Version July 2025
Dosage guidance:
Dosing: Dosage should be individualized according to the baseline LDL cholesterol (LDL-C) level, the recommended goal of therapy, and patient response; adjustments should be made at intervals of 4 weeks.
Heterozygous familial hypercholesterolemia (HeFH):
Children 6 to <10 years: Limited data available: Oral: Initial: 5 mg once daily; if target LDL-C not achieved after 4 weeks, may increase to 10 mg once daily; may continue to increase doses every 4 to 6 weeks in 10 to 20 mg increments until target LDL-C is achieved; usual maximum daily dose: 40 mg/day; however, in some cases doses up to 80 mg/day have been reported (Ref).
Children ≥10 years and Adolescents: Oral: Initial: 10 mg once daily; if target LDL-C not achieved after 4 weeks, may increase to 20 mg once daily; may continue to increase doses every 4 to 6 weeks in 10 to 20 mg increments until target LDL-C is achieved; maximum daily dose: 80 mg/day (Ref).
Homozygous familial hypercholesterolemia (HoFH):
Children ≥10 years and Adolescents: Oral: Initial: 10 to 20 mg once daily; if target LDL-C not achieved after 4 to 6 weeks, may increase incrementally by doubling dose (20 mg/day, 40 mg/day) at 4- to 6-week intervals until target LDL-C up to a maximum daily dose: 80 mg/day (Ref).
Nonfamilial hypercholesterolemia: Limited data available:
Children ≥10 years and Adolescents (males at least Tanner stage II or greater, and postmenarchal females): Oral: Initial: 10 mg once daily; if target LDL-C not achieved after 4 weeks, may increase to 20 mg once daily; may continue to increase doses every 4 to 6 weeks in 10 to 20 mg increments until target LDL-C is achieved; usual maximum daily dose: 40 mg/day; however, in some cases doses up to 80 mg/day have been reported (Ref).
Transplantation, post heart; prevention of cardiac allograft vasculopathy (CAV): Limited data available:
Note: Initiate following heart transplant regardless of baseline cholesterol levels in children ≥10 years and adolescents. Therapy can be initiated in children <10 years with hyperlipidemia, following a second transplant, or with evidence of CAV (Ref). Significant drug interactions between statins and immunosuppressant drugs are frequent; many interactions can increase statin serum concentrations and risk of toxicity (eg, myopathy) (Ref); consult drug interactions database for more detailed information.
Children ≥10 years and Adolescents: Oral: 0.2 mg/kg/day rounded to nearest 2.5 mg increment; maximum daily dose: 20 mg/day (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Dosing adjustment for toxicity: Muscle symptoms (potential myopathy): Children ≥10 years and Adolescents: Discontinue use until symptoms can be evaluated; check CPK level; based on experience in adult patients, also evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution (symptoms and any associated CPK abnormalities), resume the original or consider a lower dose of atorvastatin and retitrate. If muscle symptoms recur, discontinue atorvastatin use. After muscle symptom resolution, may reinitiate a different statin at an initial low dose; gradually increase if tolerated. Based on experience in adult patients, if muscle symptoms or elevated CPK persists for 2 months in the absence of continued statin use, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (Ref).
Altered kidney function:
Mild to severe impairment: Children ≥10 years and Adolescents: Oral: No dosage adjustment necessary.
Hemodialysis, intermittent: There are no recommendations in the manufacturer's labeling (has not been studied); however, atorvastatin is highly protein bound, making it unlikely to be cleared by dialysis. Based on adult experience, it is poorly dialyzed and no dosage adjustment or supplemental dose is recommended (Ref).
Peritoneal dialysis: There are no recommendations for dosing in patients undergoing peritoneal dialysis. Based on adult experience, it is poorly dialyzed and no dosage adjustment is necessary (Ref).
Children ≥10 years and Adolescents: Contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.
(For additional information see "Atorvastatin: Drug information")
Dosage guidance:
Dosing: Atorvastatin 40 to 80 mg/day is considered a high-intensity statin (generally reduces low-density lipoprotein cholesterol [LDL-C] by ≥50%). Atorvastatin 10 to 20 mg/day is considered a moderate-intensity statin (generally reduces LDL-C by ~30% to 49%). Assess response ~1 to 3 months after initiation of therapy or dose adjustment and every 3 to 12 months thereafter (Ref).
Clinical considerations: Use in conjunction with lifestyle modification (eg, diet, exercise). When initiating therapy and selecting dose intensity, consider age, baseline LDL-C, 10-year atherosclerotic cardiovascular disease risk, risk-enhancing factors, potential adverse effects, and drug interactions (Ref).
Atherosclerotic cardiovascular disease, primary or secondary prevention:
Note: If LDL-C goal (eg, percent reduction or absolute goal) is not met with the initial dose, may consider up-titration based on estimated 10-year ASCVD risk (see ACC/AHA ASCVD Risk Estimator Plus online), LDL-C response, and tolerability. If LDL-C goal is not met with maximally tolerated dose, additional lipid-lowering therapy may be warranted (Ref).
Primary prevention:
Patients without diabetes, age 40 to 75 years, and LDL-C 70 to 189 mg/dL:
ASCVD 10-year risk 5% to <7.5%:
Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest shared decision-making if ASCVD 10-year risk is 5% to 10%; however, in patients with a baseline LDL-C >160 mg/dL, statin therapy is usually recommended (Ref).
Moderate-intensity therapy: Oral: 10 to 20 mg once daily to reduce LDL-C by 30% to 49% (Ref).
ASCVD 10-year risk ≥7.5% to <20%:
Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest initiating moderate-intensity statin therapy in most patients if ASCVD 10-year risk is >10% to <20% and an LDL-C >100 mg/dL (Ref).
Moderate-intensity therapy: Oral: 10 to 20 mg once daily to reduce LDL-C by 30% to 49%; higher risk patients with multiple risk-enhancing factors may benefit from higher doses to reduce LDL-C by ≥50% (Ref).
ASCVD 10-year risk ≥20%: High-intensity therapy: Oral: 40 to 80 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (Ref).
Patients with diabetes:
Age 40 to 75 years without additional ASCVD risk factors: Moderate-intensity therapy: Oral: 10 to 20 mg once daily to reduce LDL-C by 30% to 49% (Ref).
ASCVD risk ≥7.5% or multiple ASCVD risk factors: High-intensity therapy: Oral: 40 to 80 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (Ref).
Patients with LDL-C ≥190 mg/dL and age 20 to 75 years:
Note: High-intensity therapy indicated regardless of ASCVD risk calculation or coexisting diabetes mellitus.
High-intensity therapy: Oral: 40 to 80 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (Ref).
Secondary prevention in patients with established atherosclerotic cardiovascular disease (eg, coronary heart disease, cerebrovascular disease [ischemic stroke or transient ischemic attack], peripheral arterial disease):
Note: Patients with high-risk ASCVD may require additional therapies to achieve LDL-C goal (eg, <70 mg/dL or <50 mg/dL if very high risk).
High-intensity therapy: Oral: 80 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (Ref).
Transplantation:
Note: Certain immunosuppressive drugs can induce or exacerbate hypercholesterolemia. Significant drug interactions between statins and immunosuppressant drugs are frequent; some interactions can increase statin serum concentrations and risk of toxicity (eg, myopathy) (Ref). Consult drug interactions database for more detailed information.
Transplantation, post heart (off-label use): Oral: Initial: 10 mg once daily starting 1 to 2 weeks after transplant, regardless of baseline cholesterol levels; increase dose based on response, tolerability, and use of concomitant medications up to 20 mg once daily (Ref).
Transplantation, post kidney (off-label use):
Note: The decision to initiate therapy for primary or secondary prevention is similar to the non-transplant population (see the "Prevention of atherosclerotic cardiovascular disease" indication). However, in patients who are 30 to 39 years of age, some experts suggest statin therapy post-kidney transplantation for primary prevention of ASCVD. For primary prevention of ASCVD in patients 18 to 29 years of age, use shared decision making while considering risks and benefits (Ref).
Oral: Initial: 10 mg once daily; increase dose based on response, tolerability, and use of concomitant medications up to 20 mg once daily (Ref).
Missed doses: Oral suspension: If a dose is missed by >12 hours, omit that dose and administer the next dose at the regularly scheduled time; do not administer extra doses to make up for a missed dose.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function: Mild to severe impairment: No dosage adjustment necessary (Ref).
Hemodialysis, intermittent (thrice weekly): Poorly dialyzed: No supplemental dose or dosage adjustment necessary (Ref).
Peritoneal dialysis: No dosage adjustment necessary (Ref).
CRRT: No dosage adjustment necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).
The liver dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Matt Harris, PharmD, MHS, BCPS, FAST, FCCP; Jeong Park, PharmD, MS, BCTXP, FCCP, FAST; Arun Jesudian, MD; Sasan Sakiani, MD.
Note: Although use is contraindicated in patients with active liver failure or decompensated cirrhosis according to the manufacturer's labeling, baseline elevation in AST/ALT should not preclude use of statins for compelling indications in patients with chronic stable liver disease including compensated cirrhosis (Ref).
Liver impairment prior to treatment initiation:
Initial or dose adjustment in patients with preexisting liver cirrhosis:
Child-Turcotte-Pugh class A: No dosage adjustment necessary (Ref).
Child-Turcotte-Pugh class B: Note: Consider use only when benefit likely outweighs risk (eg, secondary prevention in patients with established atherosclerotic cardiovascular disease, including ischemic stroke, transient ischemic attack, peripheral artery disease) (Ref).
Oral: Initial: 10 to 20 mg once daily; maximum recommended dose: 20 mg/day (Ref).
Child-Turcotte-Pugh class C: Use of a hydrophilic statin (eg, rosuvastatin) is recommended. If use of atorvastatin is deemed necessary: Initial: 10 mg once daily; maximum recommended dose: 20 mg/day (Ref).
Liver impairment developing in patient already receiving atorvastatin:
Chronic disease progression (eg, outpatient) or a cute worsening of liver function (eg, requiring hospitalization):
Baseline to Child-Turcotte-Pugh class A: Although use is contraindicated in patients with active liver failure or decompensated cirrhosis according to the manufacturer's labeling, if atorvastatin-induced hepatoxicity has been ruled out, may continue atorvastatin therapy with no dosage adjustment necessary (Ref).
Progression to Child-Turcotte-Pugh class B and C: Although use is contraindicated in patients with active liver failure or decompensated cirrhosis according to the manufacturer's labeling, if atorvastatin-induced toxicity (eg, liver injury, rhabdomyolysis) has been ruled out, may continue atorvastatin therapy with no dosage adjustment necessary; however, in patients with decompensated cirrhosis, consider not exceeding 20 mg once daily (Ref). Continued use of statin therapy may be hepatoprotective in patients with decompensated cirrhosis (Ref).
Statins are associated with increased serum transaminases and hepatotoxicity (Ref). Asymptomatic transient or persistent increases both <3 or >3 times the ULN in serum transaminases may occur with all statins; the increase in ALT is typically greater than the increase in AST (Ref). Additionally, there are postmarketing reports of fatal and nonfatal hepatic failure, consisting of a cholestatic/mixed pattern (more common with atorvastatin) or hepatocellular pattern (Ref). Drug-induced autoimmune hepatitis has also been documented (Ref).
Upon dose reduction or discontinuation, transaminase levels return to or near pretreatment levels; although, mild elevations resolve with continued use in some cases (Ref). Chronic liver injury (defined as liver biochemical or histological abnormalities that persisted for 6 months or more after onset) has been reported (Ref).
Mechanism: Unclear; inhibition of the CYP450 system, leading to increased plasma concentrations of statins has been postulated, as well as an immune-mediated response (Ref). Changes in the lipid components of the hepatocyte membrane may lead to increased permeability and leakage of liver enzymes (Ref).
Onset: Varied; most cases occur within the first 3 months of initiation or dose escalation (Ref). Duration of atorvastatin prior to development of hepatotoxicity has been reported from ∼1 month to 10 years (Ref).
Risk factors:
• Administration of high oral daily dose of lipophilic drugs that undergo extensive hepatic metabolism, such as atorvastatin, may increase the risk of developing drug-induced liver injury (Ref).
• Concurrent medications with statin drug-drug interactions or hepatotoxic properties (Ref)
• Hepatotoxicity is more commonly associated with atorvastatin than pravastatin, rosuvastatin, and simvastatin (Ref). Fluvastatin is associated with the greatest risk of developing hepatotoxicity (Ref).
• Cross-reactivity between different statins and the susceptibility to hepatotoxicity is unknown, as data have shown conflicting results (Ref).
• Chronic hepatitis B and alcohol consumption are independent risk factors for hepatic aminotransferase elevation associated with statins in patients 80 years of age or older (Ref).
Statins are associated with several muscle-related effects, including:
• Myalgia (muscle symptoms without significant creatine kinase [CK] elevations; also known as statin-associated muscle symptoms) (Ref)
• Myopathy (defined as unexplained muscle pain or weakness accompanied by a CK ≥10 times the ULN) (Ref)
• Rhabdomyolysis (CK >40 times the ULN) (Ref) often with acute renal failure secondary to myoglobinuria (Ref)
• Immune-mediated necrotizing myopathy (IMNM) (elevated CK plus the presence of antibodies against HMG-CoA) (Ref)
Mechanism: Uncertain; alterations in the mevalonate pathway and changes in the electrical and structural characteristics of the sarcolemma related to calcium ion flux possibly contribute (Ref). Decreased ubiquinone, which is essential for energy production in skeletal muscle, may also contribute (Ref). Myopathy/rhabdomyolysis risk is related to circulating active drug concentrations (Ref). IMNM is considered an immune-mediated process; autoantibodies against HMG-CoA reductase (anti-HMG-CoA) have been identified (Ref).
Onset: Delayed; often presents within a few months after starting therapy (highest risk within first year of use), when the dose of the statin is increased, or when introducing an interacting drug (Ref). Muscle symptoms often appear more promptly when patients are reexposed to the same statin (Ref). Duration of statin use prior to development of IMNM is ~2 to 3 years (Ref).
Risk factors:
• First year of therapy (Ref)
• Addition of an interacting drug (eg, concurrent use of strong CYP3A4 inhibitors or medications associated with myopathy [eg, colchicine]) (Ref)
• Older patients (Ref)
• Hypothyroidism (Ref)
• Preexisting muscle disease (Ref)
• Kidney impairment (Ref)
• Females (Ref)
• Low body mass index (Ref)
• Heavy exercise (Ref)
• Surgery (Ref)
• Higher HMG-CoA reductase inhibitory activity (Ref), rosuvastatin > atorvastatin > simvastatin > pravastatin ≈ lovastatin (Ref)
• Although incidence increases with dose for most statins, there was no difference found in incidence with atorvastatin dose (Ref)
• Asian population: Increased plasma concentrations (up to ≈ twofold with atorvastatin) may result in increased risk of myopathy (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions reported in children, adolescents, and adults.
>10%:
Gastrointestinal: Diarrhea (7% to 14%)
Neuromuscular & skeletal: Arthralgia (9% to 12%)
Respiratory: Nasopharyngitis (13%)
1% to 10%:
Endocrine & metabolic: Diabetes mellitus (6%)
Gastrointestinal: Dyspepsia (6%), nausea (7%)
Genitourinary: Urinary tract infection (7% to 8%)
Hepatic: Increased serum transaminases (≤2%) (table 1)
|
Drug (Atorvastatin) |
Placebo |
Dose |
Number of Patients (Atorvastatin) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
2% |
N/A |
80 mg |
N/A |
N/A |
|
0.9% |
0.1% |
80 mg |
2,365 |
2,366 |
|
0.6% |
N/A |
40 mg |
N/A |
N/A |
|
0.2% |
N/A |
10 mg |
N/A |
N/A |
|
0.2% |
N/A |
20 mg |
N/A |
N/A |
Nervous system: Insomnia (5%), intracranial hemorrhage (2%)
Neuromuscular & skeletal: Limb pain (3% to 9%) (table 2), muscle spasm (2% to 5%) (table 3), musculoskeletal pain (2% to 5%) (table 4), myalgia (3% to 8%) (table 5)
|
Drug (Atorvastatin) |
Placebo |
Dose |
Number of Patients (Atorvastatin) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
9% |
6% |
40 mg |
604 |
7,311 |
|
9% |
6% |
10 mg |
3,908 |
7,311 |
|
4% |
6% |
20 mg |
188 |
7,311 |
|
3% |
6% |
80 mg |
4,055 |
7,311 |
|
Drug (Atorvastatin) |
Placebo |
Dose |
Number of Patients (Atorvastatin) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
5% |
3% |
10 mg |
3,908 |
7,311 |
|
5% |
3% |
20 mg |
188 |
7,311 |
|
5% |
3% |
40 mg |
604 |
7,311 |
|
2% |
3% |
80 mg |
4,055 |
7,311 |
|
Drug (Atorvastatin) |
Placebo |
Dose |
Number of Patients (Atorvastatin) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
5% |
4% |
40 mg |
604 |
7,311 |
|
5% |
4% |
10 mg |
3,908 |
7,311 |
|
3% |
4% |
20 mg |
188 |
7,311 |
|
2% |
4% |
80 mg |
4,055 |
7,311 |
|
Drug (Atorvastatin) |
Placebo |
Dose |
Number of Patients (Atorvastatin) |
Number of Patients (Placebo) |
|---|---|---|---|---|
|
8% |
3% |
40 mg |
604 |
7,311 |
|
6% |
3% |
20 mg |
188 |
7,311 |
|
4% |
3% |
10 mg |
3,908 |
7,311 |
|
3% |
3% |
80 mg |
4,055 |
7,311 |
Respiratory: Pharyngolaryngeal pain (3% to 4%)
Frequency not defined:
Gastrointestinal: Abdominal distress, eructation, flatulence
Nervous system: Malaise
Neuromuscular & skeletal: Joint swelling, muscle fatigue, neck pain
Ophthalmic: Blurred vision
Otic: Tinnitus
Respiratory: Epistaxis
Miscellaneous: Fever
Postmarketing:
Dermatologic: Bullous rash, erythema multiforme, exacerbation of psoriasis (Ref), lichenoid eruption (Ref), Stevens-Johnson syndrome, toxic epidermal necrolysis (Ref), urticaria (Ref)
Gastrointestinal: Cholestasis (Ref), pancreatitis (Ref)
Genitourinary: Cystitis (interstitial) (Ref)
Hematologic & oncologic: Immune thrombocytopenia (Ref)
Hepatic: Autoimmune hepatitis (Ref), hepatic failure (Ref), hepatitis (Ref), increased gamma-glutamyl transferase (Ref), increased serum alkaline phosphatase (Ref)
Hypersensitivity: Anaphylaxis, angioedema (Ref), drug reaction with eosinophilia and systemic symptoms (Ref)
Immunologic: Dermatomyositis (Ref)
Infection: Reactivation of HBV (Ref)
Nervous system: Cognitive dysfunction (reversible; including amnesia, confusion, memory impairment) (Ref), depression, dizziness, fatigue, myasthenia (Ref), myasthenia gravis (including exacerbation of myasthenia gravis, ocular myasthenia), nightmares (Ref), peripheral neuropathy
Neuromuscular & skeletal: Immune-mediated necrotizing myopathy (Ref), increased creatine phosphokinase in blood specimen (Ref), myopathy (Ref), myositis (including necrotizing autoimmune myositis) (Ref), rhabdomyolysis (Ref), rupture of tendon (Ref)
Ophthalmic: Diplopia (Ref)
Renal: Acute interstitial nephritis (Ref)
Respiratory: Interstitial lung disease
Hypersensitivity (eg, anaphylaxis, angioneurotic edema, erythema multiforme, Steven Johnson syndrome, toxic epidermal necrolysis) to atorvastatin or any component of the formulation; acute liver failure or decompensated cirrhosis.
Canadian labeling: Additional contraindications (not in US labeling): Concurrent therapy with boceprevir, cyclosporine, elbasvir/grazoprevir, glecaprevir/pibrentasvir, ledipasvir/sofosbuvir, simeprevir, telaprevir, or velpatasvir/sofosbuvir.
Concerns related to adverse effects:
• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported.
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; use is contraindicated in patients with active liver disease or unexplained persistent elevations of serum transaminases.
• Myasthenia gravis: May rarely worsen or precipitate myasthenia gravis (MG); monitor for worsening MG if treatment is initiated (AAN [Narayanaswami 2021]).
• Stroke: Patients with recent stroke or TIA receiving long-term therapy with high-dose (ie, 80 mg/day) atorvastatin may be at increased risk for hemorrhagic stroke (SPARCL Investigators [Amarenco 2006]). A subsequent post-hoc analysis demonstrated that patients with lacunar or hemorrhagic stroke may be at higher risk of hemorrhagic stroke; however, this finding was determined to be hypothesis generating. The overall benefit of treatment with atorvastatin (ie, reduced risk of stroke and cardiovascular events) in this population seems to outweigh the increased risk of hemorrhagic stroke if one truly exists (Goldstein 2008).
Special populations:
• Surgical patients: Based on current research and clinical guidelines, HMG-CoA reductase inhibitors should be continued in the perioperative period for noncardiac and cardiac surgery (ACC/AHA [Fleisher 2014]; ACC/AHA [Hillis 2011]). Perioperative discontinuation of statin therapy is associated with an increased risk of cardiac morbidity and mortality.
Dosage form specific issues:
• Polysorbate 80: Some dosage forms may contain polysorbate 80 (also known as Tweens). Hypersensitivity reactions, usually a delayed reaction, have been reported following exposure to pharmaceutical products containing polysorbate 80 in certain individuals (Isaksson 2002; Lucente 2000; Shelley 1995).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Suspension, Oral, as calcium:
Atorvaliq: 20 mg/5 mL (150 mL) [contains ethylparaben, methylparaben, propylparaben]
Tablet, Oral:
Lipitor: 10 mg, 20 mg, 40 mg, 80 mg
Generic: 10 mg, 20 mg, 40 mg, 80 mg
May be product dependent
Suspension (Atorvaliq Oral)
20 mg/5 mL (per mL): $1.44
Tablets (Atorvastatin Calcium Oral)
10 mg (per each): $0.02 - $7.50
20 mg (per each): $0.03 - $10.70
40 mg (per each): $0.04 - $10.70
80 mg (per each): $0.06 - $10.70
Tablets (Lipitor Oral)
10 mg (per each): $16.01
20 mg (per each): $22.84
40 mg (per each): $22.84
80 mg (per each): $22.84
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
Lipitor: 10 mg, 20 mg, 40 mg, 80 mg [contains polysorbate 80]
Generic: 10 mg, 20 mg, 40 mg, 80 mg
Oral:
Oral suspension: Administer on an empty stomach once daily, at least 1 hour before or 2 hours after a meal; may take without regard to time of day. Measure dose using a calibrated oral measuring device with metric units (ie, mL).
Tablets: May be administered without regard to meals or time of day. The manufacturer's labeling states tablets should not be broken; however, available data do not indicate any safety or efficacy concerns with this practice.
Missed doses: If a dose is missed by >12 hours, omit that dose and administer the next dose at the regularly scheduled time; do not administer extra doses to make up for a missed dose.
Oral:
Suspension: Administer on an empty stomach, at least 1 hour before or 2 hours after a meal; may take without regard to time of day. Measure dose using a calibrated oral syringe or other oral dosing device containing scored metric units of measurement (eg, mL).
Tablet: Administer with or without food; may take without regard to time of day.
Oral suspension: Store in original container at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F). Discard any unused portion within 60 days of opening the bottle.
Tablet: Store at 20°C to 25°C (68°F to 77°F).
Adjunct to dietary therapy in patients with heterozygous familial hypercholesterolemia (HeFH) (FDA approved in ages ≥10 years and adults); adjunct to other LDL cholesterol (LDL-C)-lowering therapies to reduce LDL-C for patients with homozygous familial hypercholesterolemia (HoFH) or alone if other therapies unavailable (FDA approved in ages ≥10 years and adults); adjunct to diet to reduce LDL-C in patients with primary hypercholesterolemia (FDA approved in adults); adjunct to dietary therapy in patients with primary dysbetalipoproteinemia and hypertriglyceridemia (FDA approved in adults); to reduce the risk of myocardial infarction (MI), stroke, revascularization procedures, and angina in patients with multiple risk factors for coronary heart disease (CHD) but without clinically evident CHD (FDA approved in adults); to reduce the risk of MI and stroke in patients with type 2 diabetes mellitus with multiple risk factors for CHD but without clinically evident CHD (FDA approved in adults); to reduce risk of non-fatal MI, fatal and non-fatal stroke, revascularization procedures, hospitalization for congestive heart failure, and angina in patients with clinically evident CHD (FDA approved in adults).
Has also been used in pediatric patients for prevention of cardiac allograft vasculopathy.
Atorvastatin is identified in the Screening Tool of Older Person's Prescriptions (STOPP) criteria as a potentially inappropriate medication for primary prevention of cardiovascular disease in frail older adults ≥85 years of age with an expected life expectancy of < 3 years (O’Mahony 2023).
Atorvastatin may be confused with atomoxetine, lovastatin, nystatin, pitavastatin, pravastatin, rosuvastatin, simvastatin
HMG-CoA reductase inhibitors (when referred to as "statins") may be confused with nystatin.
Lipitor may be confused with labetalol, Levatol, lisinopril, Loniten, Lopid, Mevacor, Zocor, ZyrTEC
Substrate of BCRP, CYP3A4 (Major), NTCP, OATP1B1/1B3, P-glycoprotein (Minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program
Abiraterone Acetate: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Acipimox: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Amiodarone: May increase serum concentration of Atorvastatin. Risk C: Monitor
Antihepaciviral Combination Products: May increase serum concentration of Atorvastatin. Risk X: Avoid
Asciminib: May increase serum concentration of Atorvastatin. Risk X: Avoid
Atazanavir: May increase serum concentration of Atorvastatin. Management: Use of atorvastatin and atazanavir/cobicistat is not recommended. Use the lowest atorvastatin dose necessary and titrate carefully due to the increased risk of statin toxicities. Alternative statins include fluvastatin, pravastatin, and rosuvastatin. Risk D: Consider Therapy Modification
Belumosudil: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid coadministration of belumosudil with these substrates of BCRP for which minimal concentration increases can cause serious adverse effects. If coadministration is required, dose reductions of the BCRP substrate may be required. Risk D: Consider Therapy Modification
Bezafibrate: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Bezafibrate may increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). More specifically, bezafibrate may increase the serum concentration of fluvastatin Management: Avoid use of bezafibrate and HMG-CoA reductase inhibitors (statins) unless strictly indicated due to the increased of muscle toxicity (including rhabdomyolysis). In patients who may be predisposed to myopathy, concomitant use is contraindicated. Risk D: Consider Therapy Modification
Bulevirtide: May increase serum concentration of NTCP Substrates. Management: Coadministration of bulevirtide with sodium taurocholate co-transporting polypeptide (NTCP) substrate should be avoided when possible. If used together, close clinical monitoring is recommended. Risk D: Consider Therapy Modification
Bulevirtide: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Management: Coadministration of bulevirtide with OATP1B1/1B3 (also known as SLCO1B1/1B3) substrates should be avoided when possible. If used together, close clinical monitoring is recommended. Risk D: Consider Therapy Modification
Cardiac Glycosides: Atorvastatin may increase serum concentration of Cardiac Glycosides. Risk C: Monitor
Ceftobiprole Medocaril: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
Ciprofibrate: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Management: Avoid the use of HMG-CoA reductase inhibitors and ciprofibrate if possible. If concomitant therapy is considered, benefits should be carefully weighed against the risks, and patients should be monitored closely for signs/symptoms of muscle toxicity. Risk D: Consider Therapy Modification
Clarithromycin: May increase serum concentration of Atorvastatin. Management: Limit atorvastatin to a maximum dose of 20 mg/day when used with clarithromycin. If this combination is used, monitor patients more closely for evidence of atorvastatin toxicity. Risk D: Consider Therapy Modification
Clofazimine: May increase serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor
Cobicistat: May increase serum concentration of Atorvastatin. Management: Avoid the combined use of atorvastatin with atazanavir/cobicistat. Atorvastatin dose should not exceed 20 mg daily when combined with other cobicistat-containing regimens. Risk D: Consider Therapy Modification
Colchicine: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Colchicine may increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). HMG-CoA Reductase Inhibitors (Statins) may increase serum concentration of Colchicine. Risk C: Monitor
CycloSPORINE (Systemic): May increase serum concentration of Atorvastatin. Risk X: Avoid
CYP3A4 Inducers (Moderate): May decrease serum concentration of Atorvastatin. Risk C: Monitor
CYP3A4 Inducers (Strong): May decrease serum concentration of Atorvastatin. Risk C: Monitor
CYP3A4 Inhibitors (Moderate): May increase serum concentration of Atorvastatin. Risk C: Monitor
CYP3A4 Inhibitors (Strong): May increase serum concentration of Atorvastatin. Risk C: Monitor
Cyproterone: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Daclatasvir: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Danazol: May increase serum concentration of Atorvastatin. Risk C: Monitor
Danicopan: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
DAPTOmycin: HMG-CoA Reductase Inhibitors (Statins) may increase adverse/toxic effects of DAPTOmycin. Specifically, the risk of skeletal muscle toxicity may be increased. Management: Consider temporarily stopping statin (HMG-CoA reductase inhibitor) therapy prior to daptomycin. If daptomycin is used with a statin, creatine phosphokinase (CPK) monitoring could be considered. Risk D: Consider Therapy Modification
Darolutamide: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Darunavir: May increase serum concentration of Atorvastatin. Management: Use the lowest atorvastatin dose necessary and limit the atorvastatin dose to 20 mg daily in patients taking darunavir. Monitor patients for signs and symptoms of myopathy at initiation of therapy and with any dose increase. Risk D: Consider Therapy Modification
Elacestrant: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Elafibranor: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk of muscle toxicity may be increased. Risk C: Monitor
Elbasvir and Grazoprevir: May increase serum concentration of Atorvastatin. Management: Limit the adult dose of atorvastatin to a maximum of 20 mg/day when used together with elbasvir and grazoprevir. Use the lowest atorvastatin dose necessary and monitor closely for evidence of statin-related toxicities such as myalgia or myopathy. Risk D: Consider Therapy Modification
Elexacaftor, Tezacaftor, and Ivacaftor: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Eltrombopag: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Eltrombopag: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Encorafenib: May increase serum concentration of Atorvastatin. Encorafenib may decrease serum concentration of Atorvastatin. Risk C: Monitor
Etravirine: May decrease serum concentration of HMG-CoA Reductase Inhibitors (Statins). This applies to atorvastatin, lovastatin and simvastatin. Risk C: Monitor
Fenofibrate and Derivatives: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Fosamprenavir: May increase serum concentration of Atorvastatin. Atorvastatin may increase active metabolite exposure of Fosamprenavir. Management: Use the lowest atorvastatin dose necessary and limit the atorvastatin dose to 20 mg daily in patients taking fosamprenavir. Monitor patients for signs and symptoms of myopathy at initiation of therapy and with any dose increase. Risk D: Consider Therapy Modification
Fostemsavir: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest possible starting statin dose and monitor patients closely for statin-related adverse effects (eg, muscle aches and pains) during coadministration with fostemsavir. Risk D: Consider Therapy Modification
Fusidic Acid (Systemic): May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for muscle toxicities, including rhabdomyolysis may be significantly increased. Management: Avoid concurrent use whenever possible. Use is listed as contraindicated in product characteristic summaries in several countries, although UK labeling suggests that use could be considered under exceptional circumstances and with close supervision. Risk X: Avoid
Futibatinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Gemfibrozil: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid
Gilteritinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Glecaprevir and Pibrentasvir: May increase serum concentration of Atorvastatin. Risk X: Avoid
Grapefruit Juice: May increase serum concentration of Atorvastatin. Management: Avoid large quantities of grapefruit juice (more than 1.2 liters daily) during treatment with atorvastatin. Monitor for atorvastatin adverse effects (eg, myopathy, rhabdomyolysis) in patients who consume smaller quantities or whose intake has changed. Risk D: Consider Therapy Modification
Indinavir: May increase serum concentration of Atorvastatin. Management: Use the lowest atorvastatin dose necessary and titrate carefully in patients taking indinavir. Monitor patients carefully for signs and symptoms of myopathy and rhabdomyolysis during coadministration. Risk D: Consider Therapy Modification
Interleukin-6 (IL-6) Inhibiting Therapies: May decrease serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Istradefylline: May increase serum concentration of Atorvastatin. Risk C: Monitor
Itraconazole: May increase serum concentration of Atorvastatin. Management: Limit atorvastatin to a maximum adult dose of 20 mg/day in patients receiving itraconazole. Assess clinical response to ensure that the lowest necessary dose of atorvastatin is used. Consider use of fluva-, rosuva-, pitava-, or pravastatin when possible. Risk D: Consider Therapy Modification
Ketoconazole (Systemic): Atorvastatin may increase adverse/toxic effects of Ketoconazole (Systemic). Specifically, there is a theoretical potential for additive effects on reducing endogenous steroid concentrations. Ketoconazole (Systemic) may increase serum concentration of Atorvastatin. Risk C: Monitor
Lanthanum: May decrease serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Administer HMG-CoA reductase inhibitors (eg, statins) at least two hours before or after lanthanum. Risk D: Consider Therapy Modification
Lazertinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Ledipasvir: May increase adverse/toxic effects of Atorvastatin. Risk C: Monitor
Leflunomide: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Leniolisib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
Letermovir: May increase serum concentration of Atorvastatin. Management: Limit the atorvastatin dose to 20 mg daily when combined with letermovir. When letermovir is coadministered with cyclosporine, the use of atorvastatin (at any dose) is not recommended. Risk D: Consider Therapy Modification
Lomitapide: May increase serum concentration of Atorvastatin. Atorvastatin may increase serum concentration of Lomitapide. Management: When the lomitapide dose is 10 mg daily or greater, reduce the lomitapide dose by 50% when combined with atorvastatin. No dose adjustment is required when the lomitapide dose is 5 mg daily. Risk D: Consider Therapy Modification
Lonafarnib: May increase serum concentration of Atorvastatin. Risk X: Avoid
Lopinavir: May increase serum concentration of Atorvastatin. Management: Consider the risks and benefits of this combination. If coadministered, use the lowest dose of atorvastatin necessary and monitor patients for signs and symptoms of myopathy, especially at initiation of therapy and with any dose increase. Risk D: Consider Therapy Modification
Midazolam: Atorvastatin may increase serum concentration of Midazolam. Risk C: Monitor
Nelfinavir: May increase serum concentration of Atorvastatin. Management: Use the lowest atorvastatin dose necessary in patients taking nelfinavir, and do not exceed atorvastatin 40 mg daily. Monitor patients for signs and symptoms of myopathy at initiation of therapy and with any dose increase. Risk D: Consider Therapy Modification
Niacin: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Nirmatrelvir and Ritonavir: May increase serum concentration of Atorvastatin. Management: Consider temporarily discontinuing atorvastatin during treatment with nirmatrelvir/ritonavir. It is not necessary to hold atorvastatin either prior to or after completion of nirmatrelvir/ritonavir treatment. Risk D: Consider Therapy Modification
Osimertinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Oteseconazole: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Posaconazole: May increase serum concentration of Atorvastatin. Risk X: Avoid
Pretomanid: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
QuiNINE: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Raltegravir: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Red Yeast Rice: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid
Regorafenib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Repaglinide: HMG-CoA Reductase Inhibitors (Statins) may increase serum concentration of Repaglinide. Risk C: Monitor
Resmetirom: May increase serum concentration of Atorvastatin. Management: Do not exceed atorvastatin doses of 40 mg daily during coadministration with resmetirom. Monitor for increased atorvastatin adverse effects (eg, myalgias) during coadministration. Risk D: Consider Therapy Modification
RifAMPin: May increase serum concentration of Atorvastatin. RifAMPin may decrease serum concentration of Atorvastatin. Management: Administer atorvastatin and rifampin simultaneously if using both. Monitor atorvastatin response closely. Risk D: Consider Therapy Modification
Ritonavir: May increase serum concentration of Atorvastatin. Management: Use lowest atorvastatin dose needed. If ritonavir is combined with another protease inhibitor, see the drug interaction monograph for that protease inhibitor. Risk D: Consider Therapy Modification
Rolapitant: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Monitor patients receiving rolapitant for increased exposure to and/or effects of BCRP/ABCG2 substrates. Use the lowest effective rosuvastatin dose when used in combination with rolapitant. Risk C: Monitor
Roxadustat: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Rupatadine: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for increased CPK and/or other muscle toxicities may be increased. Risk C: Monitor
Sacubitril: May increase serum concentration of Atorvastatin. Risk C: Monitor
Saquinavir: May increase serum concentration of Atorvastatin. Management: Limit the atorvastatin dose to 20 mg in patients taking saquinavir and ritonavir. Monitor patients for signs and symptoms of myopathy at initiation of therapy and with any dose increase. Risk D: Consider Therapy Modification
Selpercatinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Simeprevir: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Sofosbuvir: May increase serum concentration of Atorvastatin. Risk C: Monitor
Sparsentan: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
St John's Wort: May decrease active metabolite exposure of HMG-CoA Reductase Inhibitors (Statins). Management: Consider avoiding the concomitant administration of St John's Wort with atorvastatin, lovastatin and simvastatin in order to avoid the potential for decreased effects statins. If coadministered, monitor for decreased statin efficacy. Risk D: Consider Therapy Modification
Tafamidis: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Talazoparib: Atorvastatin may increase serum concentration of Talazoparib. Risk C: Monitor
Taurursodiol: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid
Tedizolid: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Teriflunomide: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Ticagrelor: May increase serum concentration of Atorvastatin. Risk C: Monitor
Tipranavir: May increase serum concentration of Atorvastatin. Risk X: Avoid
Trabectedin: HMG-CoA Reductase Inhibitors (Statins) may increase myopathic (rhabdomyolysis) effects of Trabectedin. Risk C: Monitor
Trofinetide: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Management: Avoid concurrent use with OATP1B1/1B3 substrates for which small changes in exposure may be associated with serious toxicities. Monitor for evidence of an altered response to any OATP1B1/1B3 substrate if used together with trofinetide. Risk D: Consider Therapy Modification
Vadadustat: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor
Vanzacaftor, Tezacaftor, and Deutivacaftor: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Velpatasvir: May increase serum concentration of Atorvastatin. Risk C: Monitor
Verapamil: Atorvastatin may increase serum concentration of Verapamil. Verapamil may increase serum concentration of Atorvastatin. Management: Consider using lower doses of atorvastatin when used together with verapamil, and monitor closely for signs of HMG-CoA reductase inhibitor toxicity (eg, myositis, rhabdomyolysis, hepatotoxicity). Risk D: Consider Therapy Modification
Vimseltinib: May increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid concomitant use of vimseltinib and BCRP substrates when possible. If combined, monitor for increased effects and toxicities of the BCRP substrate and consider dose adjustments. Risk D: Consider Therapy Modification
Voclosporin: May increase serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor
Voxilaprevir: May increase serum concentration of Atorvastatin. Management: Use the lowest atorvastatin dose possible if combined with voxilaprevir and monitor patients for increased statin effects/toxicities (eg, myopathy, rhabdomyolysis). Risk D: Consider Therapy Modification
Atorvastatin serum concentrations may be increased by grapefruit juice. Management: Avoid concurrent intake of large quantities of grapefruit juice (>1.2 liters/day).
Before initiation of therapy, patients should be placed on a standard cholesterol-lowering diet for 3 to 6 months and the diet should be continued during drug therapy. Atorvastatin serum concentration may be increased when taken with grapefruit juice; avoid concurrent intake of large quantities (>1.2 liters/day).
Red yeast rice contains variable amounts of several compounds that are structurally similar to HMG-CoA reductase inhibitors, primarily monacolin K (or mevinolin) which is structurally identical to lovastatin; concurrent use of red yeast rice with HMG-CoA reductase inhibitors may increase the incidence of adverse and toxic effects (Lapi 2008; Smith 2003).
Adequate contraception is recommended if an HMG-CoA reductase inhibitor (statin) is required in patients who may become pregnant (AHA/ACC [Grundy 2019a]; CCS [Pearson 2021]). Patients planning to become pregnant should discuss their lifetime risk of cardiovascular disease, as well as risks and benefits of statin therapy with their health care team (CCS [Pearson 2021]). When appropriate, statins can be discontinued 1 to 2 months prior to conception (AHA/ACC [Grundy 2019a]).
When a statin is needed in a patient of reproductive potential, a more hydrophilic option (eg, pravastatin, rosuvastatin) may be preferred to limit placental transfer (CCS [Pearson 2021]).
In healthy pregnancies, changes in lipid synthesis occur that are required for normal placental and fetal growth. Low-density lipoprotein cholesterol and triglycerides increase as pregnancy progresses and decline postpartum. HMG-CoA reductase inhibitors (statins) decrease the synthesis of cholesterol and substances derived from cholesterol. Therefore, based on the mechanism of action, in utero exposure may cause fetal harm (Lecarpentier 2012); however, data from available studies have not shown an increased risk of major congenital anomalies following first trimester exposure (Bateman 2015; Chang 2021; Vahedian-Azimi 2021a). Additional data are needed to evaluate other pregnancy outcomes, such as miscarriage (Vahedian-Azimi 2021b).
Because there is potential for fetal harm, statins should be discontinued once pregnancy is recognized (AHA/ACC [Grundy 2019a]; Brunham 2018). If lipid-lowering therapy during pregnancy is required, it should be individualized based on the therapeutic needs of the patient, considering the lifetime risk of untreated disease, use of nonstatin therapies, as well as the known risks and benefits of statins. Based on limited data, when a statin is needed in a pregnant patient, a more hydrophilic option (eg, pravastatin, rosuvastatin) may be preferred. Lipophilic statins (eg, atorvastatin, fluvastatin, lovastatin, simvastatin, pitavastatin) may be more likely to cross the placenta and increase the risk of congenital malformations (AHA/ACC [Grundy 2019a]; CCS [Pearson 2021]; Lecarpentier 2012).
Additional data are needed to clarify the role of statins for the prevention of atherosclerotic cardiovascular disease in at-risk pregnant patients (AHA/ACC [Grundy 2019a]; CCS [Pearson 2021]; Parikh 2021).
Manufacturer's labeling: Consider neuromuscular and serologic testing if immune-mediated necrotizing myopathy is suspected.
Pediatric patients: Baseline: ALT, AST, and CPK; fasting lipid panel (FLP) and repeat ALT and AST should be checked after 4 weeks of therapy; if no myopathy symptoms or laboratory abnormalities, then monitor FLP, ALT, and AST every 3 to 4 months during the first year and then every 6 months thereafter (NHLBI 2011).
Adults:
2013 ACC/AHA Blood Cholesterol Guideline recommendations (Stone 2014):
Lipid panel (total cholesterol, HDL, LDL, triglycerides): Baseline lipid panel; fasting lipid profile within 4 to 12 weeks after initiation or dose adjustment and every 3 to 12 months (as clinically indicated) thereafter. If 2 consecutive LDL levels are <40 mg/dL, consider decreasing the dose.
Hepatic transaminase levels: Baseline measurement of hepatic transaminase levels (ie, ALT); measure hepatic function if symptoms suggest hepatotoxicity (eg, unusual fatigue or weakness, loss of appetite, abdominal pain, dark-colored urine or yellowing of skin or sclera) during therapy.
CPK: CPK should not be routinely measured. Baseline CPK measurement is reasonable for some individuals (eg, family history of statin intolerance or muscle disease, clinical presentation, concomitant drug therapy that may increase risk of myopathy). May measure CPK in any patient with symptoms suggestive of myopathy (pain, tenderness, stiffness, cramping, weakness, or generalized fatigue).
Evaluate for new-onset diabetes mellitus during therapy; if diabetes develops, continue statin therapy and encourage adherence to a heart-healthy diet, physical activity, a healthy body weight, and tobacco cessation.
If patient develops a confusional state or memory impairment, may evaluate patient for nonstatin causes (eg, exposure to other drugs), systemic and neuropsychiatric causes, and the possibility of adverse effects associated with statin therapy.
Manufacturer recommendation: Liver enzyme tests at baseline and repeated when clinically indicated. Measure CPK when myopathy is being considered or may measure CPK periodically in high risk patients (eg, drug-drug interaction). Upon initiation or titration, lipid panel should be analyzed within 2 to 4 weeks.
Inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism. 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 (de Denus 2002; Ray 2005).
Onset of action: Initial changes: 3 to 5 days; Maximal reduction in plasma cholesterol and triglycerides: 2 to 4 weeks; LDL reduction: 10 mg/day: 39% (for each doubling of this dose, LDL is lowered approximately 6%)
Absorption: Oral: Rapidly absorbed; extensive first-pass metabolism in GI mucosa and liver
Distribution: Vd: ~381 L
Protein binding: ≥98%
Metabolism: Hepatic via CYP3A4; forms active ortho- and parahydroxylated derivatives and an inactive beta-oxidation product; plasma concentrations are elevated in patients with chronic alcoholic liver disease and Child-Pugh class A and B liver disease
Bioavailability: ~14% (parent drug); ~30% (parent drug and equipotent metabolites)
Half-life elimination: Parent drug: ~14 hours; Equipotent metabolites: 20 to 30 hours
Time to peak, serum: 1 to 2 hours
Excretion: Bile (following hepatic and/or extra-hepatic metabolism; does not appear to undergo enterohepatic recirculation); urine (<2% as unchanged drug)
Hepatic function impairment: Cmax and AUC are each 4-fold greater in patients with Child-Pugh class A disease; Cmax and AUC are ~16-fold and 11-fold increased, respectively, in patients with Child-Pugh class B disease.
Older adult: Plasma concentrations are higher (~40% for Cmax and 30% for AUC).
Sex: Plasma concentrations in women differ from those in men (~20% higher for Cmax and 10% lower for AUC).
Molecular weight: 1,209.42.
