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pindolol 5 mg tablet

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Pindolol is used in the management of hypertension. The drug also has been used in the management of angina.

The choice of a β-adrenergic blocking agent (β-blocker) depends on numerous factors, including pharmacologic properties (e.g., relative β-selectivity, intrinsic sympathomimetic activity, membrane-stabilizing activity, lipophilicity), pharmacokinetics, intended use, and adverse effect profile, as well as the patient's coexisting disease states or conditions, response, and tolerance. While specific pharmacologic properties and other factors may appropriately influence the choice of a β-blocker in individual patients, evidence of clinically important differences among the agents in terms of overall efficacy and/or safety is limited. Patients who do not respond to or cannot tolerate one β-blocker may be successfully treated with a different agent.

In the management of hypertension or chronic stable angina pectoris, many clinicians prefer to use low dosages of a β1-selective adrenergic blocking agent (e.g., atenolol, metoprolol), rather than a nonselective agent like pindolol, in patients with chronic obstructive pulmonary disease (COPD) or insulin-dependent diabetes mellitus. However, selectivity of these agents is relative and dose dependent. Although a β-blocker with intrinsic sympathomimetic activity (ISA) (e.g., pindolol) does not eliminate sympathetic activity entirely, there is no evidence from well-controlled studies that pindolol is safer in these patients than other nonselective β-blockers that do not possess ISA. Some clinicians also will recommend using a β1-selective agent or pindolol (because of its ISA), rather than a nonselective agent, for the management of hypertension or angina pectoris in patients with peripheral vascular disease, but there is no evidence that the choice of β-blocker substantially affects efficacy.


Pindolol is used alone or in combination with other classes of antihypertensive agents in the management of hypertension. Although β-blockers were previously considered a drug of choice for the initial management of hypertension, most current guidelines no longer recommend these drugs as first-line therapy because of the lack of established superiority over other recommended drug classes and at least one study demonstrating that they may be less effective than angiotensin II receptor antagonists in preventing cardiovascular death, myocardial infarction, or stroke. However, β-blockers may still be considered in hypertensive patients who have a compelling indication (e.g., prior myocardial infarction, 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 (angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, or thiazide diuretics). and in )

In general, black hypertensive patients tend to respond better to monotherapy with thiazide diuretics or calcium-channel blocking agents than to monotherapy with β-blockers. Although β-blockers have lowered blood pressure in all races studied, monotherapy with these agents has produced a smaller reduction in blood pressure in black hypertensive patients; however, this population difference in response does not appear to occur during combined therapy with a β-blocker and a thiazide diuretic. (See Race under Hypertension: Other Special Considerations for Antihypertensive Therapy, in Uses in and in .)

Pindolol's efficacy in hypertensive patients is similar to that of other β-blockers.

For additional information on the role of β-blockers in the management of hypertension, see Uses in and in . For information on overall principles and expert recommendations for treatment of hypertension,

Chronic Stable Angina

Pindolol has been used in the management of chronic stable angina pectoris. β-Blockers are recommended as the anti-ischemic drugs of choice in most patients with chronic stable angina; despite differences in cardioselectivity, intrinsic sympathomimetic activity, and other clinical factors, all β-blockers appear to be equally effective for this indication.

Combination therapy with a β-blocker and a nitrate appears to be more effective than either drug alone because β-blockers attenuate the increased sympathetic tone and reflex tachycardia associated with nitrate therapy while nitrate therapy (e.g., nitroglycerin) counteracts the potential increase in left-ventricular wall tension associated with a decrease in heart rate. Combined therapy with a β-blocker and a dihydropyridine calcium-channel blocker also may be useful because the tendency to develop tachycardia with the calcium-channel blocker is counteracted by the β-blocker. However, caution should be exercised in the concomitant use of β-blockers and the nondihydropyridine calcium-channel blockers verapamil or diltiazem because of the potential for excessive fatigue, bradycardia, or atrioventricular (AV) block.(See Drug Interactions: Cardiovascular Drugs.)

Long-term use of β-blockers in patients with chronic stable angina has been shown to reduce the frequency of anginal attacks, allow a reduction in nitroglycerin dosage, and increase exercise tolerance. It has been suggested that pindolol may be a particularly useful β-blocker in patients with exercise-induced angina and substantial resting bradycardia and heart failure, since the drug has little effect on heart rate or cardiac output at rest; however, additional study is needed to determine the specific role of pindolol in the management of angina. In patients who do not respond to maximal dosages of a β-blocker or nitroglycerin, concurrent use of the 2 drugs may be beneficial.

Dosage and Administration


Pindolol is administered orally.


Dosage of pindolol must be individualized and adjusted according to the patient's response and tolerance. If long-term pindolol therapy is to be discontinued, dosage of the drug should be gradually reduced over a period of 1-2 weeks.(See Cautions: Precautions and Contraindications.)


Usual Dosage

For the management of hypertension, the usual initial adult dosage of pindolol is 5 mg twice daily, administered alone or in combination with other antihypertensive agents. Although a hypotensive effect usually is seen within 1 week, maximum therapeutic response may not be seen until 2 weeks or longer. If an adequate reduction in blood pressure with the initial dosage does not occur within 3-4 weeks, dosage of pindolol may be gradually increased by 10 mg daily at 3- to 4-week intervals as necessary up to a maximum dosage of 60 mg daily. The usual adult dosage range is 10-40 mg daily, given in 2 divided doses.

The panel members appointed to the Eighth Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8 expert panel) state that evidence-based dosing information (i.e., dosages shown in randomized controlled trials to reduce complications of hypertension) should be used when available to determine target dosages of antihypertensive agents. Target dosages of antihypertensive agents generally can be achieved within 2-4 weeks, but it may take up to several months. In patients who experience intolerable adverse effects with pindolol, dosage reduction should be considered; if adverse effects worsen or fail to resolve, it may be necessary to discontinue the β-blocker and initiate another class of antihypertensive agent.

Blood Pressure Monitoring and Treatment Goals

Careful monitoring of blood pressure during initial titration or subsequent upward adjustment in dosage of pindolol is recommended.

The goal of hypertension management and prevention is to achieve and maintain optimal control of blood pressure; specific target levels of blood pressure should be individualized based on consideration of multiple factors, including patient age and comorbidities, and the currently available evidence from clinical studies.

For additional information on initiating and adjusting pindolol dosage in the management of hypertension, .

Chronic Stable Angina

For the management of chronic stable angina pectoris, pindolol dosages of 15-40 mg daily, given in 3 or 4 divided doses, have been used.

Dosage in Hepatic Impairment

In patients with hepatic impairment, doses and/or frequency of administration of pindolol must be modified in response to the degree of hepatic impairment.


Pindolol shares the toxic potentials of β-adrenergic blocking agents (β-blockers). In therapeutic dosage, pindolol usually is well tolerated and has a low incidence of adverse effects. The incidence and severity of adverse reactions may occasionally be obviated by a reduction in dosage. Although there is some evidence that abrupt withdrawal of pindolol may be better tolerated than that of β-blockers that do not possess ISA, abrupt withdrawal of pindolol should be avoided, especially in patients with coronary artery disease, since it may exacerbate angina or precipitate myocardial infarction.

Cardiovascular Effects

Potentially serious adverse effects attributed to pindolol's action on the heart occur in less than 2% of patients and include bradycardia, heart block, hypotension, and precipitation of heart failure. Bradycardia and hypotension usually can be reversed with an antimuscarinic agent like IV atropine or with isoproterenol. Congestive heart failure usually responds to digitalization and diuresis. Other cardiovascular effects include peripheral edema, occurring in 6-16% of patients; dyspnea, occurring in about 10% of patients; weight gain, occurring in 3% of patients; and palpitation, claudication, coldness of the extremities, syncope, and tachycardia, usually occurring in less than 2% of patients.

Nervous System Effects

Common adverse CNS effects, occurring in 15-19% of patients receiving pindolol, include dizziness, fatigue, and insomnia. Bizarre dreams or an increased number of dreams, visual disturbances, paresthesia, weakness, and nervousness or anxiety reportedly occur in about 4-10% of patients. Hallucinations and lethargy reportedly occur in 1 and 3% of patients, respectively. Development or exacerbation of tremor (e.g., essential tremor) also has been reported in patients receiving the drug. Adverse CNS effects seen with other β-blockers that may occur with pindolol include disorientation, short-term memory impairment, emotional lability, catatonia, and impaired performance on neuropsychometric tests.

GI Effects

Adverse GI reactions, reportedly occurring in about 2-7% of patients receiving pindolol, include nausea and abdominal discomfort. Diarrhea and vomiting occur in less than 2% of patients. A few cases of mesenteric arterial thrombosis and ischemic colitis have been reported in patients receiving other β-blockers.

Endocrine Effects

Results of a large prospective cohort study of nondiabetic adults 45-64 years of age indicate that use of β-blockers in hypertensive patients is associated with increased risk (about 28%) of developing type 2 diabetes mellitus compared with hypertensive patients who were not receiving hypotensive therapy. In this study, the number of new cases of diabetes per 1000 person-years was 33.6 or 26.3 in patients receiving a β-blocker or no drug therapy, respectively. The association between the risk of developing type 2 diabetes mellitus and use of β-blockers reportedly was not confounded by weight gain, hyperinsulinemia, or differences in heart rate. It is not known if the risk of developing diabetes is affected by β-receptor selectivity. Further studies are needed to determine whether concomitant use of ACE inhibitors (which may improve insulin sensitivity) would abrogate β-blocker-induced adverse effects related to glucose intolerance. Therefore, until results of such studies are available, the proven benefits of β-blockers in reducing cardiovascular events in hypertensive patients must be weighed carefully against the possible risks of developing type 2 diabetes mellitus.

Hypoglycemia, which may result in loss of consciousness, also may occur in nondiabetic patients receiving β-blockers. Patients most at risk for the development of β-blocker-induced hypoglycemia are those undergoing dialysis, prolonged fasting, or severe exercise regimens.

β-Blockers may mask signs and symptoms of hypoglycemia (e.g., palpitation, tachycardia, tremor) and potentiate insulin-induced hypoglycemia. Although it has been suggested that nonselective β-blockers are more likely to induce hypoglycemia than selective β-blockers, such an adverse effect also has been reported with selective β-blockers (e.g., atenolol). In addition, selective β-blockers are less likely to mask symptoms of hypoglycemia or delay recovery from insulin-induced hypoglycemia than nonselective β-blockers because of their vascular sparing effects; however, selective β-blockers can decrease insulin sensitivity by approximately 15-30%, which may result in increased insulin requirements.

Other Adverse Effects

Slight but persistent increases in serum AST (SGOT) and ALT (SGPT) concentrations, without findings of liver injury, occur in about 7% of patients receiving pindolol. Rarely, increases in serum alkaline phosphatase, LDH, and uric acid concentrations may occur.

Other adverse effects noted during pindolol use include muscle, leg, or joint pain or cramps, occurring in 2-10% of patients; chest pain, occurring in 5% of patients; and wheezing, pruritus, rash, burning eyes, hyperhidrosis, pollakiuria (urinary frequency), and impotence, occurring in less than 2% of patients.

The possibility that other adverse effects associated with other β-blockers may occur during pindolol therapy should be considered. These include hematologic reactions (e.g., agranulocytosis, nonthrombocytopenic or thrombocytopenic purpura); allergic reactions characterized by fever, sore throat, laryngospasm, and respiratory distress; reversible alopecia; and Peyronie's disease.

Precautions and Contraindications

Pindolol shares the toxic potentials of β-blockers, and the usual precautions of these agents should be observed.

In patients with heart failure, sympathetic stimulation is vital for the support of circulatory function. Pindolol should be used with caution in patients with inadequate cardiac function, since heart failure may be precipitated by blockade of β-adrenergic stimulation when pindolol therapy is administered. In addition, in patients with latent cardiac insufficiency, prolonged β-adrenergic blockade may lead to cardiac failure. Although β-blockers should be avoided in patients with overt heart failure, pindolol may be administered cautiously, if necessary, to patients with well-compensated heart failure (e.g., those controlled with cardiac glycosides and/or diuretics). Patients receiving pindolol therapy should be instructed to consult their physician at the first sign or symptom of impending cardiac failure and should be adequately treated (e.g., with a cardiac glycoside and/or diuretic) and observed closely; if cardiac failure continues, pindolol should be discontinued, gradually if possible.

Abrupt withdrawal of pindolol may exacerbate angina symptoms or precipitate myocardial infarction in patients with coronary artery disease, or precipitate thyroid crisis in patients with thyrotoxicosis. Therefore, patients receiving pindolol (especially those with ischemic heart disease) should be warned not to interrupt or discontinue therapy without consulting their clinician. When discontinuance of long-term pindolol therapy is planned, particularly in patients with ischemic heart disease, dosage of the drug should be gradually reduced over a period of 1-2 weeks. When pindolol therapy is discontinued, patients should be carefully monitored. If exacerbation of angina occurs or acute coronary insufficiency develops after pindolol therapy is interrupted or discontinued, treatment with the drug should be reinstituted promptly, at least temporarily, and appropriate measures for the management of unstable angina pectoris should be initiated. Because coronary artery disease is common and may be unrecognized, the manufacturers caution that it may be prudent not to discontinue pindolol therapy abruptly, even in patients being treated only for hypertension.

Since β-blockers may inhibit bronchodilation produced by endogenous catecholamines, the drugs generally should not be used in patients with bronchospastic disease. Pindolol should be used with caution in patients with nonallergic bronchospasm (e.g., chronic bronchitis, emphysema).

Pindolol should be used with caution in hyperthyroidism, since β-blockers may mask the tachycardia associated with hyperthyroidism. In addition, it is recommended that pindolol be used with caution in patients with diabetes mellitus since β-blockers may mask the tachycardia associated with hypoglycemia (a few cases have been reported in patients with type 2 diabetes mellitus), and β-blockers, especially nonselective ones, may potentially precipitate severe, acute hyperglycemia.(see Cautions: Endocrine Effects.) However, many clinicians state that patients with diabetes mellitus may be particularly likely to experience a reduction in morbidity and mortality with the use of β-blockers. β-Blockers usually will not completely mask dizziness and sweating seen with hypoglycemia. If pindolol is administered concurrently with an antidiabetic agent, dosage of the latter agent may need to be adjusted.

Pindolol should be used with caution in patients undergoing major surgery involving general anesthesia. The necessity of withdrawing β-blocker therapy prior to major surgery is controversial, but the manufacturers state that, if possible, pindolol should be withdrawn well before surgery. Severe, protracted hypotension and difficulty in restarting or maintaining a heart beat have occurred during surgery in some patients who have received β-blockers. If patients continue to receive pindolol prior to surgery, the anesthesiologist should be advised that the patient is receiving the drug. The manufacturers recommend administration of β-agonists (e.g., dopamine, dobutamine, isoproterenol, norepinephrine) to reverse pindolol's β-adrenergic blockade if necessary during surgery.

Patients with a history of atopy or severe anaphylactic reactions to a variety of allergens may be more reactive to repeated, accidental, diagnostic, or therapeutic challenge with such allergens while receiving a β-blocker. These patients may be less responsive than other patients to usual dosages of epinephrine used to treat anaphylactic reactions.

Pindolol should be used with caution and in reduced dosage in patients with impaired hepatic function.

Pindolol also is contraindicated in patients receiving thioridazine.(See Drug Interactions: Thioridazine.)

Pindolol is contraindicated in patients with bronchial asthma, second- or third-degree AV block, severe bradycardia, cardiogenic shock, or overt cardiac failure.

Pediatric Precautions

Safety and efficacy of pindolol in children have not been established. For information on overall principles and expert recommendations for treatment of hypertension in pediatric patients, .


Studies in rats and mice using oral pindolol dosages up to 5 and 100 times the recommended maximum human doses, respectively, have not revealed evidence of carcinogenicity.

Pregnancy and Lactation


Reproduction studies in rats and rabbits using doses exceeding 100 times the recommended maximum human doses have not revealed any evidence of embryotoxicity or teratogenicity. There are no adequate and controlled studies to date using pindolol in pregnant women, and the drug should be used during pregnancy only when the potential benefits justify the possible risks to the fetus.


Nursing should not be undertaken in women receiving pindolol, since the drug is distributed into milk.

Drug Interactions

Cardiovascular Drugs

Hypotensive Agents

Concomitant administration of pindolol with reserpine may increase the incidence of hypotension and bradycardia as compared with pindolol alone, because of reserpine's catecholamine-depleting activity. Pindolol also is additive with and may potentiate the hypotensive actions of other hypotensive agents (e.g., hydralazine, hydrochlorothiazide). This effect usually is used to therapeutic advantage, but careful adjustment of dosage is necessary when these drugs are used concurrently.

Slowing or complete suppression of SA node activity with development of slow ventricular rates (e.g., 30-40 bpm), often misdiagnosed as complete AV block, has been reported in patients receiving the nondihydropyridine calcium-channel blocking agent mibefradil (no longer commercially available in the US), principally in geriatric patients and in association with concomitant β-blocker therapy.


Slight transient decreases in serum digoxin concentrations have occurred when pindolol and digoxin were used concurrently; however, this effect is not considered clinically important.


Concomitant use of pindolol and thioridazine is contraindicated because such use may be associated with prolongation of the QTc interval and a possible increase in the risk of serious, potentially fatal cardiac arrhythmia (e.g., torsades de pointes) as a result of moderate, dose-related increases in serum concentrations of thioridazine and 2 of its metabolites. Higher than expected serum concentrations of pindolol also have occurred following combined use of these drugs.



Pindolol is rapidly absorbed from the GI tract. Reported bioavailability ranges from 50-95 %; bioavailability in uremic patients may be at the lower end of this range. Food does not reduce bioavailability but may increase the rate of GI absorption. Pindolol reportedly does not undergo substantial metabolism on first pass through the liver; the manufacturers state that only about 20% of an oral dose is metabolized on first pass. Peak plasma concentrations of 45-167 ng/mL are reached within 1-2 hours after administration of a single 20-mg dose. The extent of absorption may be decreased in patients with impaired renal function. The effect of pindolol on heart rate usually is seen within 3 hours and acute hemodynamic effects persist for 24 hours after administration of the drug.


Approximately 40-60% of pindolol is bound to plasma proteins. In healthy adults, the drug has an apparent volume of distribution (Vd) of 1.2-2 L/kg; Vd may be decreased by 50% in uremic patients. Pindolol is distributed into milk.


Elimination of pindolol appears to be a first-order process over a dose range of 5-20 mg. The drug has a plasma half-life (t½) of 3-4 hours in healthy adults. Plasma t½ increases to 3-11.5 hours in patients with renal failure, to 7-15 hours in geriatric patients, and varies from 2.5-30 hours in patients with hepatic cirrhosis. Approximately 60-65% of pindolol is metabolized in the liver to hydroxylated metabolites which are then excreted in urine as glucuronides and ethereal sulfates. In healthy adults, about 35-50% of the drug is excreted in urine unchanged; in patients with creatinine clearances less than 20 mL/minute, less than 15% is excreted in urine unchanged.

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