Antihypertensive Agents may increase hypotensive effects of Prazosin. Risk C: Monitor

Prostacyclin Analogues: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Quinagolide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Reserpine: May increase hypotensive effects of Beta-Blockers. Reserpine may increase bradycardic effects of Beta-Blockers. Risk C: Monitor

Rivastigmine: May increase bradycardic effects of Beta-Blockers. Risk X: Avoid

Silodosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Siponimod: Bradycardia-Causing Agents may increase bradycardic effects of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. If combined, consider obtaining a cardiology consult regarding patient monitoring. Risk D: Consider Therapy Modification

Succinylcholine: Beta-Blockers may increase neuromuscular-blocking effects of Succinylcholine. Risk C: Monitor

Sulfonylureas: Beta-Blockers (Nonselective) may increase hypoglycemic effects of Sulfonylureas. Beta-Blockers (Nonselective) may decrease therapeutic effects of Sulfonylureas. Risk C: Monitor

Tasimelteon: Beta-Blockers may decrease therapeutic effects of Tasimelteon. Management: Consider avoiding nighttime administration of beta-blockers during tasimelteon therapy due to the potential for reduced tasimelteon efficacy. Risk D: Consider Therapy Modification

Terazosin: Antihypertensive Agents may increase hypotensive effects of Terazosin. Risk C: Monitor

Theodrenaline: May increase bradycardic effects of Beta-Blockers. Beta-Blockers may decrease therapeutic effects of Theodrenaline. Risk C: Monitor

Theophylline Derivatives: Beta-Blockers (Nonselective) may decrease bronchodilatory effects of Theophylline Derivatives. Risk C: Monitor

Urapidil: Antihypertensive Agents may increase hypotensive effects of Urapidil. Risk C: Monitor

Vimseltinib: May increase serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors). Management: Avoid concomitant use of vimseltinib and P-gp substrates when possible. If combined, administer vimseltinib at least 4 hours before the P-gp substrate. Risk D: Consider Therapy Modification

White Birch Allergen Extract: Beta-Blockers may increase adverse/toxic effects of White Birch Allergen Extract. Specifically, beta-blockers may reduce the effectiveness of beta-agonists that may be required to treat systemic reactions to white birch allergen extract. Risk X: Avoid

Reproductive Considerations

Medications considered acceptable for the treatment of chronic hypertension during pregnancy may generally be used in patients trying to conceive. Nadolol is not considered a preferred agent for use in pregnant patients; consider transitioning to a preferred agent in patients planning to become pregnant (ACC/AHA [Whelton 2018]; ACOG 2019).

Nadolol is effective for prevention of migraines. In general, preventive treatment for migraine in patients trying to become pregnant should be avoided. Options for patients planning a pregnancy should be considered as part of a shared decision-making process. Nonpharmacologic interventions should be considered initially. When needed, preventive treatment should be individualized considering the available safety data and needs of the patient should pregnancy occur. A gradual discontinuation of preventive medications is generally preferred when the decision is made to stop treatment prior to conception (ACOG 2022; AHS [Ailani 2021]).

Decreased libido and impotence are noted in product labeling following use of nadolol. As a class, outcomes from available studies evaluating beta-blockers and sexual dysfunction are inconsistent, and the negative effects on erectile function and libido are considered controversial. A clear relationship between use of beta-blockers and erectile dysfunction has not been established. Hypertension itself is associated with erectile dysfunction. Patients on a beta-blocker presenting with sexual dysfunction should be evaluated for underlying disease (Farmakis 2021; Levine 2012; Semet 2017; Terentes-Printzios 2022; Viigimaa 2020).

Pregnancy Considerations

Exposure to beta-blockers during pregnancy may increase the risk for adverse events in the neonate. Adverse events, such as bradycardia and hypoglycemia have been observed following in utero exposure to nadolol. If maternal use of a beta-blocker is needed, monitor fetal growth during pregnancy; monitor the newborn for 48 hours after delivery for bradycardia, hypoglycemia, and respiratory depression (ESC [Regitz-Zagrosek 2018]).

Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to the duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 2019).

Patients with preexisting hypertension may continue their medication during pregnancy unless contraindications exist (ESC [Regitz-Zagrosek 2018]). When treatment of hypertension is initiated during pregnancy, agents other than nadolol may be preferred (ACOG 2019; ESC [Cífková 2020]; ESC [Regitz-Zagrosek 2018]; SOGC [Magee 2022]).

In general, preventive treatment for migraine should be avoided during pregnancy. Options for pregnant patients should be considered as part of a shared decision-making process. Nonpharmacologic interventions should be considered initially. When needed, preventive treatment should be individualized considering the available safety data, the potential for adverse maternal and fetal events, and needs of the patient (ACOG 2022; AHS [Ailani 2021]). If preventive therapy is needed, beta-blockers may be considered (ACOG 2022); however, agents other than nadolol are preferred (CHS [Pringsheim 2012]).

Monitoring Parameters

Blood pressure, heart rate, fluid intake and output, weight.

Mechanism of Action

Competitively blocks response to beta1- and beta2-adrenergic stimulation; does not exhibit any membrane stabilizing or intrinsic sympathomimetic activity. Nonselective beta-adrenergic blockers (propranolol, nadolol) reduce portal pressure by producing splanchnic vasoconstriction (beta2 effect) thereby reducing portal blood flow.

Pharmacokinetics (Adult Data Unless Noted)

Duration: 17 to 24 hours

Absorption: ~30%

Distribution: Vd: ~2 L/kg

Protein binding: 30%

Metabolism: Not metabolized

Half-life elimination:

Infants 3 to 22 months (n=3): 3.2 to 4.3 hours (Mehta 1992)

Children 10 years (n=1): 15.7 hours (Mehta 1992)

Children ~15 years (n=1): 7.3 hours (Mehta 1992)

Adults: 20 to 24 hours; prolonged with renal impairment; (up to 45 hours in severe impairment) (Herrera 1979)

Time to peak, serum: 3 to 4 hours

Excretion: Urine (as unchanged drug)

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Corgard;
  • (AR) Argentina: Corgard;
  • (BE) Belgium: Corgard;
  • (BR) Brazil: Corgard;
  • (CH) Switzerland: Corgard;
  • (CL) Chile: Corgard;
  • (CO) Colombia: Corgard;
  • (CZ) Czech Republic: Apo nadol | Corgard;
  • (DE) Germany: Solgol;
  • (EG) Egypt: Corgard;
  • (ES) Spain: Solgol;
  • (FR) France: Corgard | Nadolol Dci;
  • (GB) United Kingdom: Corgard;
  • (GR) Greece: Corgard;
  • (HK) Hong Kong: Corgard;
  • (ID) Indonesia: Corgard | Farmagard;
  • (IE) Ireland: Corgard;
  • (IT) Italy: Corgard | Nadololo sanofi;
  • (JO) Jordan: Corgard;
  • (JP) Japan: Begen | Donalock | Isacol | Nadic dainippon | Nadol | Naodoriru | Saitamin;
  • (KR) Korea, Republic of: Corgard | Nadogard;
  • (KW) Kuwait: Corgard;
  • (LB) Lebanon: Corgard;
  • (LT) Lithuania: Apo nadol | Corgard;
  • (LU) Luxembourg: Corgard;
  • (LV) Latvia: Corgard;
  • (MX) Mexico: Corgard;
  • (NO) Norway: Apo-nadolol | Mint nadolol | Nadolol bluepoint;
  • (NZ) New Zealand: Apo-nadolol | Corgard;
  • (PE) Peru: Corgard;
  • (PK) Pakistan: Corgard;
  • (PL) Poland: Apo nadol | Corgard | Mint nadolol | Solgol;
  • (PR) Puerto Rico: Corgard;
  • (PT) Portugal: Anabet | Corgard;
  • (QA) Qatar: Apo-Nadolol | Solgol;
  • (RU) Russian Federation: Corgard;
  • (SA) Saudi Arabia: Apo-nadolol;
  • (SI) Slovenia: Corgard;
  • (TH) Thailand: Corgard;
  • (TW) Taiwan: Corgard;
  • (UY) Uruguay: Corgard;
  • (VE) Venezuela, Bolivarian Republic of: Corgard;
  • (ZA) South Africa: Corgard
  1. Ailani J, Burch RC, Robbins MS; Board of Directors of the American Headache Society. The American Headache Society consensus statement: update on integrating new migraine treatments into clinical practice. Headache. 2021;61(7):1021-1039. doi:10.1111/head.14153 [PubMed 34160823]
  2. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018;138(13):e272-e391. doi:10.1161/CIR.0000000000000549 [PubMed 29084731]
  3. American College of Obstetricians and Gynecologists (ACOG). ACOG practice bulletin no. 203: chronic hypertension in pregnancy. Obstet Gynecol. 2019;133(1):e26-e50. [PubMed 30575676]
  4. American College of Obstetricians and Gynecologists (ACOG). Headaches in pregnancy and postpartum: ACOG clinical practice guideline No. 3. Obstet Gynecol. 2022;139(5):944-972. doi:10.1097/AOG.0000000000004766 [PubMed 35576364]
  5. American Diabetes Association (ADA). Diabetes Care. 2019;42(suppl 1):S1-S193. http://care.diabetesjournals.org/content/42/Supplement_1. Accessed April 12, 2019.
  6. Antman EM, Anbe SC, Alpert JS, et al, "ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction - Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)," Circulation, 2004, 110(5):588-636. [PubMed 15289388]
  7. Aronoff GR, Bennett WM, Berns JS, et al, Drug Prescribing in Renal Failure: Dosing Guidelines for Adults and Children, 5th ed, Philadelphia, PA: American College of Physicians, 2007, p 33.
  8. Aronow WS, Fleg JL, Pepine CJ, et al, “ACCF/AHA 2011 Expert Consensus Document on Hypertension in the Elderly: A Report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents,” Circulation, 2011, 123(21):2434-506. [PubMed 21518977]
  9. Bahn RS, Burch HB, Cooper, DS, et.al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Endocrine Practice. 2011;17(3):1-65. [PubMed 21700562]
  10. Brauchli YB, Jick SS, Curtin F, et al, “Association Between Beta-Blockers, Other Antihypertensive Drugs and Psoriasis: Population-Based Case-Control Study,” Br J Dermatol, 2008, 158(6):1299-307. [PubMed 18410416]
  11. Bultas AC, Teshome B, Richter SK, Schafers S, Cooke E, Call WB. Use of nonselective β-blockers in patients with end-stage liver disease and select complications. Ann Pharmacother. 2020;54(6):583-593. doi:10.1177/1060028019893092 [PubMed 31810371]
  12. Chobanian AV, Bakris GL, Black HR, et al, “The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report,” JAMA, 2003, 289(19):2560-72. [PubMed 12748199]
  13. Chockalingam P, Crotti L, Girardengo G, et al. Not all beta-blockers are equal in the management of long QT syndrome types 1 and 2: higher recurrence of events under metoprolol. J Am Coll Cardiol. 2012;60(20):2092-2099. doi: 10.1016/j.jacc.2012.07.046. [PubMed 23083782]
  14. Cífková R, Johnson MR, Kahan T, et al. Peripartum management of hypertension: a position paper of the ESC Council on Hypertension and the European Society of Hypertension. Eur Heart J Cardiovasc Pharmacother. 2020;6(6):384-393. doi:10.1093/ehjcvp/pvz082 [PubMed 31841131]
  15. Claudio B, Alice M, Daniel S. A focus on pharmacological management of catecholaminergic polymorphic ventricular tachycardia. Mini Rev Med Chem. 2018;18(6):476-482. [PubMed 28685702]
  16. Corgard (nadolol) [prescribing information]. Louisville, KY: US WorldMeds LLC; December 2023.
  17. Dahlof B, Devereux RB, Kjeldsen SE, et al; Life Study Group. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet. 2002;359(9311):995-1003. [PubMed 11937178]
  18. de la Peña J, Brullet E, Sanchez-Hernández E, et al. Variceal ligation plus nadolol compared with ligation for prophylaxis of variceal rebleeding: a multicenter trial. Hepatology. 2005;41(3):572-578. [PubMed 15726659]
  19. Devlin RG, Duchin KL, and Fleiss PM, "Nadolol in Human Serum and Breast Milk," Br J Clin Pharmacol, 1981, 12(3):393-6. [PubMed 6117304]
  20. Farmakis IT, Pyrgidis N, Doundoulakis I, Mykoniatis I, Akrivos E, Giannakoulas G. Effects of major antihypertensive drug classes on erectile function: a network meta-analysis. Cardiovasc Drugs Ther. 2022;36(5):903-914. doi:10.1007/s10557-021-07197-9 [PubMed 33945044]
  21. Foster CA and Aston SJ, “Propranolol-Epinephrine Interaction: A Potential Disaster,” Plast Reconstr Surg, 1983, 72(1):74-8. [PubMed 6867180]
  22. Fox RE, Marx C, and Stark AR, "Neonatal Effects of Maternal Nadolol Therapy," Am J Obstet Gynecol, 1985, 152(8):1045-6. [PubMed 4025452]
  23. Funder JW, Carey RM, Mantero F, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(5):1889-1916. doi: 10.1210/jc.2015-4061. [PubMed 26934393]
  24. Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: Risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the study of liver diseases. Hepatology. 2017;65(1):310-335. [PubMed 27786365]
  25. Garcia-Tsao G, Sanyal AJ, Grace ND, et al, “Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis,” Hepatology, 2007, 46(3):922-38. [PubMed 17879356]
  26. Go AS, Bauman M, King SM, et al. An effective approach to high blood pressure control: a science advisory from the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention [published online November 15, 2013]. Hypertension. [PubMed 24243703]
  27. Gold MH, Holy AK, and Roenigk HH Jr, "Beta-Blocking Drugs and Psoriasis. A Review of Cutaneous Side Effects and Retrospective Analysis of Their Effects on Psoriasis," J Am Acad Dermatol, 1988, 19(5 Pt 1):837-41. [PubMed 2903871]
  28. Goldenberg I, Bradley J, Moss A, et al; International LQTS Registry Investigators. Beta-blocker efficacy in high-risk patients with the congenital long-QT syndrome types 1 and 2: implications for patient management. J Cardiovasc Electrophysiol. 2010;21(8):893-901. doi: 10.1111/j.1540-8167.2010.01737.x. [PubMed 20233272]
  29. Hayashi M, Denjoy I, Extramiana F, et al. Incidence and risk factors of arrhythmic events in catecholaminergic polymorphic ventricular tachycardia. Circulation. 2009;119(18):2426-2434. doi: 10.1161/CIRCULATIONAHA.108.829267. [PubMed 19398665]
  30. Herrera J, Vukovich RA, and Griffith DL, “Elimination of Nadolol by Patients With Renal Impairment,” Br J Clin Pharmacol, 1979, 7(Suppl 2):227-31. [PubMed 37878]
  31. Ito S. Drug therapy for breast-feeding women. N Engl J Med. 2000;343(2):118-126. [PubMed 10891521]
  32. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5):507-520. [PubMed 24352797]
  33. Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation: a report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines. Circulation. 2024;149(1):e1-e156. doi:10.1161/CIR.0000000000001193 [PubMed 38033089]
  34. Juul AB, Wetterslev J, Gluud C, et al, “Effect of Perioperative Beta Blockade in Patients With Diabetes Undergoing Major Non-Cardiac Surgery: Randomized Placebo Controlled, Blinded Multicentre Trial. DIPOM Trial Group,” BMJ, 2006, 332(7556):1482. [PubMed 16793810]
  35. Lang DM, “Anaphylactoid and Anaphylactic Reactions. Hazards of Beta-Blockers,” Drug Saf, 1995, 12(5):299-304. [PubMed 7669259]
  36. Levine GN, Steinke EE, Bakaeen FG, et al; American Heart Association Council on Clinical Cardiology; Council on Cardiovascular Nursing; Council on Cardiovascular Surgery and Anesthesia; Council on Quality of Care and Outcomes Research. Sexual activity and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2012;125(8):1058-1072. doi:10.1161/CIR.0b013e3182447787 [PubMed 22267844]
  37. Lo GH, Chen WC, Chan HH, et al. A randomized, controlled trial of banding ligation plus drug therapy versus drug therapy alone in the prevention of esophageal variceal rebleeding. J Gastroenterol Hepatol. 2009;24(6):982-987. [PubMed 19638080]
  38. Lo GH, Chen WC, Chen MH, et al. Endoscopic ligation vs. nadolol in the prevention of first variceal bleeding in patients with cirrhosis. Gastrointest Endosc. 2004;59(3):333-338. [PubMed 14997127]
  39. Lo GH, Chen WC, Wang HM, Lee CC. Controlled trial of ligation plus nadolol versus nadolol alone for the prevention of first variceal bleeding. Hepatology. 2010;52(1):230-237. [PubMed 20578138]
  40. Lo GH, Chen WC, Wang HM, Lee CC. Randomized, controlled trial of carvedilol versus nadolol plus isosorbide mononitrate for the prevention of variceal rebleeding. J Gastroenterol Hepatol. 2012;27(11):1681-1687. [PubMed 22849337]
  41. Magee LA, Smith GN, Bloch C, et al. Guideline No. 426: hypertensive disorders of pregnancy: diagnosis, prediction, prevention, and management. J Obstet Gynaecol Can. 2022;44(5):547-571.e1. doi:10.1016/j.jogc.2022.03.002 [PubMed 35577426]
  42. Mayer S, Hillis LD. Prinzmetal's variant angina. Clin Cardiol. 1998;21(4):243-246. doi:10.1002/clc.4960210403 [PubMed 9562933]
  43. Mehta AV and Chidambaram B, “Efficacy and Safety of Intravenous and Oral Nadolol for Supraventricular Tachycardia in Children,” J Am Coll Cardiol, 1992a, 19(3):630-5. [PubMed 1538020]
  44. Mehta AV, Chidambaram B, and Rice PJ, Pharmacokinetics of nadolol in children with supraventricular tachycardia. J Clin Pharmacol. 1992;32(1):1023-1027. [PubMed 1474163]
  45. Merkel C, Marin R, Angeli P, et al; Gruppo Triveneto per l'Ipertensione Portale. A placebo-controlled clinical trial of nadolol in the prophylaxis of growth of small esophageal varices in cirrhosis. Gastroenterology. 2004;127(2):476-484. doi:10.1053/j.gastro.2004.05.004 [PubMed 15300580]
  46. Michaels RS, Duchin KL, Akbar S, Meister J, Levin NW. Nadolol in hypertensive patients maintained on long-term hemodialysis. Am Heart J. 1984;108(4, pt 2):1091-1094. doi:10.1016/0002-8703(84)90587-8 [PubMed 6148869]
  47. Mint-Nadolol (nadolol) [product monograph]. Mississauga, Ontario, Canada: Mint Pharmaceuticals Inc; February 2020.
  48. Moss AJ, Zareba W, Hall WJ, et al. Effectiveness and limitations of beta-blocker therapy in congenital long-QT syndrome. Circulation. 2000;101(6):616-623. [PubMed 10673253]
  49. Nadolol [prescribing information]. Peapack, NJ: Greenstone LLC; November 2019.
  50. Nadolol [product monograph]. Vaughan, Ontario, Canada: AA Pharma Inc; June 2016.
  51. Nahata MC, Pai VB. Pediatric Drug Formulations. 6th ed. Cincinnati, OH: Harvey Whitney Books, 2011.
  52. Nishimura RA, Otto CM, Bonow RO, et al, 2014 AHA/ACC Guideline for the Management of Patients with Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):2440-92. doi: 10.1161/CIR.0000000000000029. [PubMed 24589852]
  53. O'Mahony D, Cherubini A, Guiteras AR, et al. STOPP/START criteria for potentially inappropriate prescribing in older people: version 3. Eur Geriatr Med. 2023;14(4):625-632. doi:10.1007/s41999-023-00777-y [PubMed 37256475]
  54. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67(13):e27-e115. [PubMed 26409259]
  55. POISE Study Group, Devereaux PJ, Yang H, et al, “Effects of Extended-Release Metoprolol Succinate in Patients Undergoing Non-Cardiac Surgery (POISE Trial): A Randomised Controlled Trial,” Lancet, 2008, 371(9627):1839-47. [PubMed 18479744]
  56. Poynard T, Calès P, Pasta L, et al; Franco-Italian Multicenter Study Group. Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clinical trials. N Engl J Med. 1991;324(22):1532-1538. [PubMed 1674104]
  57. Pringsheim T, Davenport W, Mackie G, et al; Canadian Headache Society Prophylactic Guidelines Development Group. Canadian Headache Society guideline for migraine prophylaxis. Can J Neurol Sci. 2012;39(2 suppl 2):S1-S59. [PubMed 22683887]
  58. Redelmeier D, Scales D, and Kopp A, "Beta Blockers for Elective Surgery in Elderly Patients: Population Based, Retrospective Cohort Study," BMJ, 2005, 331(7522):932. [PubMed 16210252]
  59. Refer to the manufacturer's labeling.
  60. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, et al. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J. 2018;39(34):3165-3241. [PubMed 30165544]
  61. Rosendorff C, Lackland DT, Allison M, et al. Treatment of hypertension in patients with coronary artery disease: a scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension. J Am Soc Hypertens. 2015;9(6):453-498. doi:10.1016/j.jash.2015.03.002 [PubMed 25840695]
  62. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343-1421. doi: 10.1089/thy.2016.0229 [PubMed 27521067]
  63. Sauer AJ, Moss AJ, McNitt S, et al. Long QT syndrome in adults. J Am Coll Cardiol. 2007;49(3):329-337. doi: 10.1016/j.jacc.2006.08.057. [PubMed 17239714]
  64. Schön MP and Boehncke WH, “Psoriasis,” N Eng J Med, 2005, 352(18):1899-1912. [PubMed 15872205]
  65. Schwedt TJ, Garza I. Preventive treatment of episodic migraine in adults. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed June 19, 2022.
  66. Semet M, Paci M, Saïas-Magnan J, et al. The impact of drugs on male fertility: a review. Andrology. 2017;5(4):640-663. doi:10.1111/andr.12366 [PubMed 28622464]
  67. Silberstein SD. Preventive migraine treatment. Continuum (Minneap Minn). 2015;21(4 Headache):973-989. doi:10.1212/CON.0000000000000199 [PubMed 26252585]
  68. Silberstein SD, Holland S, Freitag F, et al. Evidence-based guideline update: pharmacologic treatment for episodic migraine prevention in adults: report of the Quality Standard Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2012;78(17):1337-1345. [PubMed 22529202]
  69. Smith SC Jr, Benjamin EJ, Bonow RO, et al, “AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update: A Guideline From the American Heart Association and American College of Cardiology Foundation,” Circulation, 2011, 124(22):2458-73. [PubMed 22052934]
  70. Song G, Yoon HY, Yee J, Kim MG, Gwak HS. Antihypertensive drug use and psoriasis: a systematic review, meta- and network meta-analysis. Br J Clin Pharmacol. Published online October 5, 2021. doi:10.1111/bcp.15060 [PubMed 34611920]
  71. Steiner TJ, Jensen R, Katsarava Z, et al. Aids to management of headache disorders in primary care (2nd edition): on behalf of the European Headache Federation and Lifting The Burden: the Global Campaign Against Headache. J Headache Pain. 2019;20(1):57. doi:10.1186/s10194-018-0899-2 [PubMed 31113373]
  72. Terentes-Printzios D, Ioakeimidis N, Rokkas K, Vlachopoulos C. Interactions between erectile dysfunction, cardiovascular disease and cardiovascular drugs. Nat Rev Cardiol. 2022;19(1):59-74. doi:10.1038/s41569-021-00593-6 [PubMed 34331033]
  73. Tripathi D, Stanley AJ, Hayes PC, et al; Clinical Services and Standards Committee of the British Society of Gastroenterology. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. Gut. 2015;64(11):1680-1704. [PubMed 25887380]
  74. UK Prospective Diabetes Study Group, “Efficacy of Atenolol and Captopril in Reducing Risk of Macrovascular and Microvascular Complications in Type 2 Diabetes: UKPDS 39,” BMJ, 1998, 317(7160):713-20. [PubMed 9732338]
  75. Viigimaa M, Vlachopoulos C, Doumas M, et al; European Society of Hypertension Working Group on Sexual Dysfunction. Update of the position paper on arterial hypertension and erectile dysfunction. J Hypertens. 2020;38(7):1220-1234. doi:10.1097/HJH.0000000000002382 [PubMed 32073535]
  76. Villaneuva C, Minana J, Ortiz J, et al, “Endoscopic Ligation Compared With Combined Treatment With Nadolol and Isosorbide Mononitrate to Prevent Recurrent Variceal Bleeding,” N Engl J Med, 2001, 345(9):647-55. [PubMed 11547718]
  77. Virani SS, Newby LK, Arnold SV, et al. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA guideline for the management of patients with chronic coronary disease: a report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023;148(9):e9-e119. doi:10.1161/CIR.0000000000001168 [PubMed 37471501]
  78. von Alvensleben JC, LaPage MJ, Caruthers R, Bradley DJ. Nadolol for treatment of supraventricular tachycardia in infants and young children. Pediatr Cardiol. 2017;38(3):525-530. [PubMed 27995288]
  79. Weber MA, Schiffrin EL, White WB, et al, Clinical practice guidelines for the management of hypertension in the community: a statement by the American Society of Hypertension and the International Society of Hypertension. J Clin Hypertens (Greenwich). 2014;16(1):14-26. [PubMed 24341872]
  80. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. Hypertension. 2018;71(6):1269-1324. doi:10.1161/HYP.0000000000000066 [PubMed 29133354]
  81. Wong DG, Spence JD, Lamki L, et al, “Effect of Nonsteroidal Anti-inflammatory Drugs on Control of Hypertension of Beta-Blockers and Diuretics,” Lancet, 1986, 1(8488):997-1001. [PubMed 2871333]
  82. Wynn RL, “Dental Nonsteroidal Anti-inflammatory Drugs and Prostaglandin-Based Drug Interactions, Part Two,” Gen Dent, 1992, 40(2):104, 106, 108. [PubMed 1354194]
  83. Wynn RL, “Epinephrine Interactions With Beta-Blockers,” Gen Dent, 1994, 42(1):16, 18. [PubMed 7911769]
  84. Yang H, Raymer K, Butler R, et al, “The Effects of Perioperative Beta-Blockade: Results of the Metoprolol After Vascular Surgery (MaVS) Study, a Randomized Controlled Trial,” Am Hear J, 2006, 152(5):983-90. [PubMed 17070177]
Topic 12625 Version 411.0