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Special Alerts
HMG-CoA Reductase Inhibitors: Evidence Does Not Suggest Increased Incidence of Amyotrophic Lateral Sclerosis (ALS) - Results of FDA Analysis - September 30, 2008
The U.S. Food and Drug Administration's (FDA) review of 41 long-term controlled clinical trials of HMG-CoA reductase inhibitors finds no evidence of an increased incidence of ALS (also known as Lou Gehrig's disease) related to these medications. This analysis occurred after the FDA had received notice of numerous adverse events of which 109 of these reports mentioned ALS, Lou Gehrig's disease, or motor neurone disease. The clinical trials included in the analysis had a median duration of treatment of 3.3 years (range of duration: 6 months to 5 years) and involved 120,964 patients. The analysis identified a total of 19 cases of ALS – 9 cases per 64,602 patients (0.014%) with statin therapy and 10 cases per 56,362 patients (0.017%) with placebo. The incidence rates, based on approximately 400,000 person-years, were 4.2 per 100,000 person-years in the statin-treated group and 5 per 100,000 person-years in the placebo-treated group.
The FDA recommends that health care providers continue to prescribe, and patients continue to use these products as described within their labeling.
For more information, healthcare professionals may refer to the following:
http://www.fda.gov/medwatch/safety/2008/safety08.htm#Statin
Colman E, Szarfman A, Wyeth J, et al, “An Evaluation of a Data Mining Signal for Amyotrophic Lateral Sclerosis and Statins Detected in FDA's Spontaneous Adverse Event Reporting System,” Pharmacoepidemiol Drug Saf, 2008 (epub ahead of print)
Medication Safety Issues
Sound-alike/look-alike issues:
Lovastatin may be confused with Leustatin®, Livostin®, Lotensin®
Mevacor® may be confused with Mivacron®
International issues:
Lovacol® [Chile and Finland] may be confused with Levatol® which is a brand name for penbutolol in the U.S.
Lovastin® [Poland] may be confused with Livostin® which is a brand name for levocabastine in the U.S.
Pronunciation
(LOE va sta tin)
U.S. Brand Names
Index Terms
Generic Available
Yes: Immediate release tablet
Canadian Brand Names
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Adjunct to dietary therapy to decrease elevated serum total and LDL-cholesterol concentrations in primary hypercholesterolemia
Primary prevention of coronary artery disease (patients without symptomatic disease with average to moderately elevated total and LDL-cholesterol and below average HDL-cholesterol); slow progression of coronary atherosclerosis in patients with coronary heart disease
Adjunct to dietary therapy in adolescent patients (10-17 years of age, females >1 year postmenarche) with heterozygous familial hypercholesterolemia having LDL >189 mg/dL, or LDL >160 mg/dL with positive family history of premature cardiovascular disease (CVD), or LDL >160 mg/dL with the presence of at least two other CVD risk factors
Pregnancy Risk Factor
X
Pregnancy Considerations
Cholesterol biosynthesis may be important in fetal development. Contraindicated in pregnancy. Administer to women of childbearing potential only when conception is highly unlikely and patients have been informed of potential hazards.
Lactation
Excretion unknown/contraindicated
Contraindications
Hypersensitivity to lovastatin or any component of the formulation; active liver disease; unexplained persistent elevations of serum transaminases; pregnancy; breast-feeding
Warnings/Precautions
Concerns related to adverse effects:
• Myopathy/rhabdomyolysis: Patients receiving HMG-CoA reductase inhibitors have developed rhabdomyolysis with acute renal failure and/or myopathy; patients should be monitored closely. This risk is dose-related and is increased with concurrent use of other lipid lowering medications. Temporarily discontinue for elective major surgery, acute medical or surgical conditions, or in any patient experiencing an acute or serious condition predisposing to renal failure (eg, sepsis, hypotension, trauma, uncontrolled seizures). Based upon current evidence, HMG-CoA reductase inhibitor therapy should be continued in the perioperative period unless risk outweighs cardioprotective benefit. Use caution in patients with renal impairment, inadequately treated hypothyroidism, and those taking other drugs associated with myopathy (eg, colchicine); these patients are predisposed to myopathy. Patients should be instructed to report unexplained muscle pain, tenderness, weakness, or brown urine.
Disease-related concerns:
• Hepatic impairment and/or ethanol use: Use with caution in patients who consume large amounts of ethanol or have a history of liver disease.
Concurrent drug therapy issues:
• High potential for interactions: Use with caution in patients taking strong CYP3A4 inhibitors (see drug interactions); consider alternative agents that avoid or lessen potential for CYP-mediated interactions.
Special populations:
• Elderly: Use with caution in patients with advanced age, these patients are predisposed to myopathy.
• Pediatrics: Safety and efficacy of the immediate release tablet has not been evaluated in prepubertal patients, patients <10 years of age, or doses >40 mg/day; extended release tablets have not been studied in patients <20 years of age.
Other warnings/precautions:
• Hyperlipidemia: Secondary causes of hyperlipidemia should be ruled out prior to therapy.
• Liver function tests: Must be monitored by periodic laboratory assessment.
Adverse Reactions
Percentages as reported with immediate release tablets; similar adverse reactions seen with extended release tablets.
>10%: Neuromuscular & skeletal: CPK increased (>2x normal) (11%)
1% to 10%:
Central nervous system: Headache (2% to 3%), dizziness (0.5% to 1%)
Dermatologic: Rash (0.8% to 1%)
Gastrointestinal: Abdominal pain (2% to 3%), constipation (2% to 4%), diarrhea (2% to 3%), dyspepsia (1% to 2%), flatulence (4% to 5%), nausea (2% to 3%)
Neuromuscular & skeletal: Myalgia (2% to 3%), weakness (1% to 2%), muscle cramps (0.6% to 1%)
Ocular: Blurred vision (0.8% to 1%)
<1% (Limited to important or life-threatening): Acid regurgitation, alopecia, arthralgia, chest pain, dermatomyositis, eye irritation, insomnia, leg pain, paresthesia, pruritus, vomiting, xerostomia
Additional class-related events or case reports (not necessarily reported with lovastatin therapy): Alkaline phosphatase increased, alopecia, alteration in taste, anaphylaxis, angioedema, anorexia, anxiety, arthritis, cataracts, chills, cholestatic jaundice, cirrhosis, CPK increased (>10x normal), depression, dryness of skin/mucous membranes, dyspnea, eosinophilia, erectile dysfunction, erythema multiforme, ESR increased, facial paresis, fatty liver, fever, flushing, fulminant hepatic necrosis, GGT increased, gynecomastia, hemolytic anemia, hepatitis, hepatoma, hyperbilirubinemia, hypersensitivity reaction, impaired extraocular muscle movement, impotence, leukopenia, libido decreased, malaise, memory loss, myopathy, nail changes, nodules, ophthalmoplegia, pancreatitis, paresthesia, peripheral nerve palsy, peripheral neuropathy, photosensitivity, polymyalgia rheumatica, positive ANA, pruritus, psychic disturbance, purpura, rash, renal failure (secondary to rhabdomyolysis), rhabdomyolysis, skin discoloration, Stevens-Johnson syndrome, systemic lupus erythematosus-like syndrome, thrombocytopenia, thyroid dysfunction, toxic epidermal necrolysis, transaminases increased, tremor, urticaria, vasculitis, vertigo, vomiting
Metabolism/Transport Effects
Substrate of CYP3A4 (major); Inhibits CYP2C9 (weak), 2D6 (weak), 3A4 (weak)
Drug Interactions
Amiodarone: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Management: Dose of simvastatin should not exceed 20 mg/day during concurrent therapy. Risk D: Consider therapy modification
Antifungal Agents (Azole Derivatives, Systemic): May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Bosentan: May increase the metabolism of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
Calcium Channel Blockers (Nondihydropyridine): May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Colchicine: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors. Colchicine may increase the serum concentration of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
CycloSPORINE: May increase the serum concentration of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Risk D: Consider therapy modification
Danazol: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
DAPTOmycin: HMG-CoA Reductase Inhibitors may enhance the adverse/toxic effect of DAPTOmycin. Specifically, the risk of skeletal muscle toxicity may be increased. Management: Consider temporarily stopping HMG-CoA reductase inhibitor therapy prior to daptomycin. If used together, regular (i.e., at least weekly) monitoring of CPK concentrations is recommended. Risk D: Consider therapy modification
Etravirine: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. This applies to atorvastatin, lovastatin and simvastatin. Conversely, levels of fluvastatin may be increased. Management: Dose adjustment of the HMG-CoA reductase inhibitor may be warranted. No interaction is expected with rosuvastatin or pravastatin. Risk C: Monitor therapy
Fenofibrate: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
Fluconazole: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors. Gemfibrozil may increase the serum concentration of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Grapefruit Juice: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Macrolide Antibiotics: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Exceptions: Azithromycin; Dirithromycin [Off Market]; Spiramycin. Risk D: Consider therapy modification
Nefazodone: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
Niacinamide: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
P-Glycoprotein Inducers: May decrease the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inducers may also further limit the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
P-Glycoprotein Inhibitors: May increase the serum concentration of P-Glycoprotein Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
Phenytoin: May increase the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Protease Inhibitors: May increase the serum concentration of HMG-CoA Reductase Inhibitors. Limited data suggest pravastatin may slightly decrease protease inhibitor concentrations. Management: Lovastatin and simvastatin are contraindicated with many protease inhibitors; use lowest possible HMG-CoA reductase inhibitor dose and monitor for signs and symptoms of rhabdomyolysis if these agents are used concomitantly. Risk D: Consider therapy modification
Rifamycin Derivatives: May increase the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Sildenafil: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
St Johns Wort: May increase the metabolism of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): HMG-CoA Reductase Inhibitors may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid excessive ethanol consumption (due to potential hepatic effects).
Food: Food decreases the bioavailability of lovastatin extended release tablets and increases the bioavailability of lovastatin immediate release tablets. Lovastatin serum concentrations may be increased if taken with grapefruit juice; avoid concurrent intake of large quantities (>1 quart/day). Red yeast rice contains an estimated 2.4 mg lovastatin per 600 mg rice.
Herb/Nutraceutical: St John's wort may decrease lovastatin levels.
Storage
Tablet, immediate release: Store between 5°C to 30°C (41°F to 86°F). Protect from light.
Tablet, extended release: Store between 20°C to 25°C (68°F to 77°F). Avoid excessive heat and humidity.
Mechanism of Action
Lovastatin acts by competitively inhibiting 3-hydroxyl-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis
Pharmacodynamics/Kinetics
Onset of action: LDL-cholesterol reductions: 3 days
Absorption: 30%; increased with extended release tablets when taken in the fasting state
Protein binding: 95%
Metabolism: Hepatic; extensive first-pass effect; hydrolyzed to B-hydroxy acid (active)
Bioavailability: Increased with extended release tablets
Half-life elimination: 1.1-1.7 hours
Time to peak, serum: 2-4 hours
Excretion: Feces (~80% to 85%); urine (10%)
Dosage
Oral:
Adolescents 10-17 years: Immediate release tablet:
LDL reduction <20%: Initial: 10 mg/day with evening meal
LDL reduction ?20%: Initial: 20 mg/day with evening meal
Usual range: 10-40 mg with evening meal, then adjust dose at 4-week intervals
Adults: Initial: 20 mg with evening meal, then adjust at 4-week intervals; maximum dose: 80 mg/day immediate release tablet or 60 mg/day extended release tablet
Dosage modification/limits based on concurrent therapy:
Cyclosporine and other immunosuppressant drugs: Initial dose: 10 mg/day with a maximum recommended dose of 20 mg/day
Concurrent therapy with fibrates, danazol, and/or lipid-lowering doses of niacin (>1 g/day): Maximum recommended dose: 20 mg/day. Concurrent use with fibrates should be avoided unless risk to benefit favors use.
Concurrent therapy with amiodarone or verapamil: Maximum recommended dose: 40 mg/day of regular release or 20 mg/day with extended release.
Dosage adjustment in renal impairment: Clcr <30 mL/minute: Use doses >20 mg/day with caution.
Administration: Oral
Administer immediate release tablet with meals. Administer extended release tablet at bedtime; do not crush or chew.
Monitoring Parameters
Obtain baseline LFTs and total cholesterol profile. LFTs should also be assessed prior to upwards dosage adjustment to ?40 mg daily or when otherwise indicated clinically. Enzyme levels should be followed periodically thereafter as clinically warranted.
Reference Range
NCEP classification of pediatric patients with familial history of hypercholesterolemia or premature CVD: Acceptable total cholesterol: <170 mg/dL, LDL: <110 mg/dL
Test Interactions
Altered thyroid function tests
Dietary Considerations
Before initiation of therapy, patients should be placed on a standard cholesterol-lowering diet for 6 weeks and the diet should be continued during drug therapy. Avoid intake of large quantities of grapefruit juice (?1 quart/day); may increase toxicity. Red yeast rice contains an estimated 2.4 mg lovastatin per 600 mg rice.
Patient Education
Do not take any new prescription or OTC medications or herbal products during therapy without consulting prescriber. Take as directed with food at evening meal. Follow diet and exercise regimen as prescribed. You will have periodic blood tests to assess effectiveness. You may experience mild nausea or vomiting (small, frequent meals, frequent mouth care, chewing gum, or sucking lozenges may help); diarrhea (buttermilk, boiled milk, or yogurt may help); constipation (increased exercise, fruit, fluids, or fiber may help); or headache, dizziness, or insomnia (use caution when driving or engaged in potentially hazardous tasks until response to drug in known). Contact prescriber immediately with persistent muscle pain or cramping, skeletal or joint pain, or numbness. Report other persistent adverse effects. Pregnancy/breast-feeding precautions: Inform prescriber if you are pregnant. Consult prescriber for appropriate barrier contraceptive measures to use during and for 1 month following therapy. This drug may cause severe fetal defects. Do not breast-feed.
Geriatric Considerations
The definition of and, therefore, when to treat hyperlipidemia in the elderly is a controversial issue. The National Cholesterol Education Program recommends that all adults maintain a plasma cholesterol <160 mg/dL. Elderly with one additional risk factor, goal LDL would be <130 mg/dL. It is the authors' belief that pharmacologic treatment be reserved for those who are unable to obtain a desirable plasma cholesterol concentration by diet alone and for whom the benefits of treatment are believed to outweigh the potential adverse effects, drug interactions, and cost of treatment.
Anesthesia and Critical Care Concerns/Other Considerations
Myopathy: Currently-marketed HMG-CoA reductase inhibitors appear to have a similar potential for causing myopathy. Incidence of severe myopathy is about 0.08% to 0.09%. The factors that increase risk include advanced age (especially >80 years), gender (occurs in women more frequently than men), small body frame, frailty, multisystem disease (eg, chronic renal insufficiency especially due to diabetes), multiple medications, and drug interactions (use with caution or avoid).
Based on current research, HMG-CoA reductase inhibitors should be continued in the perioperative period. Postoperative discontinuation of statin therapy is associated with an increased risk of cardiac morbidity and mortality.
Cardiovascular Considerations
HMG-CoA reductase inhibitors are effective in primary and secondary prevention of cardiovascular events in patients with hyperlipidemia. For primary prevention, a patient's major risk factors (cigarette smoking, hypertension or currently taking antihypertensives, low HDL-C, family history, age, gender) should be evaluated. Patients with multiple risk factors (?2) require more intensive therapy guided by the calculation of a 10-year absolute CHD risk (eg, the percent probability of having a CHD event in next 10 years). An individual's 10-year absolute CHD risk can be calculated at www.med-decisions.com/cvtool/phys/phys.html. LDL cholesterol goals, therapeutic lifestyle changes, and drug therapy are determined based upon a patient's risk factor profile.
Primary prevention trials show that cholesterol-lowering drugs reduce the risk of major coronary events, coronary death, and cerebrovascular events even in the first 6-12 months of use. The WOSCOP trial suggested a trend towards enhanced survival using pravastatin in their patients (mean LDL-cholesterol of 192 mg/dL and no history of MI). In a recent trial (Sever, 2003), patients with HTN and at least three other risk factors were randomized to 10 mg daily of atorvastatin or placebo. These patients had a total nonfasting cholesterol <250 mg/dL before treatment. LDL-C levels were 132 mg/dL before treatment and fell to an average of 90 mg/dL in the atorvastatin-treated group. There was a significant reduction in stroke, cardiovascular events, and coronary events in the atorvastatin-treated group as compared to the placebo group. There was no difference in mortality between the groups.
Secondary prevention trials indicate that “statin” therapy reduces mortality, major coronary events, coronary artery procedures, and stroke. The Heart Protection Study proved that lowering serum cholesterol levels reduces the rate of major vascular events among high-risk individuals with documented vascular disease (CHD, cerebrovascular, peripheral vascular) or diabetes regardless of initial cholesterol concentrations. PROVE IT is a randomized, double-blind trial evaluating hospitalized patients with acute coronary syndrome to determine the effects of intense LDL-C lowering therapy. Four thousand patients with an LDL-C levels of 106 mg/dL were randomized to pravastatin 40 mg daily or atorvastatin 80 mg daily. After 2 years, the combined cardiovascular endpoint (death, MI, unstable angina requiring hospitalization, revascularization and stroke) was ~26% in the pravastatin patients (median LDL-C 95 mg/dL) and ~22% in the atorvastatin treated patients (median LDL-C 62 mg/dL).
LaRosa and colleagues assessed the efficacy and safety of lowering LDL cholesterol <100 mg/dL in patients with stable coronary heart disease (LaRosa, 2005). Ten thousand and one patients with baseline LDL levels <130 mg/dL were randomized to atorvastatin 10 mg or 80 mg daily and followed for a median of 4.9 years. The primary endpoint was the occurrence of the first major cardiovascular event (death from CVD, MI, resuscitation after cardiac arrest, or stroke). A primary event occurred in 434 patients (8.7%) receiving 80 mg daily (mean LDL 77 mg/dL) and 548 patients (10.9%) receiving 10 mg dose (mean LDL 101 mg/dL) (95% CI, 0.69-0.89; p <0.001). There was no mortality difference between the two treatment groups.
HMG-CoA reductase inhibitors decrease levels of high-sensitivity C-reactive protein (hs-CRP). They also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects. These nonlipid effects may be beneficial when HMG-CoA reductase inhibitors are introduced early in the management of acute coronary syndromes (de Denus, 2002).
Myopathy: Currently-marketed HMG-CoA reductase inhibitors appear to have a similar potential for causing myopathy. Incidence of severe myopathy is about 0.08% to 0.09%. The factors that increase risk include advanced age (especially >80 years of age), women more frequently than men, small body frame, frailty, multisystem disease (eg, chronic renal insufficiency especially due to diabetes), multiple medications, drug interactions (use with caution or avoid). The combination of a HMG-CoA reductase inhibitor plus nicotinic acid seems to carry a lower risk of myopathy than does a HMG-CoA reductase inhibitor plus a fibrate. Other medications, when used concurrently, may enhance the risk of myopathy associated with statins; these include drugs that inhibit CYP3A4 isoenzymes (lovastatin, simvastatin, atorvastatin) or CYP2C9 isoenzymes (fluvastatin). HMG-CoA reductase inhibitors may exacerbate exercise-induced skeletal muscle injury. Many experts favor getting a baseline creatine kinase (CK) measurement before initiating therapy (asymptomatic CK elevations are common). Obtain a CK measurement if patient complains of muscle soreness, tenderness, or pain.
Dental Health: Effects on Dental Treatment
No significant effects or complications reported
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
May cause dizziness
Mental Health: Effects on Psychiatric Treatment
None reported
Nursing: Physical Assessment/Monitoring
Use caution with history of hepatic disease. Assess potential for interactions with other pharmacological agents or herbal products patient may be taking (eg, other lipid-lowering agents may increase risk of myopathy or rhabdomyolysis). Evaluate results of laboratory tests (LFTs and lipid profile) at baseline and periodically. Assess patient response on a regular basis throughout therapy (eg, rash, myalgia, gastrointestinal effects). Teach patient proper use (as adjunct to diet and exercise program), possible side effects/appropriate interventions, and adverse symptoms to report. Pregnancy risk factor X: Determine that patient is not pregnant before starting therapy. Do not give to women of childbearing age unless they are capable of complying with effective contraceptive use. Instruct patient in appropriate contraceptive measures.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet: 10 mg, 20 mg, 40 mg
Mevacor®: 20 mg, 40 mg
Tablet, extended release:
Altoprev®: 20 mg, 40 mg, 60 mg
Pricing: U.S. (www.drugstore.com)
Tablet, 24-hour (Altoprev)
10 mg (30): $77.98
20 mg (30): $140.38
60 mg (30): $158.75
Tablets (Lovastatin)
10 mg (45): $47.99
20 mg (30): $22.99
40 mg (30): $35.99
Tablets (Mevacor)
10 mg (30): $45.99
20 mg (30): $74.99
40 mg (30): $125.99
References
de Denus S and Spinler SA, “Early Statin Therapy for Acute Coronary Syndromes,” Ann Pharmacother, 2002, 36(11):1749-58.
“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(19):2486-97.
Fleisher LA, Beckman JA, Brown KA, et al, “ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery) Developed in Collaboration With the American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, and Society for Vascular Surgery,” J Am Coll Cardiol, 2007, 50(17):e159-241.
Fonarow GC, French WJ, Parsons LS, et al, “Use of Lipid-Lowering Medications at Discharge in Patients With Acute Myocardial Infarction: Data From the National Registry of Myocardial Infarction 3,” Circulation, 2001, 103(1):38-44.
Grundy SM, Cleeman JI, Merz CN, “Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines,” Arterioscler Thromb Vasc Biol, 2004, 24(8):E149-61.
Heeschen C, Hamm CW, Laufs U, et al, “Withdrawal of Statins Increases Event Rates in Patients With Acute Coronary Syndromes,” Circulation, 2002, 105(12):1446-52.
Koren MJ, Smith DG, Hunninghake DB, et al, “The Cost of Reaching National Cholesterol Education Program (NCEP) Goals in Hypercholesterolaemic Patients. A Comparison of Atorvastatin, Simvastatin, Lovastatin, and Fluvastatin,” Pharmacoeconomics, 1998, 14(1):59-70.
LaRosa JC, Grundy SM, Waters DD, et al, “Intensive Lipid Lowering With Atorvastatin in Patients With Stable Coronary Disease,” N Engl J Med, 2005, 352(14):1425-35.
LeManach Y, Godet G, Coriat P, et al, “The Impact of Postoperative Discontinuation or Continuation of Chronic Statin Therapy on Cardiac Outcome After Major Vascular Surgery,” Anesth Analg, 2007, 104(6):1326-33.
“MRC/BHF Heart Protection Study of Cholesterol Lowering With Simvastatin in 20,536 High-Risk Individuals: A Randomised Placebo-Controlled Trial. Heart Protection Study Collaborative Group,” Lancet, 2002, 360(9326):7-22.
“National Cholesterol Education Program (NCEP): Highlights of the Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents,” Pediatrics, 1992, 89(3):495-501.
Pasternak RC, Smith SC Jr, Bairey-Merz CN, et al, “ACC/AHA/NHLBI Clinical Advisory on the Use and Safety of Statins,” Stroke, 2002, 33(9):2337-41. Available at: http://www.acc.org/clinical/alerts/statins_june02.htm. accessed June 18, 2003.
Pearson TA, Mensah GA, Alexander RW, et al, “Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association,” Circulation, 2003, 107(3):499-511.
Phillips BG, Yim JM, Brown EJ Jr, et al, “Pharmacologic Profile of Survivors of Acute Myocardial Infarction at United States Academic Hospitals,” Am Heart J, 1996, 131(5):872-8.
Poldermans D, Bax JJ, Kertai MD, et al, “Statins Are Associated With a Reduced Incidence of Perioperative Mortality in Patients Undergoing Major Noncardiac Vascular Surgery,” Circulation, 2003, 107(14):1848-51.
Sever PS, Dahlof B, Poulter NR, et al, “Prevention of Coronary and Stroke Events With Atorvastatin in Hypertensive Patients Who Have Average or Lower-Than-Average Cholesterol Concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial - Lipid Lowering Arm (ASCOT-LLA): A Multicentre Randomised Controlled Trial,” Lancet, 2003, 361(9364):1149-58.
Shepherd J, Cobbe SM, Ford I, et al, “Prevention of Coronary Heart Disease With Pravastatin in Men With Hypercholesterolemia. West of Scotland Coronary Prevention Study Group,” N Engl J Med, 1995, 333(20):1301-7.
Sun JX, Niecestro R, Phillips G, et al, “Comparative Pharmacokinetics of Lovastatin Extended-Release Tablets and Lovastatin Immediate-Release Tablets in Humans,” J Clin Pharmacol, 2002, 42(2):198-204.
International Brand Names
Lexi-Comp.com
Last full review/revision October 2008
Content last modified October 2008
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