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Pronunciation
(LOE va sta tin)
Generic Available (U.S.)
Yes: Exludes extended release tablet
Index Terms
U.S. Brand Names
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 in breast milk 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.
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 (≤1%)
Dermatologic: Rash (≤1%)
Gastrointestinal: Flatulence (4% to 5%), constipation (2% to 4%), abdominal pain (2% to 3%), diarrhea (2% to 3%), nausea (2% to 3%), dyspepsia (1% to 2%)
Neuromuscular & skeletal: Myalgia (2% to 3%), weakness (1% to 2%), muscle cramps (≤1%)
Ocular: Blurred vision (≤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, alteration in taste, anaphylaxis, angioedema, anorexia, anxiety, arthritis, cataracts, chills, cholestatic jaundice, cirrhosis, 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, interstitial lung disease, leukopenia, libido decreased, malaise, memory loss, myopathy, nail changes, nodules, ophthalmoplegia, pancreatitis, peripheral nerve palsy, peripheral neuropathy, photosensitivity, polymyalgia rheumatica, positive ANA, psychic disturbance, purpura, 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
Metabolism/Transport Effects
Substrate of CYP3A4 (major), P-glycoprotein; Inhibits CYP2C9 (weak), 2D6 (weak), 3A4 (weak)
Drug Interactions
Amiodarone: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Management: Dose of HMG-CoA reductase inhibitor may need to be reduced (e.g., simvastatin prescribing information recommends not exceeding 20 mg/day for adults during concurrent therapy). Risk D: Consider therapy modification
Antacids: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
Antifungal Agents (Azole Derivatives, Systemic): May decrease the metabolism of HMG-CoA Reductase Inhibitors. Management: Consider use of HMG-CoA reductase inhibitors posing the least rhabdomyolysis risk (e.g. fluva- or pravastatin), and monitor for signs/symptoms of rhabdomyolysis. Do not use keto- or itraconazole with lova- or simvastatin, or posaconazole with simvastatin. Risk D: Consider therapy modification
Boceprevir: May increase the serum concentration of Lovastatin. Risk X: Avoid combination
Bosentan: May increase the metabolism of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
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
Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Management: Upon completion/discontinuation of conivaptan, allow at least 7 days before initiating therapy with drugs that are CYP3A4 substrates. Risk D: Consider therapy modification
CycloSPORINE: May increase the serum concentration of HMG-CoA Reductase Inhibitors. Management: Use of cyclosporine with pitavastatin is contraindicated. U.S. and Canadian recommendations for some statins may differ, see appropriate prescribing information. Monitor closely for myotoxicity with concomitant use of statins and cyclosporine. Risk D: Consider therapy modification
CycloSPORINE (Systemic): May increase the serum concentration of HMG-CoA Reductase Inhibitors. Management: Use of cyclosporine with pitavastatin is contraindicated. U.S. and Canadian recommendations for some statins may differ, see appropriate prescribing information. Monitor closely for myotoxicity with concomitant use of statins and cyclosporine. Risk D: Consider therapy modification
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
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 increase the serum concentration of HMG-CoA Reductase Inhibitors. Management: Limit doses of simvastatin (max 10 mg/day) and lovastatin (max 20 mg/day) with concomitant danazol. Monitor for toxic effects of HMG-CoA reductase inhibitors with any such combination. Fluvastatin, pravastatin and rosuvastatin may pose lower risk. Risk D: Consider therapy modification
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
Dasatinib: May increase the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Diltiazem: May increase the serum concentration of Lovastatin. Lovastatin may increase the serum concentration of Diltiazem. Management: Avoid concurrent use of diltiazem with lovastatin when possible. If used together, consider using lower lovastatin doses (max of 40 mg/day for adults). Risk D: Consider therapy modification
Dronedarone: May increase the serum concentration of Lovastatin. Management: Consider using lower lovastatin doses; consider limiting lovastatin to a max of 40 mg/day (in adults). Increase monitoring for signs of lovastatin toxicity (e.g., myositis, rhabdomyolysis). Risk D: Consider therapy modification
Efavirenz: May decrease the serum concentration of Lovastatin. Risk C: Monitor therapy
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, pravastatin, or pitavastatin. Risk C: Monitor therapy
Fenofibrate: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Risk C: Monitor therapy
Fenofibric Acid: 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
Fosphenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of Lovastatin. Gemfibrozil may increase the serum concentration of Lovastatin. More specifically, gemfibrozil may increase the serum concentrations of lovastatin acid (active form of parent drug). Management: If possible, avoid concomitant use of lovastatin and gemfibrozil or consider using micronized fenofibrate instead of gemfibrozil. If gemfibrozil use can not be avoided, limit lovastatin to 20 mg/day and closely monitor for signs of rhabdomyolysis. Risk D: Consider therapy modification
Grapefruit Juice: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Lanthanum: HMG-CoA Reductase Inhibitors may decrease the serum concentration of Lanthanum. Management: Administer HMG-CoA reductase inhibitors at least two hours before or after lanthanum. Risk D: Consider therapy modification
Macrolide Antibiotics: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Management: Avoid lovastatin or simvastatin with erythro-, clarithro-, or telithromycin. Limit pitavastatin to a 1 mg/day maximum adult dose with erythromycin. Atorvastatin dose adjustments may be required. Increase monitoring for toxicity with any such combination. Exceptions: Azithromycin; Azithromycin (Systemic); Spiramycin. Risk D: Consider therapy modification
Nefazodone: May decrease the metabolism of HMG-CoA Reductase Inhibitors. Management: Monitor for evidence of myositis and rhabdomyolysis if an HMG-CoA reductase inhibitor is used with nefazodone. Fluvastatin, pravastatin, and rosuvastatin may be less likely to interact. Avoid use of nefazodone with simvastatin and lovastatin. Risk D: Consider therapy modification
Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Management: This is of greatest concern with niacin doses of 1 g or greater daily. Avoid simvastatin 80 mg in combination with niacin 1 g or greater in Chinese patients. Canadian labeling contraindicates use of niacin with rosuvastatin 40 mg. Risk D: Consider therapy modification
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 decrease the serum concentration of HMG-CoA Reductase Inhibitors. Risk D: Consider therapy modification
Protease Inhibitors: May increase the serum concentration of Lovastatin. Risk X: Avoid combination
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 protease inhibitors; also, avoid rosuvastatin with indinavir. Use lowest possible HMG-CoA reductase inhibitor dose and monitor for signs of toxicity if these agents are used concomitantly. Risk D: Consider therapy modification
QuiNINE: May increase the serum concentration of HMG-CoA Reductase Inhibitors. Management: Consider using a lower starting dose and lower maintenance/maximum doses of atorvastatin, simvastatin, or lovastatin when used together with quinine. Risk D: Consider therapy modification
Red Yeast Rice: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Risk X: Avoid combination
Rifamycin Derivatives: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. Rifamycin Derivatives may increase the serum concentration 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
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Trabectedin: HMG-CoA Reductase Inhibitors may enhance the myopathic (rhabdomyolysis) effect of Trabectedin. Risk C: Monitor therapy
Verapamil: May increase the serum concentration of Lovastatin. Management: Avoid concurrent use of verapamil with lovastatin when possible. If used together, use lower lovastatin doses (max of 40 mg/day for adults). Risk D: Consider therapy modification
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 at 20°C to 25°C (68°F to 77°F). Protect from light
Tablet, extended release: Store between 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C to 30°C (59°F to 86°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 β-hydroxyacid (active)
Bioavailability: Increased with extended release tablets
Half-life elimination: 1.1-1.7 hours
Time to peak, serum: Immediate release: 2-4 hours; extended release: 12-14 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; maximum dose per manufacturer: 40 mg/day
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
Note: Doses should be individualized according to the baseline LDL-cholesterol levels, the recommended goal of therapy, and patient response.
Dosage modification/limits based on concurrent therapy:
Cyclosporine or danazol: Initial dose: 10 mg/day with a maximum recommended dose of 20 mg/day
Concurrent therapy with fibrates 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 immediate 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 the evening meal. 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, at 6 and 12 weeks after initiation, and periodically thereafter; baseline CPK (recheck CPK in any patient with symptoms suggestive of myopathy).
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. Immediate release tablet should be taken with the evening meal.
Patient Education
Take with food at evening meal. Follow prescribed diet and exercise regimen. You will have periodic blood tests to assess effectiveness. Avoid excessive alcohol. Report unusual muscle cramping or weakness, yellowing of skin or eyes, easy bruising or bleeding, or unusual fatigue.
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
Clinical Pearls/Comments: 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 and clinical guidelines (Fleisher, 2007), 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
Primary Prevention: 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.
HMG-CoA reductase inhibitors decrease C-reactive protein (CRP), an inflammatory marker and an acute phase reactant. Elevated levels of high sensitive CRP (hsCRP), which detects CRP levels as low as 0.175 mg/L, have been shown to be associated with an increased risk of cardiovascular events. Recently, the JUPITER trial demonstrated that the use of rosuvastatin in healthy patients (men ≥50 years and women ≥60 years) without a history of cardiovascular disease with LDL <130 mg/dL and a hsCRP level ≥2 mg/L reduced the risk of major cardiovascular events (eg, nonfatal MI, stroke, death from cardiovascular causes), The number needed to treat over 5 years to prevent 1 cardiovascular event is 25. Current guidelines do not recommend drug treatment for patients with an LDL <130 mg/dL. However, identification of the patient at higher risk of cardiovascular events within this subgroup using hsCRP is now important given that statins may prevent the occurrence of these serious cardiovascular events (Ridker, 2008).
Secondary Prevention: 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.
In addition to the ability of HMG-CoA reductase inhibitors to decrease levels of high-sensitivity C-reactive protein (hsCRP), 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 risk potential for interactions with other prescriptions or herbal products patient may be taking that may increase risk of myopathy or rhabdomyolysis. Evaluate LFTs and lipid profile prior to treatment and at regular intervals. Teach proper diet and exercise program.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, oral: 10 mg, 20 mg, 40 mg
Mevacor®: 20 mg, 40 mg
Tablet, extended release, oral:
Altoprev®: 20 mg, 40 mg, 60 mg
Pricing: U.S. (www.drugstore.com)
Tablet, 24-hour (Altoprev)
20 mg (30): $240.00
60 mg (30): $321.01
Tablets (Lovastatin)
10 mg (45): $47.99
20 mg (30): $22.99
40 mg (30): $35.99
Tablets (Mevacor)
20 mg (30): $80.16
40 mg (30): $134.69
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International Brand Names
Lexi-Comp.com
Last full review/revision May 2011
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