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Generic Name: Pindolol
Class: beta-Adrenergic Blocking Agents
VA Class: CV100
Chemical Name: 1-(Indol-4-yloxy)-3-(isopropylamino)-2-propanol
Molecular Formula: C14H20N2O2
CAS Number: 13523-86-9
A nonselective β-adrenergic blocking agent (β-blocker).1 2 3 4
Uses for Visken
Management of hypertension (alone or in combination with other classes of antihypertensive agents).1 2 500
β-Blockers generally not preferred for initial management of hypertension, but may be considered in patients who have a compelling indication (e.g., prior MI, ischemic heart disease, heart failure) for their use or as add-on therapy in those who do not respond adequately to the preferred drug classes (ACE inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, or thiazide diuretics).101 501 502 503 504 515 523 524 527 800
Black hypertensive patients generally tend to respond better to monotherapy with calcium-channel blockers or thiazide diuretics than to β-blockers. 85 89 90 500 501 504 However, diminished response to β-blockers is largely eliminated when administered concomitantly with a thiazide diuretic.500
Management of chronic stable angina pectoris†.2 5 15 22
Visken Dosage and Administration
Individualize dosage according to patient response and tolerance.1
If long-term therapy is discontinued, reduce dosage gradually over a period of about 1–2 weeks.1 (See Abrupt Withdrawal of Therapy under Cautions.)
BP Monitoring and Treatment Goals
Carefully monitor BP during initial titration or subsequent upward adjustment in dosage.500 501
When available, use evidence-based dosing information (i.e., dosages shown in randomized controlled trials to reduce complications of hypertension) to determine target dosages; target dosages usually can be achieved within 2–4 weeks but may take up to several months.501
Goal is to achieve and maintain optimal control of BP; individualize specific target BP based on consideration of multiple factors, including patient age and comorbidities, and currently available evidence from clinical studies.500 501
Administer orally, usually twice daily;1 bioavailability does not appear to be affected by food.1 (See Absorption under Pharmacokinetics.)
Initially, 5 mg twice daily, either alone or in combination with other antihypertensives.1 52 600 Increase dosage gradually by 10 mg daily at 3- to 4-week intervals as necessary up to 60 mg daily.1 The usual maintenance dosage range is 10–40 mg daily, given in 2 divided doses.2 11 15 500
If intolerable adverse effects occur, consider dosage reduction; if adverse effects worsen or fail to resolve, may need to discontinue and switch to another antihypertensive drug class.501
15–40 mg daily, given in 3 or 4 divided doses.2 5 22
Maximum 60 mg daily.1
Dosage must be modified in response to the degree of hepatic impairment.1
Cautions for Visken
Bronchial asthma, heart block greater than first degree, cardiogenic shock, overt cardiac failure, or severe bradycardia.1
Possible precipitation of CHF.1 2
Avoid use in patients with decompensated heart failure, may use cautiously in patients with well-compensated heart failure (e.g., those controlled with ACE inhibitors, cardiac glycosides, and/or diuretics).1
Adequate treatment (e.g., with a cardiac glycoside and/or diuretic) and close observation recommended if signs or symptoms of impending heart failure occur; if heart failure continues, discontinue therapy, gradually if possible.1
Abrupt Withdrawal of Therapy
Abrupt discontinuance of therapy is not recommended as it may exacerbate angina symptoms or precipitate MI in patients with CAD.1 Gradually decrease dosage over a period of about 1–2 weeks.1 Monitor patients carefully and advise to temporarily limit their physical activity.1 If exacerbation of angina occurs, reinstitute therapy promptly, and initiate appropriate measures for the management of unstable angina pectoris.1
Possible inhibition of bronchodilation produced by endogenous catecholamines.1
Generally should not be used in patients with bronchospastic disease, but may be used with caution in patients with nonallergic bronchospasm (e.g., chronic bronchitis, emphysema).1 (See Contraindications under Cautions.)
Possible risks associated with general anesthesia (e.g., severe hypotension, difficulty maintaining heart beat) due to decreased ability of the heart to respond to reflex β-adrenergic stimuli.1 Use with caution in patients undergoing major surgery involving general anesthesia.1
Diabetes and Hypoglycemia
Possible decreased signs and symptoms of hypoglycemia (e.g., tachycardia, palpitation, BP changes, tremor, feelings of anxiety, but not sweating or dizziness).1 68
Use with caution in patients with diabetes mellitus receiving hypoglycemic drugs.1
Signs of hyperthyroidism (e.g., tachycardia) may be masked.1 Possible thyroid storm if therapy is abruptly withdrawn;1 carefully monitor patients having or suspected of developing thyrotoxicosis.1
Possible increased reactivity to repeated, accidental, diagnostic, or therapeutic challenges with a variety of allergens while taking β-blockers in patients with a history of anaphylactic reactions to a variety of allergens.1 Such patients may be unresponsive to usual doses of epinephrine.1
Distributed into milk.1 Use not recommended.1
Safety and efficacy not established.1
Hepatic elimination; use with caution.1
Common Adverse Effects
Insomnia, dizziness, fatigue, nervousness, bizarre dreams or increased dreaming, weakness, paresthesia, edema, dyspnea, muscle pain, joint pain, chest pain, muscle cramps, nausea, abdominal discomfort, pruritus.1
Interactions for Visken
Pharmacokinetic interaction unlikely1
Possible decreases in serum digoxin concentrations 1
Not considered clinically important1 18
Monitor for signs of hypotension and bradycardia (e.g., vertigo, syncope, postural hypotension)1
Hypotensive agents (hydralazine, hydrochlorothiazide)
Possible increased hypotensive effects1
Adjust dosage carefully1
Increased serum concentrations of thioridazine1 and metabolites; higher than expected serum concentrations of pindolol1 73 1
Increased thioridazine concentrations may cause prolongation of the QTc interval and a possible increase in the risk of serious, potentially fatal cardiac arrhythmia (e.g., torsades de pointes)73 1
Concomitant use is contraindicated73
Pharmacokinetic interaction unlikely1
Rapidly absorbed from the GI tract with peak plasma concentrations reached within 1–2 hours.1 2
Bioavailability 502 –95%.1 2
Effect on heart rate is seen within 3 hours.2
Hypotensive effect is usually seen within 1 week, but maximum therapeutic response may not be observed until 2 weeks or longer.1
Acute hemodynamic effects persist for 24 hours after administration.2
Food may increase the rate,2 but not the extent of absorption.1
Bioavailability may be at the lower end of the range in uremic patients;2 extent of absorption may be decreased in patients with impaired renal function.19
Distributed into milk.1
Plasma Protein Binding
Approximately 40–60%.1 2
Extensively metabolized in the liver (approximately 60–65%) to metabolites.1 2
Excreted in urine (35–50%) unchanged.1 2 18
3–4 hours.1 2
In patients with creatinine clearances <20 mL/minute, <15% is excreted in urine unchanged.1 18 20
In patients with renal failure, plasma half-life is 3–11.5 hours.2 20
In geriatric patients, plasma half-life is 7–15 hours.1
In patients with hepatic cirrhosis, half-life is 2.5–30 hours.1
Tight, light-resistant containers at 15–30°C.1 31
Inhibits response to adrenergic stimuli by competitively blocking β-adrenergic receptors within the myocardium (β1-receptors) and within bronchial and vascular smooth muscle (β2-receptors).2 4 5
In addition, causes slight activation of the β-receptors, making the drug a partial β-agonist.2 4 5
At higher than therapeutically obtained plasma concentrations, the drug has membrane-stabilizing activity or a quinidine-like effect.4
Decreases stress- and exercise-stimulated heart rate.1 2 4 5 Has a lesser effect on resting heart rate (usually decreasing resting heart rate only by about 4–8 bpm or not at all),1 2 4 5 15 22 slowing of conduction in the AV node,4 and cardiac output,2 4 13 22 than do β-blockers that do not possess intrinsic sympathomimetic activity (ISA).1 2 4 5 15 22
The precise mechanism of hypotensive effect has not been determined;1 the drug does not consistently affect cardiac output or renin release, and other mechanisms (e.g., decreased peripheral resistance) probably contribute to its hypotensive effect.1 15 16
May increase airway resistance,1 2 4 depending on the patient’s pretreatment sympathetic tone; patients with high pretreatment tone show a decrease in forced expiratory volume in 1 second (FEV1), whereas those with low pretreatment tone may show little, if any, change in FEV1.17
Advice to Patients
Importance of taking pindolol exactly as prescribed.1
Importance of not interrupting or discontinuing therapy without consulting clinician.1
Importance of immediately informing clinician at the first sign or symptom of impending cardiac failure (e.g., weight gain, increased shortness of breath) or if any difficulty in breathing occurs.1
In patients with heart failure, importance of informing clinician of signs or symptoms of exacerbation (e.g., weight gain, difficulty in breathing).1
Importance of patients informing anesthesiologist or dentist that they are receiving pindolol therapy prior to undergoing major surgery.1
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.1
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1
Importance of informing patients of other important precautionary information.1 (See Cautions.)
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
AHFS DI Essentials. © Copyright 2017, Selected Revisions February 28, 2017. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.
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