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Pravastatin

Class: HMG-CoA Reductase Inhibitors
- Statins
VA Class: CV350
Chemical Name: [1S-[1α(βS*,δS*),2α,6α,8β(R*),8aα]]-1,2,6,7,8,8a-Hexahydro-β,δ,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-1-naphthalene-heptanoic acid monosodium salt
CAS Number: 81131-70-6
Brands: Pravachol

Medically reviewed by Drugs.com. Last updated on June 16, 2020.

Introduction

Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).1 2 3 4 5 6

Uses for Pravastatin

Prevention of Cardiovascular Events

ACC/AHA cholesterol management guideline recommends statins as first-line therapy for prevention of atherosclerotic cardiovascular disease (ASCVD) in adults; extensive evidence demonstrates that statins can substantially reduce ASCVD risk when used for secondary prevention or primary prevention (in high-risk patients).336 337 338 350 Relative reduction in ASCVD risk is correlated with degree of LDL-cholesterol lowering; therefore, use maximum tolerated statin intensity to achieve optimum ASCVD benefits.350 According to ACC/AHA, pravastatin may be used for primary or secondary prevention in adults when moderate-intensity statin therapy is indicated.350 (See Prevention of Cardiovascular Events under Dosage and Administration.)

Adjunct to nondrug therapies (i.e., lifestyle modifications) in patients with hypercholesterolemia without clinical evidence of CHD to reduce the risk of MI, to reduce the risk of undergoing myocardial revascularization procedures, and to reduce the risk of cardiovascular mortality (with no increase in death from noncardiovascular causes).1 12 350 Consider benefits, adverse effects, drug interactions, and patient preferences before initiating statin therapy for primary prevention.350

Adjunct to nondrug therapies (i.e., lifestyle modifications350 ) in patients with clinical evidence of CHD to reduce the risk of total mortality by reducing coronary death, to reduce the risk of MI, to reduce the risk of undergoing myocardial revascularization procedures, and to reduce the risk of stroke or TIA.1 Unless contraindicated, statins are considered first-line therapy in patients 21–75 years of age with clinical ASCVD (i.e., acute coronary syndromes; history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin).350 Addition of a nonstatin drug (i.e., niacin) to statin-based therapy (i.e., simvastatin with or without ezetimibe) in patients with established cardiovascular disease not shown to provide incremental ASCVD risk reduction benefit beyond that provided by statin monotherapy.350 354

Adjunct to nondrug therapies (i.e., lifestyle modifications350 ) in patients with clinical evidence of CHD to slow the progression of coronary atherosclerosis.1 13 14 16 Has been shown to slow the progression and/or induce regression of atherosclerosis in a few patients without clinical evidence of CHD† who had mild to moderate elevations of LDL-cholesterol concentrations.61

Intensive antilipemic therapy (atorvastatin 80 mg daily) shown to be more effective than moderate antilipemic therapy (pravastatin 40 mg daily) in reducing the risk of cardiovascular events in patients hospitalized for acute coronary syndrome (16% reduction in composite risk of death or major cardiovascular events for atorvastatin compared with pravastatin regimen).69 Intensive antilipemic therapy also more effective in slowing progression of coronary atherosclerosis in patients with CHD.70

Current recommendations from ACC/AHA regarding prevention of ASCVD and lifestyle modifications to reduce cardiovascular risk are available at [Web] or [Web].350 352

Dyslipidemias

Adjunct to nondrug therapies (e.g., dietary management) in adults to decrease elevated serum total and LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia or mixed dyslipidemia (Fredrickson type IIa or IIb).1 2 3 5 17 Also used in combination with fenofibrate to decrease triglyceride concentrations and increase HDL-cholesterol concentrations in patients with mixed dyslipidemia and CHD (or CHD risk equivalents) who are on optimal statin therapy; however, no incremental benefit on cardiovascular morbidity and mortality beyond that provided by statin monotherapy.74 353

Adjunct to dietary therapy and lifestyle modification in the management of heterozygous familial hypercholesterolemia in children ≥8 years of age who, despite an adequate trial of dietary management, have a serum LDL-cholesterol concentration of ≥190 mg/dL or a serum LDL-cholesterol concentration of ≥160 mg/dL and either a family history of premature cardiovascular disease or ≥2 other cardiovascular risk factors.1

Adjunct to nondrug therapies (e.g., dietary management) in the treatment of primary dysbetalipoproteinemia (Fredrickson type III) in patients who do not respond adequately to diet.1

Adjunct to nondrug therapies (e.g., dietary management) in the treatment of elevated serum triglyceride concentrations (Fredrickson type IV).1 However, fibric acid derivatives provide greater benefit in patients with elevated triglyceride concentrations compared with statins.356

Reduction of total and LDL-cholesterol concentrations in patients with hypercholesterolemia associated with or exacerbated by diabetes mellitus† (diabetic dyslipidemia),51 62 cardiac† or liver† transplantation,19 63 or nephrotic syndrome† (nephrotic hyperlipidemia).20

Pravastatin Dosage and Administration

General

  • Patients should be placed on a standard lipid-lowering diet before initiation of pravastatin therapy and should remain on this diet during treatment with the drug.1

Monitoring during Antilipemic Therapy

  • Manufacturer recommends obtaining lipoprotein concentrations within 4 weeks following initiation of pravastatin and adjusting dosage accordingly.1 ACC/AHA cholesterol management guideline recommends obtaining lipoprotein concentrations within 4–12 weeks following initiation of statin therapy (to assess response and adherence) and monitoring every 3–12 months thereafter as clinically indicated.350

  • Periodically reinforce adherence to lifestyle modifications.350

Administration

Oral Administration

Administer orally at any time of day without regard to meals.1

Dosage

Available as pravastatin sodium; dosage expressed in terms of pravastatin.1

Pediatric Patients

Dyslipidemias
Oral

Children 8–13 years of age: 20 mg once daily.1 Dosages >20 mg daily have not been evaluated.1

Adolescents 14–18 years of age: 40 mg once daily.1 Dosages >40 mg daily have not been evaluated.1

Re-evaluate in adulthood and modify therapy appropriately.1

Adults

Prevention of Cardiovascular Events

Select appropriate statin intensity to achieve optimal ASCVD risk reduction.350 Giving maximally tolerated statin intensity is preferred over giving lower statin dosages in combination with nonstatin drugs, a strategy not yet shown to reduce ASCVD risk.350

Although 80 mg once daily is an FDA-labeled dosage, it was not evaluated in randomized controlled studies reviewed by the ACC/AHA expert panel.350

Primary Prevention in Patients with LDL-cholesterol Concentrations ≥190 mg/dL (≥21 years of age)
Oral

ACC/AHA cholesterol management guideline recommends initiating high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin) unless contraindicated.350

Primary Prevention in Patients with Type 1 or 2 Diabetes Mellitus† (40–75 years of age)
Oral

ACC/AHA cholesterol management guideline recommends moderate-intensity statin therapy (e.g., pravastatin 40–80 mg once daily).350

If estimated 10-year ASCVD risk ≥7.5%, consider high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin) unless contraindicated.350

In patients <40 or >75 years of age, consider potential benefits, adverse effects, drug interactions, and patient preferences when deciding to initiate, continue, or intensify statin therapy.350

Primary Prevention in Patients with LDL-cholesterol Concentrations 70–189 mg/dL and Elevated ASCVD Risk (40–75 years of age)
Oral

Estimated 10-year ASCVD risk ≥7.5%: ACC/AHA cholesterol management guideline recommends moderate- (e.g., pravastatin 40–80 mg once daily) to high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin).350

Estimated 10-year ASCVD risk of 5 to <7.5%: ACC/AHA cholesterol management guideline states may consider moderate-intensity statin therapy.350

Consider potential benefits, adverse effects, drug interactions, and patient preferences before initiating statin therapy.350

Secondary Prevention in Patients with Clinical ASCVD (i.e., acute coronary syndromes; history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin) (21–75 years of age)
Oral

ACC/AHA cholesterol management guideline recommends high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin) unless contraindicated.350

In patients at increased risk for developing statin-associated adverse effects or in whom high-intensity statin therapy is inappropriate or contraindicated, consider moderate-intensity statin therapy (e.g., pravastatin 40–80 mg once daily) if tolerated.350

Patients >75 years of age: Individualize therapy based on potential benefits, adverse effects, drug interactions, and patient preferences; may consider moderate-intensity statin therapy if tolerated.350

Dyslipidemias
Oral

Initially, 40 mg once daily.1 If antilipemic response is inadequate, increase dosage to 80 mg daily.1 Adjust dosage at intervals of ≥4 weeks until the desired effect on lipoprotein concentrations is observed.1

Dosage Modification
Oral

ACC/AHA cholesterol management guideline states may consider decreasing statin dosage when LDL-cholesterol concentrations are <40 mg/dL on 2 consecutive measurements; however, no data to suggest that LDL-cholesterol concentrations <40 mg/dL increase risk of adverse effects.350

Special Populations

Hepatic Impairment

No specific dosage recommendations at this time.1

Use with caution in patients who consume substantial amounts of alcohol, have a recent (<6 months) history of liver disease, or exhibit manifestations of liver disease (e.g., unexplained increases in aminotransferase concentrations, jaundice).1

Contraindicated in patients with active liver disease or unexplained, persistent increases in serum aminotransferase concentrations.1

Renal Impairment

Initially, 10 mg once daily in patients with severe renal impairment.1

Detailed Pravastatin dosage information

Cautions for Pravastatin

Contraindications

  • Active liver disease or unexplained, persistent elevations of serum aminotransferases.1

  • Pregnancy or lactation.1 Administer to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards.1

  • Known hypersensitivity to pravastatin or any ingredient in the formulation.1

Warnings/Precautions

Fetal/Neonatal Morbidity and Mortality

Suppression of cholesterol biosynthesis could cause fetal harm.1 Congenital anomalies following intrauterine exposure to statins reported rarely.1

Administer to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards; these women should be advised to use effective contraception.1 If the patient becomes pregnant while taking the drug, immediately discontinue therapy and apprise the patient of the potential hazard to the fetus.1

Musculoskeletal Effects

Myopathy (manifested as muscle pain, tenderness, or weakness and serum creatine kinase [CK, creatine phosphokinase, CPK] concentration increases >10 times the ULN) reported occasionally.1

Rhabdomyolysis (characterized by muscle pain or weakness with marked increases [>10 times the ULN] in serum CK concentrations and increases in Scr [usually accompanied by brown urine and urinary myoglobinuria])138 with acute renal failure secondary to myoglobinuria has been reported.1

Immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, reported rarely in patients receiving statins.1 Characterized by proximal muscle weakness and elevated CK concentrations that persist despite discontinuance of statin therapy, necrotizing myopathy without substantial inflammation, and improvement following therapy with immunosuppressive agents.1

Risk of myopathy is increased in patients receiving higher dosages of statins; risk also may be increased in geriatric patients (≥65 years of age) and patients with renal impairment or uncontrolled hypothyroidism.1

Certain drug interactions also may increase risk of myopathy and/or rhabdomyolysis.1 (See Specific Drugs under Interactions.)

Measure baseline serum CK concentrations prior to initiation of therapy, particularly in black men or in patients receiving concomitant therapy with fibric acid derivatives.66 138

ACC/AHA cholesterol management guideline does not recommend routine monitoring of CK concentrations in adults; however, may obtain CK concentrations before initiating therapy in adults at increased risk of developing adverse musculoskeletal effects (e.g., patients with personal or family history of statin intolerance or muscle disease, patients receiving concomitant therapy with myotoxic drugs).350 During statin therapy, may measure CK concentrations in adults with muscle symptoms (e.g., pain, tenderness, stiffness, cramping, weakness, generalized fatigue).350

National Heart, Lung, and Blood Institute (NHLBI) expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents recommends obtaining CK concentrations in pediatric patients before initiating statin therapy and routinely monitoring for muscle toxicity during therapy.357

Obtain serum CK concentrations and compare with baseline concentrations in patients presenting with musculoskeletal symptoms suggestive of myopathy; because hypothyroidism may be a predisposing factor, thyrotropin (thyroid-stimulating hormone, TSH) concentrations also should be obtained in such patients.138

Consider myopathy in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevation in CK.1 Discontinue if serum CK concentrations increase markedly or if myopathy is diagnosed or suspected.1

Monitor patients weekly if myalgia (muscle pain, tenderness) is present with either no CK elevation or a moderate elevation (3–10 times the ULN) until manifestations improve; discontinue if manifestations worsen.138

Dosage reduction or temporary discontinuance may be prudent in patients with muscle discomfort and/or weakness in the presence of progressive elevation of CK concentrations on serial measurements.138

Temporarily withhold therapy in any patient experiencing an acute or serious condition predisposing to the development of renal failure secondary to rhabdomyolysis (e.g., sepsis; hypotension; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).1

Hepatic Effects

Associated with increases in serum aminotransferase (AST, ALT) concentrations.1

Pancreatitis,1 hepatitis (including chronic active hepatitis),1 cholestatic jaundice,1 fatty change in liver, cirrhosis,1 fulminant hepatic necrosis,1 hepatoma,1 and fatal and nonfatal hepatic failure1 have been reported.1

Perform liver function tests before initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage201 ).1 Although manufacturer previously recommended more frequent monitoring, FDA concluded that serious statin-related liver injury is rare and unpredictable, and that routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.200 ACC/AHA cholesterol management guideline recommends obtaining liver function tests in adults with symptoms of hepatotoxicity (e.g., unusual fatigue or weakness, loss of appetite, abdominal pain, dark colored urine, yellowing of skin or sclera).350 However, NHLBI expert panel on cardiovascular health and risk reduction in children and adolescents strongly recommends routine monitoring of hepatic function in children and adolescents receiving statins.357

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt pravastatin therapy.1 If an alternate etiology is not found, do not restart pravastatin.1

Also see Hepatic Impairment under Cautions.

Hyperglycemic Effects

Increases in HbA1c and fasting serum glucose concentrations reported.200 Possible increased risk of developing diabetes.200 May need to monitor glucose concentrations following initiation of statin therapy.201

FDA states that cardiovascular benefits of statins outweigh these small increased risks.200

ACC/AHA cholesterol management guideline recommends evaluating patients for new-onset diabetes mellitus according to current diabetes screening guidelines.350

If diabetes mellitus develops during statin therapy, encourage patients to adhere to a heart-healthy diet, engage in physical activity, achieve and maintain a healthy body weight, cease tobacco use, and continue statin therapy to reduce the risk of ASCVD.350

Endogenous Steroid Production

Statins interfere with cholesterol synthesis and theoretically may blunt adrenal and/or gonadal steroid production.1

Effects of pravastatin on basal steroid hormone levels not established.1 Effects on pituitary-gonadal axis in premenopausal women unknown.1

If clinical evidence of endocrine dysfunction is present, evaluate patients appropriately.1

Caution advised if a statin or another antilipemic agent is used concomitantly with drugs that may decrease concentrations or activity of endogenous steroid hormones (e.g., ketoconazole, spironolactone, cimetidine).1

Cognitive Impairment

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) reported rarely.1

Generally nonserious and reversible, with variable times to symptom onset (1 day to years) and resolution (median of 3 weeks following discontinuance of therapy).1 200 Not associated with fixed or progressive dementia (e.g., Alzheimer’s disease) or clinically important cognitive decline.200 Not associated with any specific statin, patient's age, statin dosage, or concomitant drug therapy.200

FDA states that cardiovascular benefits of statins outweigh the small increased risk of cognitive impairment.200

If manifestations consistent with cognitive impairment occur, National Lipid Association (NLA) statin safety assessment task force recommends evaluating and managing patients appropriately.202

If patients present with confusion or memory impairment, ACC/AHA cholesterol management guideline recommends evaluating patient for statin as well as nonstatin causes (e.g., other drugs, systemic or neuropsychiatric causes).350

Hypersensitivity Reactions

Anaphylaxis, angioedema, lupus erythematosus-like syndrome, polymyalgia rheumatica, dermatomyositis, vasculitis, purpura, hemolytic anemia, positive antinuclear antibody (ANA), increased erythrocyte sedimentation rate (ESR), arthritis, arthralgia, asthenia, photosensitivity, chills, malaise, toxic epidermal necrolysis, and erythema multiforme (including Stevens-Johnson syndrome) reported during postmarketing surveillance.1

Role as Adjunct Therapy

Prior to institution of antilipemic therapy, vigorously attempt to control serum cholesterol by appropriate dietary regimens, weight reduction, exercise, and treatment of any underlying disorder that might be the cause of lipid abnormality.1

Specific Populations

Pregnancy

Safety in pregnant women not established; no known benefits with use during pregnancy.1 Discontinue immediately if pregnancy is known or suspected.1 (See Contraindications and also see Fetal/Neonatal Morbidity and Mortality under Cautions.)

Lactation

Distributed into milk; effects of drug on breast-fed infants or milk production not known.1 Use contraindicated in nursing women; women who require pravastatin therapy should not breast-feed their infants.1

Pediatric Use

Safety and efficacy not established in children <8 years of age.1 Advise adolescent girls to use effective and appropriate contraceptive methods during therapy to reduce the likelihood of unintended pregnancy.1

Geriatric Use

No substantial differences in safety or efficacy relative to younger adults.1

Use with caution, since age ≥65 years is a predisposing factor for myopathy.1 In patients >75 years of age, consider benefits, adverse effects, drug interactions, and patient preferences before initiating statin therapy.350

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol, have a recent (<6 months) history of liver disease, or exhibit manifestations of liver disease (e.g., unexplained increases in aminotransferase concentrations, jaundice).1

Contraindicated in patients with active liver disease or unexplained, persistent increases in liver function test results.1

Renal Impairment

Monitor closely for adverse musculoskeletal effects, since history of renal impairment may be a risk factor for development of rhabdomyolysis.1

Dosage adjustments necessary in patients with severe renal impairment.1 (See Renal Impairment under Dosage and Administration.)

Common Adverse Effects

Musculoskeletal pain, nausea or vomiting, upper respiratory infection, diarrhea, headache.1

Interactions for Pravastatin

Minimally metabolized by CYP3A4; pharmacokinetic interaction unlikely.1

Specific Drugs

Drug

Interaction

Comments

Aspirin

Increased pravastatin peak plasma concentration and AUC1

Bile acid sequestrants (i.e., cholestyramine, colestipol)

Variable effects on pravastatin concentrations1

Administer pravastatin 1 hour before or 4 hours after the resin66

Calcium-channel blocking agents (diltiazem, verapamil)

Increased pravastatin peak plasma concentration and AUC1

Cimetidine

Increased pravastatin peak plasma concentration and AUC1

Colchicine

Myopathy, including rhabdomyolysis, reported1

Use concomitantly with caution1

Cyclosporine

Substantially increased pravastatin concentrations; possible increased risk of myopathy or rhabdomyolysis1 339

If used concomitantly, initiate pravastatin at 10 mg daily; do not exceed pravastatin dosage of 20 mg daily1

Digoxin

Slight increases in plasma digoxin and pravastatin concentrations1

Fibric acid derivatives (e.g., fenofibrate, gemfibrozil)

Increased risk of myopathy or rhabdomyolysis1

Gemfibrozil: Decreased pravastatin peak plasma concentration and AUC1

Gemfibrozil: Avoid concomitant use1

Other fibric acid derivatives (e.g., fenofibrate): Use concomitantly with caution and only if benefits outweigh risks; consider using only low- or moderate-intensity statin therapy during concomitant therapy1 350

Fluconazole

Decreased pravastatin peak plasma concentration and AUC1

HIV protease inhibitors

Ritonavir-boosted darunavir: Increased pravastatin peak plasma concentration and AUC1

Lopinavir/ritonavir: Increased pravastatin peak plasma concentration and AUC1

Ritonavir-boosted darunavir: Some experts recommend using the lowest necessary dosage of pravastatin and carefully monitoring patients72

Lopinavir/ritonavir: Dosage adjustment not necessary72

Ritonavir-boosted saquinavir: Dosage adjustment not necessary72 73

Itraconazole

Increased pravastatin concentrations1

Macrolides (e.g., azithromycin. clarithromycin, erythromycin)

Azithromycin: Potential increased pravastatin concentrations1

Clarithromycin: Increased pravastatin peak plasma concentration and AUC;1 increased risk of myopathy or rhabdomyolysis1

Erythromycin: Potential increased pravastatin concentrations and increased risk of myopathy1

Azithromycin and erythromycin: Use concomitantly with caution1

Clarithromycin: Use concomitantly with caution; if used concomitantly, do not exceed pravastatin dosage of 40 mg daily1

Niacin (antilipemic dosages [≥1 g daily])

Decreased pravastatin peak plasma concentration and AUC;1 possible increased risk of myopathy1

Increased risk of severe adverse effects (disturbances in glycemic control requiring hospitalization, development of diabetes mellitus, adverse GI effects, myopathy, gout, rash, skin ulceration, infection, bleeding) with concomitant use of niacin (1.5–2 g daily) and simvastatin (40–80 mg daily, with or without ezetimibe)369 371

Use concomitantly with caution; consider reducing pravastatin dosage1

Warfarin

Increased warfarin peak plasma concentration and AUC; increased PT1 339

Monitor INR more closely after initiating or changing dosage of pravastatin339
Pravastatin drug interactions (more detail)

Pravastatin Pharmacokinetics

Absorption

Bioavailability

Rapidly absorbed following oral administration; undergoes extensive first-pass metabolism in the liver.1 129 130 131 132 Mean peak plasma concentrations occur at 1–1.5 hours.1 133

Absolute bioavailability is 17%.1 130

Evening administration of the drug is associated with a decrease in the extent of absorption;1 however, the antilipemic activity remains unchanged and may be superior to the activity achieved with morning administration.1

Onset

A therapeutic response to pravastatin is usually apparent within 1 week after initiating therapy, with a maximal response occurring within 4 weeks.1 37 38 132

Food

Food appears to reduce the systemic bioavailability of pravastatin;1 129 131 however, antilipemic effects are similar whether pravastatin is administered with or 1 hour prior to meals.1

Distribution

Extent

Distributed mainly to the liver.1

Distributed into human milk.1

Plasma Protein Binding

Approximately 50%.1

Elimination

Metabolism

Undergoes enzymatic and nonenzymatic biotransformation independent of the CYP enzyme system.131 136 The principal metabolites are pharmacologically inactive.129 130 131 137

Elimination Route

Excreted in urine (20%) and feces (70%).1 129 130 132

Half-life

1.8 hours.1

Special Populations

Renal impairment may reduce clearance of pravastatin and/or active metabolites.1

Hepatic impairment may reduce clearance of pravastatin and/or active metabolites.1

Stability

Storage

Oral

Tablets

Tight containers at 25°C (may be exposed to 15–30°C); protect from light and moisture.1

Actions

  • Inhibits HMG-CoA reductase, causing subsequent reduction in hepatic cholesterol synthesis.1 Reduces serum concentrations of total cholesterol, LDL-cholesterol, apolipoprotein B (apo B), and triglycerides.1

  • Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries,14 15 16 26 27 114 119 120 121 122 modulate blood pressure in hypercholesterolemic patients with hypertension,124 125 and possess anti-inflammatory activity.126 127

Advice to Patients

  • Importance of adhering to nondrug therapies and measures, including adherence to a heart-healthy diet, regular exercise, avoidance of tobacco products, and maintenance of a healthy weight.1 350

  • Risk of myopathy and/or rhabdomyolysis; risk is increased with higher dosages or when used concomitantly with certain drugs.1 Importance of patients promptly reporting muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever, or if manifestations persist after discontinuance of therapy.1

  • Risk of adverse hepatic effects.1 Importance of promptly reporting any symptoms suggestive of liver injury (e.g., fatigue, anorexia, right upper abdominal discomfort, dark urine, jaundice).1

  • Risk of nonserious, reversible cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion).1 200

  • Risk of increased glucose concentrations and development of type 2 diabetes.200 May need to monitor glucose concentrations following initiation of statin therapy.201

  • Importance of advising women and adolescent girls to avoid pregnancy (i.e., using effective and appropriate contraceptive methods) during therapy and informing pregnant women of risk to fetus.1

  • Importance of avoiding breast-feeding during therapy.1

  • Importance of informing clinician of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.1

  • Importance of informing patients of other important precautionary information.1 (See Cautions.)

Preparations

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

Pravastatin Sodium

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets

10 mg (of pravastatin)*

Pravastatin Sodium Tablets

20 mg (of pravastatin)*

Pravachol

Bristol-Myers Squibb

Pravastatin Sodium Tablets

40 mg (of pravastatin)*

Pravachol

Bristol-Myers Squibb

Pravastatin Sodium Tablets

80 mg (of pravastatin)*

Pravachol

Bristol-Myers Squibb

Pravastatin Sodium Tablets

AHFS DI Essentials™. © Copyright 2021, Selected Revisions June 26, 2017. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

References

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3. Anon. Pravastatin, simvastatin, and pravastatin for lowering serum cholesterol concentrations. Med Lett Drugs Ther. 1992; 34:57-8. http://www.ncbi.nlm.nih.gov/pubmed/1593973?dopt=AbstractPlus

4. Rosen T, Heathcock CH. The synthesis of mevinic acids. Tetrahedron. 1986; 42:4909-51.

5. Raasch RH. Pravastatin sodium, a new HMG-CoA reductase inhibitor. DICP. 1991; 25:388-94. http://www.ncbi.nlm.nih.gov/pubmed/1926908?dopt=AbstractPlus

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8. Goldstein JL, Brown MS. The low-density lipoprotein pathway and its relation to atherosclerosis. Ann Rev Biochem. 1977; 46:897-930. http://www.ncbi.nlm.nih.gov/pubmed/197883?dopt=AbstractPlus

9. Brown MS, Goldstein JL. Lipoprotein receptors in the liver: control signals for plasma cholesterol traffic. J Clin Invest. 1983; 72:743-7. http://www.ncbi.nlm.nih.gov/pubmed/6309907?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=1129238&blobtype=pdf

10. The Expert Panel. Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Arch Intern Med. 1988; 148:36-69. http://www.ncbi.nlm.nih.gov/pubmed/3422148?dopt=AbstractPlus

11. National Institutes of Health Office of Medical Applications of Research. Consensus conference: lowering blood cholesterol to prevent heart disease. JAMA. 1985; 25:2080-6.

12. Shepherd J, Cobbe SM, Ford I et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med. 1995; 333:1301-7. http://www.ncbi.nlm.nih.gov/pubmed/7566020?dopt=AbstractPlus

13. Byington RP, Jukema JW, Salonen JT et al. Reduction in cardiovascular events during pravastatin therapy. Pooled analysis of clinical events of the Pravastatin Atherosclerosis Intervention Program. Circulation. 1995; 92:2419-25. http://www.ncbi.nlm.nih.gov/pubmed/7586340?dopt=AbstractPlus

14. Pitt B, Mancini GBJ, Ellis SG et al. Pravastatin limitation of atherosclerosis in the coronary arteries (PLAC I): reduction in atherosclerosis progression and clinical events. J Am Coll Cardiol. 1995; 26:1133-9. http://www.ncbi.nlm.nih.gov/pubmed/7594023?dopt=AbstractPlus

15. Crouse JR III, Byington RP, Bond MG et al. Pravastatin, lipids, and atherosclerosis in the carotid arteries (PLAC-II). Am J Cardiol. 1995; 75:455-9. http://www.ncbi.nlm.nih.gov/pubmed/7863988?dopt=AbstractPlus

16. Jukema JW, Bruschke AVG, van Boven AJ et al. Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation. 1995; 91:2528-40. http://www.ncbi.nlm.nih.gov/pubmed/7743614?dopt=AbstractPlus

17. Sacks FN, Pfeffer MA, Maye LA et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med. 1996; 335:1001-9. http://www.ncbi.nlm.nih.gov/pubmed/8801446?dopt=AbstractPlus

18. Walter DH, Schachinger V, Elsner M et al. Effect of statin therapy on restenosis after coronary stent implantation. Am J Cardiol. 2000; 85:962-8. http://www.ncbi.nlm.nih.gov/pubmed/10760335?dopt=AbstractPlus

19. Keogh A, Macdonald P, Kaan A et al. Efficacy and safety of pravastatin vs simvastatin after cardiac transplantation. Clin Heart Lung Transplant. 2000; 19:529-37.

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