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Fluvastatin

Class: HMG-CoA Reductase Inhibitors
- Statins
VA Class: CV350
Chemical Name: [R*,S*-(E)]-(±)-7-[3-(4-Fluorophenyl)-1-(1-methylethyl)-1H-indol-2-yl]-3,5-dihydroxy-6-heptenoic acid monosodium salt
Molecular Formula: C24H26FNO4•Na
CAS Number: 93957-55-2
Brands: Lescol

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

Introduction

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

Uses for Fluvastatin

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, fluvastatin 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 CHD to reduce the risk of undergoing coronary revascularization procedures.72 350 Unless contraindicated, statins are considered first-line therapy in patients 21–75 years of age who have 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 (e.g., dietary management) in patients with CHD to slow the progression of coronary atherosclerosis.72

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

Dyslipidemias

Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total cholesterol, LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia (heterozygous familial and nonfamilial) or mixed dyslipidemia (Fredrickson type IIa or IIb).1 72 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.73 353

Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total cholesterol, LDL-cholesterol, and apo B concentrations in the management of heterozygous familial hypercholesterolemia in boys and girls (≥1 year postmenarchal) 10–16 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 72

Reduction of total and LDL-cholesterol concentrations in patients with hypercholesterolemia associated with or exacerbated by diabetes mellitus† (diabetic dyslipidemia),54 renal insufficiency†,63 cardiac† or renal transplantation†,20 21 22 21 27 55 57 64 or nephrotic syndrome† (nephrotic hyperlipidemia).24 65

Fluvastatin Dosage and Administration

General

  • Patients should be placed on a standard lipid-lowering diet before initiation of fluvastatin therapy and should remain on this diet during treatment with the drug.1 60

Monitoring during Antilipemic Therapy

  • Manufacturer recommends obtaining lipoprotein concentrations periodically during fluvastatin therapy.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 during statin therapy.350

Administration

Oral Administration

Administer orally without regard to meals.1

Administer conventional capsules once (in the evening) or twice daily;1 do not administer two 40-mg capsules at one time.72 Do not open capsules prior to administration.1

Administer extended-release tablets as a single dose at any time of day.1 Do not break, crush, or chew tablets.1

Dosage

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

Pediatric Patients

Dyslipidemias
Oral

Children 10–16 years of age: Initially, 20 mg once daily.1

Adjust dosage at 6-week intervals until the desired effect on lipoprotein concentrations is observed or a daily dosage of 80 mg (administered as 40 mg twice daily as conventional capsules or 80 mg once daily as extended-release tablets) is reached.1 72

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 dosages of 20–40 mg once daily (as conventional capsules) or 80 mg once daily (as extended-release tablets) are FDA-labeled dosages, these dosages were 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., fluvastatin 40 mg twice daily [as conventional capsules], fluvastatin 80 mg once daily [as extended-release tablets]).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., fluvastatin 40 mg twice daily [as conventional capsules], fluvastatin 80 mg once daily [as extended-release tablets]) 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., fluvastatin 40 mg twice daily [as conventional capsules], fluvastatin 80 mg once daily [as extended-release tablets]) 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

Patients who require reductions in LDL-cholesterol concentrations of <25%: Initially, 20 mg once daily in the evening.1

Patients who require reductions of >25% in LDL-cholesterol concentrations or patients with primary hypercholesterolemia or mixed dyslipidemia: Initially, 40 mg (as conventional capsules) once daily in the evening, 80 mg (as extended-release tablets) once daily at any time of day, or 40 mg (as conventional capsules) twice daily.1 72

Adjust dosage at intervals of ≥4 weeks until the desired effect on lipoprotein concentrations is observed.1

Usual maintenance dosage is 20–80 mg daily.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

Prescribing Limits

Pediatric Patients

Oral

Children 10–16 years of age: Maximum 80 mg daily.1

Special Populations

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of liver disease; monitor such patients closely.1

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

Renal Impairment

Dosage modification is not necessary in patients with mild to moderate renal impairment.1

Dosages >40 mg daily have not been studied in patients with severe renal impairment; use caution when administering higher dosages to such patients.1

Cautions for Fluvastatin

Contraindications

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

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

  • Known hypersensitivity to fluvastatin 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 they are highly unlikely to conceive and have been informed of the potential hazards.1 If the patient becomes pregnant while taking the drug, 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 CK [CPK] concentration increases >10 times the ULN) has been reported.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 72

Immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, reported rarely in patients receiving statins.72 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.72

Risk of myopathy is increased in geriatric patients (≥65 years of age) and patients with renal impairment or inadequately treated hypothyroidism.72

Certain drug interactions also may increase risk of myopathy and/or rhabdomyolysis.1 72 (See Specific Drugs under Interactions.)

Use with caution in patients with predisposing factors for myopathy (e.g., advanced age [>65 years of age], renal impairment, inadequately treated hypothyroidism).72

Measure baseline serum CK concentrations prior to initiation of therapy, particularly in patients at high risk of developing musculoskeletal toxicity (e.g., geriatric patients, black men, patients receiving concomitant therapy with myotoxic drugs).70 138 202

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, TSH concentrations also should be obtained in such patients.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

Consider myopathy in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked CK elevation.72 Discontinue therapy if serum CK concentrations become markedly elevated 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 acute renal failure secondary to rhabdomyolysis (e.g., sepsis; hypotension; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).1 Initiate IV hydration therapy (in a hospital setting) in patients experiencing rhabdomyolysis as needed.202

Hepatic Effects

Increases in serum aminotransferase (AST, ALT) concentrations reported.1 Generally transient and resolve or improve with continued therapy or after temporary interruption in therapy.72

Persistent aminotransferase elevations (>3 times the ULN on 2 consecutive weekly measurements) are more common at higher dosages (40 or 80 mg daily).72 Most cases occurred within 12 weeks of therapy.72

Fatal and nonfatal hepatic failure reported rarely.72 Possibly drug-related hepatitis, which resolved following discontinuance of therapy, reported very rarely.72

Perform liver function tests before initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage201 ).72 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 statin.357

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt fluvastatin therapy.72 If an alternate etiology is not found, do not restart fluvastatin.72

Also see Hepatic Impairment under Cautions.

Hyperglycemic Effects

Increases in HbA1c and fasting serum glucose concentrations reported.72 200 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.72

Fluvastatin had no effect on nonstimulated cortisol concentrations, adrenal response to corticotropin (adrenocorticotropic hormone, ACTH) stimulation, or thyroid metabolism.72 Small declines in total serum testosterone concentrations reported, but no commensurate elevation in LH concentrations, and no effect on FSH concentrations in men.72 Data insufficient to determine effect on female sex hormones.72

If clinical evidence of endocrine dysfunction is present, evaluate patients appropriately.72

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).72

Cognitive Impairment

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) reported rarely.72

Generally nonserious and reversible, with variable times to symptom onset (1 day to years) and resolution (median of 3 weeks following discontinuance of therapy).72 200 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

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

Category X.1 (See Contraindications and also see Fetal/Neonatal Morbidity and Mortality, under Cautions.)

Lactation

Distributed into milk in animals.72 Use is contraindicated in nursing women; women who require fluvastatin therapy should not breast-feed their infants.72

Pediatric Use

Safety and efficacy not established in children <9 years of age or in premenarchal girls.1 72 (See Advice to Patients.)

Geriatric Use

Fluvastatin exposures not substantially different between patients ≥65 years of age and younger adults.72

Use with caution, since age ≥65 years is a predisposing factor for myopathy.72 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 and/or have a history of liver disease.1

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

Common Adverse Effects

Headache, dyspepsia, myalgia, abdominal pain, nausea.72

Interactions for Fluvastatin

Metabolized principally by CYP2C9; CYP2C8 and CYP3A4 also contribute to fluvastatin metabolism.1

Specific Drugs

Drug

Interaction

Comments

Bile acid sequestrants (e.g., cholestyramine)

Additive cholesterol-lowering effects45

Decreased fluvastatin peak plasma concentration and AUC when administered 4 hours after cholestyramine and a meal72

Administer statins 1 hour before or 4 hours after the resin69

Colchicine

Myopathy, including rhabdomyolysis, reported72

Use concomitantly with caution72

Cyclosporine

Increased fluvastatin concentrations;1 339 increased risk of myopathy and/or rhabdomyolysis1

If used concomitantly, limit fluvastatin dosage to 20 mg twice daily72

Diclofenac

Increased fluvastatin and diclofenac concentrations72

Digoxin

Slight increase in digoxin peak plasma concentration72

Erythromycin

Increased risk of myopathy and/or rhabdomyolysis1

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

Increased risk of myopathy and/or rhabdomyolysis1

Gemfibrozil: Avoid concomitant use72

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 therapy72 350

Fluconazole

Increased peak plasma concentration and AUC of fluvastatin1

If used concomitantly, limit fluvastatin dosage to 20 mg twice daily72

Glyburide

Increased fluvastatin and glyburide concentrations;1 no change in glucose, insulin, or C-peptide concentrations1

Monitor appropriately72

Histamine H2-receptor antagonists (e.g., cimetidine, ranitidine)

Increased plasma concentrations and decreased clearance of fluvastatin1

Niacin (antilipemic dosages [≥1 g daily])

Increased risk of myopathy and/or rhabdomyolysis1

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

If used concomitantly, consider reducing fluvastatin dosage72

Phenytoin

Increased fluvastatin and phenytoin concentrations1

Patients receiving phenytoin should be monitored appropriately when fluvastatin is initiated or dosage is adjusted1

Proton-pump inhibitors (e.g., omeprazole)

Increased plasma concentrations and decreased clearance of fluvastatin1

Rifampin

Decreased peak plasma concentration and AUC of fluvastatin72

Warfarin

Bleeding and/or increased PT observed with other statins1 339

Closely monitor PT until stabilized if fluvastatin is initiated or dosage is adjusted in patients receiving warfarin1 339

Fluvastatin Pharmacokinetics

Pharmacokinetic data in pediatric patients not available.1

Absorption

Bioavailability

Rapidly and completely absorbed.1

Absolute bioavailability of conventional capsules is 24%.1

The mean relative bioavailability of extended-release tablets is approximately 29% compared with conventional capsules administered under fasting conditions.1

Mean peak plasma concentrations occur within 1 or 3 hours following oral administration of conventional capsules or extended-release tablets, respectively.1

Onset

A therapeutic response usually is apparent within 2 weeks after initiating therapy, with a maximal response occurring within 4 weeks.1

Food

Peak plasma concentration decreased and time to peak plasma concentrations increased following administration of fluvastatin conventional capsules with the evening meal; however, no substantial differences in lipid-lowering effects following administration with food.1 72

Bioavailability increased and absorption delayed following administration of extended-release tablets with a high-fat meal; however, peak plasma concentrations achieved with the extended-release tablets following a high-fat meal are much less than those achieved with a single or twice-daily dose of 40 mg.1

Distribution

Extent

Distributed mainly to the liver.1

Distributed into milk (milk to plasma ratio 2:1).1

Plasma Protein Binding

About 98%.1

Elimination

Metabolism

Metabolized in the liver, principally by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8.1

Elimination Route

Excreted in feces (90%) and urine (5%) mainly as metabolites; <2% excreted as unchanged drug.1

Half-life

<3 hours (conventional capsules) and 9 hours (extended-release tablets).1

Special Populations

Patients with hepatic impairment may have increased exposure to fluvastatin due to decreased presystemic metabolism.1

Stability

Storage

Oral

Capsules and Extended-release Tablets

Tight containers at 25°C (may be exposed to 15–30°C).1 Protect from light.1

Actions

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

  • Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries,33 72 114 115 116 117 118 119 120 121 122 123 modulate BP 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.71 350

  • Risk of myopathy and/or rhabdomyolysis; risk is increased when used concomitantly with certain other drugs.72 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 72

  • Risk of adverse hepatic effects.72 Importance of promptly reporting any symptoms suggestive of liver injury (e.g., fatigue, anorexia, right upper abdominal discomfort, dark urine, jaundice).72

  • Risk of nonserious, reversible cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion).72 200

  • Risk of increased glucose concentrations and development of type 2 diabetes.72 200 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; if the patient becomes pregnant, importance of immediately discontinuing fluvastatin and contacting a clinician.1 72

  • Importance of avoiding breast-feeding during therapy.72 If the patient has a lipid disorder and is breast-feeding, importance of contacting a clinician to discuss other antilipemic treatment options.72

  • 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

Fluvastatin Sodium

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Capsules

20 mg (of fluvastatin)*

Fluvastatin Sodium Capsules

Lescol

Novartis

40 mg (of fluvastatin)*

Fluvastatin Sodium Capsules

Lescol

Novartis

Tablets, extended-release

80 mg (of fluvastatin)*

Fluvastatin Sodium Extended-Release Tablets

Lescol XL

Novartis

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

1. Novartis. Lescol (fluvastatin sodium) capsules and Lescol XL (fluvastatin sodium) extended-release tablets prescribing information. East Hanover, NJ: 2006 Apr.

2. 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

3. Grundy SM, Bilheimer D, Chait A et al. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA. 1993; 269:3015-23. http://www.ncbi.nlm.nih.gov/pubmed/8501844?dopt=AbstractPlus

4. Anon. Fluvastatin for lowering cholesterol. Med Lett Drugs Ther. 1994; 36:45-6. http://www.ncbi.nlm.nih.gov/pubmed/8177137?dopt=AbstractPlus

5. Jokubatis LA. Updated clinical safety experience with fluvastatin. Am J Cardiol. 1994; 73(suppl D):18D-24D. http://www.ncbi.nlm.nih.gov/pubmed/8198019?dopt=AbstractPlus

6. Baggio G, De Candia O, Forte PL et al. Efficacy and safety of fluvastatin in elderly hypercholesterolemic patients: a pilot study. Curr Ther Res. 1994; 55:401-7.

7. Davidson MH on behalf of the FLUENT Investigators Group. Fluvastatin long-term extension trial (FLUENT): summary of efficacy and safety. Am J Med. 1994; 96(suppl 6A):41S-4S.

8. Peters TK, Muratti EN, Mehra M. Fluvastatin in primary hypercholesterolemia: efficacy and safety in patients at high risk. An analysis of a clinical trial database. Am J Med. 1994; 96(suppl 6A):79S-83S. http://www.ncbi.nlm.nih.gov/pubmed/8017471?dopt=AbstractPlus

9. Banga JD, Jacotot B, Pfister P et al. Long-term treatment of hypercholesterolemia with fluvastatin: a 52-week multicenter safety and efficacy study. Am J Med. 1994; 96(suppl 6A):87S-93S. http://www.ncbi.nlm.nih.gov/pubmed/8017473?dopt=AbstractPlus

10. Peters TK. Safety profile of fluvastatin. Br J Clin Pract. 1996; 77(suppl A):20-3.

11. Suzumura K, Yasuhara M, Tanaka K et al. Protective effect of fluvastatin sodium (XU-62-320), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on oxidative modification of human low-density lipoprotein in vitro. Biochem Pharmacol. 1999; 57:697-703. http://www.ncbi.nlm.nih.gov/pubmed/10037456?dopt=AbstractPlus

12. Pauciullo P, Borgnino C, Paoletti R et al. Efficacy and safety of a combination of fluvastatin and bezafibrate in patients with mixed hyperlipidaemia (FACT) study. Atherosclerosis. 2000; 150:429-36. http://www.ncbi.nlm.nih.gov/pubmed/10856536?dopt=AbstractPlus

13. Pedersen TR, Tobert JA. Benefits and risks of HMG-CoA reductase inhiitors in the prevention of coronary heart disease: a reappraisal. Drug Safety. 1996; 14:11-24. http://www.ncbi.nlm.nih.gov/pubmed/8713485?dopt=AbstractPlus

14. Food and Drug Administration. Specific requirements on content and format of labeling for human prescription drugs; proposed addition of “geriatric use“ subsection in the labeling. 21 CFR Part 201. Proposed rule. [Docket No. 89N-0474] Fed Regist. 1990; 55:46134-7.

15. Woodhouse K, Wynne HA. Age-related changes in hepatic function: implications for drug therapy. Drugs Aging. 1992; 2:243-55. http://www.ncbi.nlm.nih.gov/pubmed/1606355?dopt=AbstractPlus

16. Montamat SC, Cusack BJ, Vestal RE. Management of drug therapy in the elderly. N Engl J Med. 1989; 321:303-9. http://www.ncbi.nlm.nih.gov/pubmed/2664519?dopt=AbstractPlus

17. Durnas C, Loi CM, Cusack BJ. Hepatic drug metabolism and aging. Clin Pharmacokinet. 1990; 19:359-89. http://www.ncbi.nlm.nih.gov/pubmed/2268986?dopt=AbstractPlus

18. Pomara N, Stanley B, Block R et al. Caution in the use of drugs in the elderly. N Engl J Med. 1983; 308:1600-1.

19. Lipsitz L. Orthostatic hypotension in the elderly. N Engl J Med. 1989; 321:952-7. http://www.ncbi.nlm.nih.gov/pubmed/2674714?dopt=AbstractPlus

20. Schrama YC, Hene RJ, de Jonge N et al. Efficacy and muscle safety of fluvastatin in cyclosporine-treated cardiac and renal transplant recipients. Transplantation. 1998; 66:1175-81. http://www.ncbi.nlm.nih.gov/pubmed/9825814?dopt=AbstractPlus

21. Austen JL, Shifrin FA, Bartucci MR et al. Effects of fluvastatin on hyperlipidemia after renal transplantation: influence of steroid therapy. Ann Pharmacother. 1996; 30:1386-9. http://www.ncbi.nlm.nih.gov/pubmed/8968448?dopt=AbstractPlus

22. Goldberg R, Roth D. Evaluation of fluvastatin in the treatment of hypercholesterolemia in renal transplant recipients taking cyclosporine. Transplantation. 1996; 62:1559-64. http://www.ncbi.nlm.nih.gov/pubmed/8970607?dopt=AbstractPlus

23. Li PKT, Mak TWL, Wang AYM et al. The interaction of fluvastatin and cyclospori A in renal transplant patients. Int J Clin Pharmacol Ther. 1995:33:246-8.

24. Matzkies FK, Bahner U, Teschner M et al. Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients. Am J Nephrol. 1999; 19:492-4. http://www.ncbi.nlm.nih.gov/pubmed/10460940?dopt=AbstractPlus

25. Eliav O, Schurr D, Pfister P et al. High-dose fluvastatin and bezafibrate combination treatment for heterozygous familial hypercholesterolemia. Am J Cardiol. 1995; 76:76-9A. http://www.ncbi.nlm.nih.gov/pubmed/7793410?dopt=AbstractPlus

26. Smit JWA, Jansen GH, de Bruin TWA et al. Treatment of combined hyperlipidemia with fluvastatin and gemfibrozil, alone or combination, does not induce muscle damage. Am J Cardiol. 1995; 76:126-8A.

27. Goldberg RB, Roth D. A preliminary report of the safety and efficacy of fluvastatin for hypercholesterolemia in renal transplant patients receiving cyclosporine. Am J Cardiol. 1995; 76:107-9A. http://www.ncbi.nlm.nih.gov/pubmed/7611141?dopt=AbstractPlus

28. Teramoto T, Goto Y, Kurokawa K et al. Clinical efficacy of fluvastatin for hyperlipidemia in Japanese patients. Am J Cardiol. 1995; 76:33-6A.

29. American Heart Association Committee to Design a Dietary Treatment of Hyperlipoproteinemia. Recommendations for treatment of hyperlipidemia in adults: a joint statement of the Nutrition Committee and the Council on Arteriosclerosis. Circulation. 1984; 69:1065-90A. http://www.ncbi.nlm.nih.gov/pubmed/6713610?dopt=AbstractPlus

30. Reviewers’ comments (personal observations) on Lovastatin 24:06.08.

31. Zavoral JH, Haggerty BJ, Winick AG et al. Efficacy of fluvastatin, a totally synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Am J Cardiol. 1995; 76:37-40A.

32. Broyles FE, Walden CE, Hunninghake DB et al. Effect of fluvastatin on intermediate density lipoprotein (remnants) and other lipoprotein levels in hypercholesterolemia. Am J Cardiol. 1995; 76:129-35A.

33. Herd JA, Ballantyne CM, Farmer JA et al. Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study [LCAS]). Am J Cardiol. 1997; 80:278-86. http://www.ncbi.nlm.nih.gov/pubmed/9264419?dopt=AbstractPlus

34. Ballantyne CM. Clinical trial endpoints: angiograms, events, and plaque instability. Am J Cardiol. 1998; 82:5M-11M. http://www.ncbi.nlm.nih.gov/pubmed/9766342?dopt=AbstractPlus

35. Tomlinson B, Mak TWL, Tsui JYY et al. Effects of fluvastatin on lipid profile and apolipoproteins in Chinese patients with hypercholesterolemia. Am J Cardiol. 1995; 76:136-9A.

36. Buzzi AP, Pastore MA, on behalf of the argentine and multicenter evaluation investigators. Argentine multicenter evaluation of fluvastatin in the treatment of patients with hypercholesterolemia. Curr Ther. 1997; 58:1013-28.

37. Rindone JP, Hiller D, Arriola G. A comparison of fluvastatin 40 mg every other day versus 20 mg every day in patients with hypercholesterolemia. Pharmacotherapy. 1998; 18:836-9. http://www.ncbi.nlm.nih.gov/pubmed/9692657?dopt=AbstractPlus

38. Insull W, Black D, Dujovne C et al. Efficacy and safety of once-daily vs twice-daily dosing with fluvastatin, a synthetic reductase inhibitor, in primary hypercholesterolemia. Arch Intern Med. 1994; 154:2449-55. http://www.ncbi.nlm.nih.gov/pubmed/7979841?dopt=AbstractPlus

39. Dujovne CA, Davidson MH. Fluvastatin administration at bedtime versus with the evening meal: a multicenter comparison of bioavailability, safety, and efficacy. Am J Med. 1994; 96(suppl 6A):37-40S.

40. Jones P, Kafonek S, Laurora I et al. Comparative dose efficacy study of atorvastatin versus fluvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study). Am J Cardiol. 1998; 81:582-7. http://www.ncbi.nlm.nih.gov/pubmed/9514454?dopt=AbstractPlus

41. Nash DT. Meeting national cholesterol education goals in clinical practice-a comparison of lovastatin and fluvastatin in primary prevention. Am J Cardiol. 1996(suppl 6A):26-31.

42. Ose L, Scott RS, and the fluvastatin-Fluvastatin Study Group. Double-blind comparison of the efficacy and tolerability of fluvastatin and fluvastatin in patients with primary hypercholesterolaemia. Clin Drug Invest. 1995; 10:127-38.

43. Deslypere JP. fluvastatin-fluvastatin comparative study. Clin Drug Invest. 1995; 11:362-4.

44. Schulte KL, Beil S. Efficacy and tolerability of fluvastatin and fluvastatin in hypercholesterolaemic patients. Clin Drug Invest. 1996; 12:119-26.

45. Sprecher DL, Abrams J, Allen JW et al. Low-dose combined therapy with fluvastatin and cholestyramine in hyperlipidemic patients. Ann Intern Med. 1994; 120:537-43. http://www.ncbi.nlm.nih.gov/pubmed/8093139?dopt=AbstractPlus

46. Jacotot B, Banga JD, Waite R et al. Long-term efficacy with fluvastatin as monotherapy and combined with cholestyramine (a 156-week multicenter study). Am J Cardiol. 1995; 76:41-6A.

47. Fanghanel G, Espinosa J, Olivares D et al. Open-label study to assess the efficacy, safety, and tolerability of fluvastatin versus bezafibrate for hypercholesterolemia. Am J Cardiol. 1995; 76:57-61A.

48. Jacobson TA, Chin MM, Fromell GJ et al. Fluvastatin with and without niacin for hypercholesterolemia. Am J Cardiol. 1994; 74:149-54. http://www.ncbi.nlm.nih.gov/pubmed/8023779?dopt=AbstractPlus

49. Leitersdorf E, Muratti EN, Eliav O et al. Efficacy and safety of a combination fluvastatin-bezafibrate treatment for familial hypercholesterolemia: comparative analysis with a fluvastatin-cholestyramine combination. Am J Med. 1994; 96:401-7. http://www.ncbi.nlm.nih.gov/pubmed/8192170?dopt=AbstractPlus

50. Leitersdorf E, Muratti EN, Eliav O et al. Efficacy and safety of triple therapy (fluvastatin-bezafibrate-cholestyramine) for severe familial hypercholesterolemia. Am J Cardiol. 1995; 76:84-8A.

51. Sigurdsson G, Haraldsdottir SO, Melberg TH et al. fluvastatin compared to fluvastatin in the reduction of serum lipids and apolipoproteins in patients with ischaemic heart disease and moderate hypercholesterolaemia. Acta Cardiol. 1998; 1:7-14.

52. Ballantyne CM, Herd JA, Ferlic LL et al. Influence of low HDL on progression of coronary artery disease and response to fluvastatin therapy. Circulation. 1999; 99:736-43. http://www.ncbi.nlm.nih.gov/pubmed/9989957?dopt=AbstractPlus

53. Serruys PW, Foley DP, Jackson G et al. A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty. Eur Heart J. 1999; 20:58-69. http://www.ncbi.nlm.nih.gov/pubmed/10075142?dopt=AbstractPlus

54. Knopp RH, Frolich JJ. Efficacy and safety of fluvastatin in patients with non-insulin-dependent diabetes mellitus and hyperlipidemia: preliminary report. Am J Cardiol. 1994; 73:39-41D.

55. Locsey L, Asztalos L, Kincses Z et al. Fluvastatin (Lescol) treatment of hyperlipidaemia in patients with renal transplants. Int Urol and Nephrol. 1997; 29:95-106.

56. Christians U, Jacobsen W, Floren LC. Metabolism and drug interactions of 3-hydroxy-3-methylglutaryl Coenzyme A reductase inhibitors in transplant patients: are the statins mechanistically similar? Pharmacol Ther. 1998; 80:1-34.

57. Podder H, Gero L, Foldes K et al. Treatment of metabolic disorders with fluvastatin after renal transplantation. Transplantation Proc. 1997; 29:216-9.

58. Novartis. Lescol formulary information. East Hanover, NJ. 1998 Nov.

59. Buemi M, Allegra A, Corica F et al. Effect of fluvastatin on proteinuria in patients with immunoglobulin A nephropathy. Clin Pharmacol Ther. 2000; 67:427-31. http://www.ncbi.nlm.nih.gov/pubmed/10801253?dopt=AbstractPlus

60. Langtry HD, Markham A. Fluvastatin. A review of its use in lipid disorders. Drugs. 1999; 57:583-606. http://www.ncbi.nlm.nih.gov/pubmed/10235694?dopt=AbstractPlus

61. Plosker GL, Wagstaff AJ. Fluvastatin. A review of its pharmacology and use in the management of hypercholesterolemia. Drugs. 1996; 51:433-59. http://www.ncbi.nlm.nih.gov/pubmed/8882381?dopt=AbstractPlus

62. Lennernas H, Fager G. Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Clin Pharmacokinet. 1997; 32:403-25. http://www.ncbi.nlm.nih.gov/pubmed/9160173?dopt=AbstractPlus

63. Lintott CJ, Scott RS, Bremer JM et al. Fluvastatin for dyslipoproteinemia, with or without concomitant chronic renal insufficiency. Am J Cardiol. 1995; 76:97-101A. http://www.ncbi.nlm.nih.gov/pubmed/7793418?dopt=AbstractPlus

64. Holdaas H, Hartmann A, Stenstrom J et al. Effect of fluvastatin for safely lowering atherogenic lipids in renal transplant patients receiving cyclosporine. Am J Cardiol. 1995; 76:102-6A.

65. Matzkies FK, Bahner U, Teschner M et al. Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients with nephrotic syndrome. Am J Nephrol. 1999; 19:492-4. http://www.ncbi.nlm.nih.gov/pubmed/10460940?dopt=AbstractPlus

66. Hagen E, Istad H, Ose L et al. Fluvastatin efficacy and tolerability in comparison and in combination with cholestyramine. Eur J Clin Pharmacol. 1994; 46:445-9. http://www.ncbi.nlm.nih.gov/pubmed/7957541?dopt=AbstractPlus

67. National Institutes of Health, National Heart, Lung, and Blood Institute, National Cholesterol Education Program. Cholesterol lowering in the patient with coronary heart disease. Physician monograph. NIH Publication. 1997; 97-3794.

68. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA. 1993;269:3015-23.

69. Expert Panel on Detection, Evaluation, and Treatment of high Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of high Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001; 285:2486-97. http://www.ncbi.nlm.nih.gov/pubmed/11368702?dopt=AbstractPlus

70. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Adult Treatment Panel III Report. From AHA web site. http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm

71. Serruys PWJC, de Feyter P, Macaya C et al for the Lescol Intervention Prevention Study (LIPS) investigators. Fluvastatin for prevention of cardiac events following successful first percutaneous coronary intervention: a randomized controlled trial. JAMA. 2002; 287:3215-22. http://www.ncbi.nlm.nih.gov/pubmed/12076217?dopt=AbstractPlus

72. Novartis. Lescol (fluvastatin sodium) capsules and Lescol XL (fluvastatin sodium) extended-release tablets prescribing information. East Hanover, NJ: 2012 Oct.

73. Abbvie. Trilipix (fenofibric acid) capsules prescribing information. North Chicago, IL; 2013 Mar.

74. ACCORD Study Group, Ginsberg HN, Elam MB et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010; 362:1563-74. http://www.ncbi.nlm.nih.gov/pubmed/20228404?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2879499&blobtype=pdf

114. MAAS Investigators. Effect of simvastatin on coronary atheroma: the multicentre anti-atheroma study (MAAS). Lancet. 1994; 344:633-8. http://www.ncbi.nlm.nih.gov/pubmed/7864934?dopt=AbstractPlus

115. 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

116. 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

117. 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

118. Salonen R, Nyyssonen K, Porkkala-Sarataho E et al. The Kuopio Atherosclerosis Prevention Study (KAPS): Effect of pravastatin treatment on lipids, oxidation resistance of lipoproteins, and atherosclerotic progression. Am J Cardiol. 1995; 76:34-9C.

119. Blankenhorn DH, Azen SP, Kramsch DM et al. Coronary angiographic changes with lovastatin therapy. The Monitored Atherosclerosis Regression Study (MARS). The MARS Research Group. Ann Intern Med. 1993; 119:969-76.

120. Waters D, Higginson L, Gladstone P et al. Effects of cholesterol lowering on the progression of coronary atherosclerosis in women. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. Circulation. 1995; 92:2404-10.

121. Brown G, Albers JJ, Fisher LD et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med. 1990; 323:1289-98. http://www.ncbi.nlm.nih.gov/pubmed/2215615?dopt=AbstractPlus

122. Furberg CD, Adams HP, Applegate WB et al for the Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Circulation. 1994; 90:1679-87. http://www.ncbi.nlm.nih.gov/pubmed/7734010?dopt=AbstractPlus

123. DeGroot E, Jukema JW, Montauban AD et al. B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). J Am Coll Cardiol. 1998; 31:1561-7. http://www.ncbi.nlm.nih.gov/pubmed/9626835?dopt=AbstractPlus

124. Glorioso N, Troffa C, Filigheddu F et al. Effect of the HMG-CoA reductase inhibitors on blood pressure in patients with essential hypertension and primary hypercholesterolemia. Hypertension. 1999; 34:1281-6. http://www.ncbi.nlm.nih.gov/pubmed/10601131?dopt=AbstractPlus

125. Borghi C, Prandin MG, Costa FV et al. Use of statins and blood pressure control in treated hypertensive patients with hypercholesterolemia. J Cardiovasc Pharmacol. 2000; 35:549-55. http://www.ncbi.nlm.nih.gov/pubmed/10774784?dopt=AbstractPlus

126. Ridker PM, Rifai N, Pfeffer MA et al. Long-term effects of pravastatin on plasma concentration of C-reactive protein. Circulation. 1999; 100:230-5. http://www.ncbi.nlm.nih.gov/pubmed/10411845?dopt=AbstractPlus

127. Kluft C, de Maat MPM, Leuven JAG et al. Statins and C-reactive protein. Lancet. 1999; 353:1274-5.

138. Pasternak RC, Smith SC Jr, Bairey-Merz CN et al. ACC/AHA/NHLBI clinical advisory on the use and safety of statins. American College of Cardiology/American Heart Association/National Heart, Lung and Blood Institute. Circulation. 2002;106:1024-8.

200. Food and Drug Administration. FDA drug safety communication: Important safety label changes to cholesterol-lowering statin drugs. Rockville, MD; 2012 Feb 28. From FDA website. http://www.fda.gov/Drugs/DrugSafety/ucm293101.htm

201. Food and Drug Administration. FDA expands advice on statin risks. Rockville, MD; 2012 Feb 27. From FDA website. http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm293330.htm

202. McKenney JM, Davidson MH, Jacobson TA et al. Final conclusions and recommendations of the National Lipid Association Statin Safety Assessment Task Force. Am J Cardiol. 2006; 97(suppl):89-94C.

309. Cannon CP, Blazing MA, Giugliano RP et al. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes. N Engl J Med. 2015; 372:2387-97. http://www.ncbi.nlm.nih.gov/pubmed/26039521?dopt=AbstractPlus

336. Cholesterol Treatment Trialists' (CTT) Collaborators, Mihaylova B, Emberson J et al. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012; 380:581-90. http://www.ncbi.nlm.nih.gov/pubmed/22607822?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=3437972&blobtype=pdf

337. Baigent C, Keech A, Kearney PM et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet. 2005; 366:1267-78. http://www.ncbi.nlm.nih.gov/pubmed/16214597?dopt=AbstractPlus

338. Cholesterol Treatment Trialists’ (CTT) Collaboration, Baigent C, Blackwell L et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010; 376:1670-81. http://www.ncbi.nlm.nih.gov/pubmed/21067804?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2988224&blobtype=pdf

339. Wiggins BS, Saseen JJ, Page RL et al. Recommendations for Management of Clinically Significant Drug-Drug Interactions With Statins and Select Agents Used in Patients With Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2016; 134:e468-e495.

350. Stone NJ, Robinson J, Lichtenstein AH et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013; :. http://circ.ahajournals.org/content/early/2013/11/11/01.cir.0000437738.63853.7a

351. Stone NJ, Robinson JG, Lichtenstein AH et al. Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Disease Risk in Adults: Synopsis of the 2013 ACC/AHA Cholesterol Guideline. Ann Intern Med. 2014; :. http://www.ncbi.nlm.nih.gov/pubmed/24474185?dopt=AbstractPlus

352. Eckel RH, Jakicic JM, Ard JD et al. 2013 AHA/ACC Guideline on Lifestyle Management to Reduce Cardiovascular Risk: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63:2960-84. http://www.ncbi.nlm.nih.gov/pubmed/24239922?dopt=AbstractPlus

353. ACCORD Study Group, Ginsberg HN, Elam MB et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010; 362:1563-74. http://www.ncbi.nlm.nih.gov/pubmed/20228404?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2879499&blobtype=pdf

354. AIM-HIGH Investigators, Boden WE, Probstfield JL et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011; 365:2255-67. http://www.ncbi.nlm.nih.gov/pubmed/22085343?dopt=AbstractPlus

356. Miller M, Stone NJ, Ballantyne C et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011; 123:2292-333. http://www.ncbi.nlm.nih.gov/pubmed/21502576?dopt=AbstractPlus

357. Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents, National Heart, Lung, and Blood Institute. Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report. Pediatrics. 2011; 128 Suppl 5:S213-56. http://www.ncbi.nlm.nih.gov/pubmed/22084329?dopt=AbstractPlus

369. HPS2-THRIVE Collaborative Group, Landray MJ, Haynes R et al. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med. 2014; 371:203-12. http://www.ncbi.nlm.nih.gov/pubmed/25014686?dopt=AbstractPlus

371. Anderson TJ, Boden WE, Desvigne-Nickens P et al. Safety profile of extended-release niacin in the AIM-HIGH trial. N Engl J Med. 2014; 371:288-90. http://www.ncbi.nlm.nih.gov/pubmed/25014706?dopt=AbstractPlus http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=4156937&blobtype=pdf

388. Holdaas H, Fellström B, Jardine AG et al. Effect of fluvastatin on cardiac outcomes in renal transplant recipients: a multicentre, randomised, placebo-controlled trial. Lancet. 2003; 361:2024-31. http://www.ncbi.nlm.nih.gov/pubmed/12814712?dopt=AbstractPlus

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