- Encourage adherence to a heart-healthy lifestyle. A healthy diet, regular aerobic physical activity, smoking cessation and maintenance of a healthy weight are critical components of ASCVD risk reduction. Control hypertension and diabetes, when present.
- Statin therapy is recommended for adults in groups demonstrated to benefit. ASCVD risk reduction clearly outweighs the risk of adverse events based on a strong body of evidence in 4 groups:
- Secondary prevention in individuals with clinical ASCVD
- Primary prevention in individuals age â¥21 years with primary elevations of LDL-C â¥190 mg/dL
- Primary prevention in individuals with diabetes 40 to 75 years of age who have LDL-C 70 to 189 mg/dL
- Primary prevention in individual without diabetes and with estimated
10-year ASCVD risk â¥7.5%, 40 to 75 years of age who have LDL-C 70 to 189 mg/dL
- Statins have an acceptable margin of safety when used in properly selected individuals and appropriately monitored. If no baseline abnormality, monitoring of hepatic transaminases is not routinely needed. CK should not be routinely measured unless there is a personal or family history of muscle problems. You may need to discontinue and then restart the statin to determine the cause of muscle symptoms.
- Engage in a clinician-patient discussion before initiating statin therapy, especially for primary prevention. Discuss the potential for ASCVD event reduction, adverse effects, drugâdrug interactions, and patient preferences.
Additional factors may be considered when a risk-based decision is uncertain.
- These include LDL-C â¥160 mg/dL, family history of premature
ASCVD, hs-CRP â¥2.0 mg/L, CAC â¥300 Agatson units, ABI <0.9;
lifetime risk of ASCVD.
- Use the newly developed Pooled Cohort Equations for estimating 10-year ASCVD risk. Calculating the estimated 10-year ASCVD risk should be the start of the clinician-patient discussion and should not automatically lead to statin initiation.
- For other ethnic groups, use the equations for non-Hispanic whites, although these estimates may underestimate the risk for persons from some race/ethnic groups, especially American Indians, some Asian Americans (e.g., of south Asian ancestry), and some Hispanics (e.g., Puerto Ricans), and may overestimate the risk for others, including some Asian Americans (e.g., of east Asian ancestry) and some Hispanics (e.g., Mexican Americans).
- Initiate the appropriate intensity of statin therapy to reduce
- Evidence is inadequate to support treatment to specific LDL-C or nonâHDL-C treatment goals. "Treating to goal" may result in treatment with less-than-optimum statin intensity or adding unproven nonstatin therapy.
- Regularly monitor patients for adherence to lifestyle and appropriate intensity of statin therapy. Obtain a fasting lipid panel before and after initiating statin or other drug therapy.
- Nonstatin drug therapy may be considered in selected individuals.
Table 1. Summary of Major Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults
|Recommendations||ACC/AHA COR||ACC/AHA LOE|
|A. Heart-healthy lifestyle habits should be encouraged for all individuals.|
|B. The appropriate intensity of statin therapy should be initiated or continued:|
|1. Clinical ASCVDa|
|a. Age â¤75 y and no safety concerns: High-intensity statin||I||A|
|b. Age >75 y or safety concerns: Moderate-intensity statin||I||A|
|2. Primary prevention â Primary LDL-C â¥190 mg/dL|
|a. Rule out secondary causes of hyperlipidemia (Table 3)||I||B|
|b. Age â¥21y: High-intensity statin||I||B|
|c. Achieve at least a 50% reduction in LDL-C||IIa||B|
|d. LDL-C lowering nonstatin therapy may be considered to further reduce LDL-C||IIb||C|
|3. Primary prevention - Diabetes 40-75 years of age and LDL-C 70-189 mg/dL|
|a. Moderate-intensity statin||I||A|
|b. Consider high-intensity statin when â¥7.5% 10-y ASCVD risk using the Pooled Cohort Equationsb||IIa||B|
|4. Primary prevention â No diabetes 40-75 years of age and LDL-C 70-189 mg/dL|
|a. Estimate 10-y ASCVD risk using the Risk Calculator based on the Pooled Cohort Equationsb in those NOT receiving a statin. Estimate risk every 4-6 y.||I||B|
|b. To determine whether to initiate a statin, engage in a clinician-patient discussion of the potential for ASCVD risk reduction, adverse effects, drugâdrug interactions, and patient preferences. Re-emphasize heart-healthy lifestyle habits and address other risk factors.||IIa||C|
|i. â¥7.5% 10-y ASCVD risk:|
Moderate- or high-intensity statin
|ii. 5 to <7.5% 10-y ASCVD risk:|
Consider moderate-intensity statin
|iii. Other factors may be consideredc:|
LDL-C â¥160 mg/dL, family history of premature ASCVD, hs-CRP â¥2.0 mg/L, CAC score â¥300 Agaston units, ABI <0.9 or lifetime ASCVD risk
|5. Primary prevention when LDL-C <190 mg/dL and age <40 or >75 y, or <5% 10-y ASCVD risk||IIb||C|
|a. Statin therapy may be considered in selected individuals when a risk decision is uncertain.c|
|6. The panel makes no recommendation for initiation of statin therapy for individuals with NYHA class II-IV heart failure or who are receiving maintenance hemodialysis.|
|C. Regularly monitor adherence to lifestyle and drug therapy with lipid and safety assessments.|
|1. Assess adherence, response to therapy, and adverse effects within 4-12 wk following statin initiation or change in therapy.||I||A|
|a. Measure a fasting lipid panel||I||A|
|b. Do not routinely monitor ALT or CK unless symptomatic||IIa||C|
|c. Screen and treat type 2 diabetes according to current practice guidelines. Heart-healthy lifestyle habits should be encouraged to prevent progression to diabetes||I||B|
|d. Anticipated therapeutic response: approximately â¥50% reduction in LDL-C from baseline for high-intensity statin and 30% to <50% for moderate-intensity statin||IIa||B|
|i. Insufficient evidence for LDL-C or nonâHDL-C treatment targets from RCTs|
|ii. For those with unknown baseline LDL-C, an LDL-C <100 mg/dL was observed in RCTs of high-intensity statin therapy|
|e. Less than anticipated therapeutic response:|
|i. Reinforce improved adherence to lifestyle and drug therapy||I||A|
|ii. Evaluate for secondary causes of hyperlipidemia if indicated (Table 3)||I||A|
|iii. Increase statin intensity, or if on maximally-tolerated statin intensity, consider addition of nonstatin therapy in selected high-risk individualsd||IIb||C|
|f. Regularly monitor adherence to lifestyle and drug therapy every 3-12 mo once adherence has been established. Continued assessment of adherence for optimal ASCVD risk reduction and safety.||I||A|
|D. In individuals intolerant of the recommended intensity of statin therapy, use the maximally-tolerated intensity of statin.||I||B|
|1. If there are muscle or other symptoms, establish that they are related to the statin||IIa||B|
|2. For specific recommendations on managing muscle symptoms (Table 8)|
|a Clinical ASCVD includes acute coronary syndromes, history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin.|
b Estimated 10-year or âhardâ ASCVD risk includes first occurrence of nonfatal MI, CHD death, and nonfatal and fatal stroke as used by the Risk Assessment Work Group in developing the Pooled Cohort Equations (http://www.cardiosource.org/en/Science-And-Quality/Practice-Guidelines-and-Quality-Standards/2013-Prevention-Guideline-Tools.aspx or http://my.americanheart.org/cvriskcalculator).
c These factors may include primary LDL-C â¥160 mg/dL or other evidence of genetic hyperlipidemias; family history of premature ASCVD with onset <55 years of age in a first-degree male relative or <65 years of age in a first-degree female relative; hs-CRP â¥2 mg/L; CAC score â¥300 Agatston units or â¥75th percentile for age, sex, and ethnicity (for additional information, see http://www.mesa-nhlbi.org/CACReference.aspx); ABI <0.9; or lifetime risk of ASCVD. Additional factors that might aid in individual risk assessment could be identified in the future.
d High-risk individuals include those with clinical ASCVD, an untreated LDL-C â¥190 mg/dL suggesting genetic hypercholesterolemia, or diabetes 40-75 years of age and LDL-C 70-189 mg/dL.
Table 2. High- Moderate- and Low-Intensity Statin Therapy (Used in the RCTs reviewed by the Expert Panel)a
|Daily dose lowers LDL-C on average by approximately â¥50%||Daily dose lowers LDL-C on average by approximately 30%-<50%||Daily dose lowers LDL-C on average by <30%|
|Atorvastatin (40b)-80 mg|
Rosuvastatin 20 (40) mg
|Atorvastatin 10 (20) mg|
Rosuvastatin (5) 10 mg
Simvastatin 20-40 mgc
Pravastatin 40 (80) mg
Lovastatin 40 mg
Fluvastatin XL 80 mg
Fluvastatin 40 mg
bid Pitavastatin 2-4 mg
|Simvastatin 10 mg|
Pravastatin 10-20 mg
Lovastatin 20 mg
Fluvastatin 20-40 mg
Pitavastatin 1 mg
|Boldface type indicates specific statins and doses that were evaluated in RCTs. All of these RCTs demonstrated a reduction in major cardiovascular events. Italic type indicates statins and doses that have been approved by the FDA but were not tested in the RCTs reviewed.|
a Individual responses to statin therapy varied in the RCTs and should be expected to vary in clinical practice. There might be a biological basis for a less-than-average response.
b Evidence from 1 RCT only: down-titration if unable to tolerate atorvastatin 80 mg in the IDEAL (Incremental Decrease through Aggressive Lipid Lowering) study.
c Although simvastatin 80 mg was evaluated in RCTs, initiation of simvastatin 80 mg or titration to 80 mg is not recommended by the FDA because of the increased risk of myopathy, including rhabdomyolysis.
Table 3. Secondary Causes of Hyperlipidemia Most Commonly Encountered in Clinical Practice
|Secondary Cause||Elevated LDL-C||Elevated Triglycerides|
|Diet||Saturated or trans fats, weight gain, anorexia||Weight gain, very low-fat diets, high intake of refined carbohydrates, excessive alcohol intake|
|Drugs||Diuretics, cyclosporine, glucocorticoids, amiodarone||Oral estrogens, glucocorticoids, bile acid sequestrants, protease inhibitors, retinoic acid, anabolic steroids, sirolimus, raloxifene, tamoxifen, beta blockers (not carvedilol), thiazides|
|Diseases||Biliary obstruction, nephrotic syndrome||Nephrotic syndrome, chronic renal failure, lipodystrophies|
|Disorders and altered states of metabolism||Hypothyroidism, obesity, pregnancya||Diabetes (poorly controlled), hypothyroidism, obesity; pregnancya|
|a Cholesterol and triglycerides rise progressively throughout pregnancy. Treatment with statins, niacin, and ezetimibe are contraindicated during pregnancy and lactation|
Table 4. Recommendations for Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in AdultsâStatin Treatment (High-, moderate-, and low-statin intensities are defined in Table 2)
- Treatment Targets
- The panel makes no recommendations for or against specific LDL-C or non-HDL-C targets for the primary or secondary prevention of ASCVD.
- Secondary Prevention
- High-intensity statin therapy should be initiated or continued as first-line therapy in women and men â¤75 years of age who have clinical ASCVDa, unless contraindicated. (I-A)
- In individuals with clinical ASCVDa in whom high-intensity statin therapy would otherwise be used, when high-intensity statin therapy is contraindicatedb or when characteristics predisposing to statin-associated adverse effects are present, moderate-intensity statin should be used as the second option if tolerated (Table 5 for Safety of Statins, Recommendation 1). (I-A)
- In individuals with clinical ASCVD >75 years of age, it is reasonable to evaluate the potential for ASCVD risk-reduction benefits and for adverse effects, drugâdrug interactions and to consider patient preferences when initiating a moderate- or high-intensity statin. It is reasonable to continue statin therapy in those who are tolerating it. (IIa-B)
- Primary Prevention in Individuals â¥21 Years of Age With LDL-C â¥190 mg/dL
- Individuals with LDL-C â¥190 mg/dL or triglycerides â¥500 mg/dL should be evaluated for secondary causes of hyperlipidemia (Table 1). (Ic-B)
- Adults â¥21 years of age with primary LDL-C â¥190 mg/dL should be treated with statin therapy (10-year ASCVD risk estimation is not required): (Id-B)
- For individuals â¥21 years of age with an untreated primary LDL-C â¥190 mg/dL, it is reasonable to intensify statin therapy to achieve at least a 50% LDL-C reduction. (IIa-B)
- For individuals â¥21 years of age with an untreated primary LDL-C â¥190 mg/dL, after the maximum intensity of statin therapy has been achieved, addition of a nonstatin drug may be considered to further lower LDL-C. Evaluate the potential for ASCVD risk-reduction benefits, adverse effects, drugâdrug interactions, and consider patient preferences. (IIb-C)
- Primary Prevention in Individuals With Diabetes and LDL-C 70-189 mg/dL
- Moderate-intensity statin therapy should be initiated or continued for adults 40-75 years of age with diabetes mellitus. (I-A)
- High-intensity statin therapy is reasonable for adults 40-75 years of age with diabetes mellitus with a â¥7.5% estimated 10-year ASCVD riske unless contraindicated. (IIa-B)
- In adults with diabetes mellitus, who are <40 or >75 years of age or with LDL-C <70 mg/dL, it is reasonable to evaluate the potential for ASCVD benefits and for adverse effects and drugâdrug interactions and to consider patient preferences when deciding to initiate, continue, or intensify statin therapy. (IIa-C)
- Primary Prevention in Individuals Without Diabetes and With LDL-C 70-189 mg/dL
- The Pooled Cohort Equations should be used to estimate
10-year ASCVD riske for individuals with LDL-C 70-189 mg/dL without clinical ASCVDa to guide initiation of statin therapy for the primary prevention of ASCVD. (Ic-B)
- The Pooled Cohort Equations should be used to estimate
- Adults 40-75 years of age with LDL-C 70-189 mg/dL, without clinical ASCVDa or diabetes, and with an estimated 10-year ASCVD riske â¥7.5% should be treated with moderate- to high-intensity statin therapy. (Id-A)
- It is reasonable to offer treatment with a moderate-intensity statin to adults 40-75 years of age, with LDL-C 70-189 mg/dL, without clinical ASCVDa or diabetes and an estimated 10-year ASCVD riske of 5% to <7.5%. (IIa-B)
- Before initiating statin therapy for the primary prevention of ASCVD in adults with LDL-C 70-189 mg/dL without clinical ASCVDa or diabetes, it is reasonable for clinicians and patients to engage in a discussion which considers the potential for ASCVD risk reduction benefits and for adverse effects, for drugâdrug interactions, as well as patient preferences for treatment. (IIa-C)
- In adults with LDL-C <190 mg/dL who are not otherwise identified in a statin benefit group, or for whom after quantitative risk assessment a risk-based treatment decision is uncertain, additional factorsf may be considered to inform treatment decision making. In these individuals, statin therapy for primary prevention may be considered after evaluating the potential for ASCVD risk-reduction benefits, adverse effects, and drugâdrug interactions and consider patient preferences. (IIb-C)
- Heart Failure and Hemodialysis
- The Expert Panel makes no recommendations regarding the initiation or discontinuation of statins in patients with NYHA class II-IV ischemic systolic heart failure or in patients on maintenance hemodialysis.
- a Clinical ASCVD includes acute coronary syndromes, history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin.
b Contraindications, warnings, and precautions are defined for each statin according to the manufacturerâs prescribing information.
c Individuals with secondary causes of hyperlipidemia were excluded from RCTs reviewed. A triglyceride level â¥500 mg/dL was an exclusion criterion for almost all RCTs. Therefore, ruling out secondary causes is necessary to avoid inappropriate statin therapy.
d No RCTs included only individuals with LDL-C â¥190 mg/dL. However, many trials did include individuals with LDL-C â¥190 mg/dL and all of these trials consistently demonstrated a reduction in ASCVD events. In addition, the CTT meta-analyses have shown that each 39 mg/dL reduction in LDL-C with statin therapy reduced ASCVD events by 22%, and the relative reductions in ASCVD events were consistent across the range of LDL-C levels. Therefore, individuals with primary LDL-C â¥190 mg/dL should be treated with statin therapy.
e Estimated 10-year or âhardâ ASCVD risk includes first occurrence of nonfatal MI, CHD death, and nonfatal and fatal stroke as used by the Risk Assessment Work Group in developing the Pooled Cohort Equations.
f These factors may include primary LDL-C â¥160 mg/dL or other evidence of genetic hyperlipidemias; family history of premature ASCVD with onset <55 years in a first degree male relative or <65 years in a first degree female relative; high sensitivity-C-reactive protein â¥2 mg/L; CAC score â¥300 Agatston units or â¥75th percentile for age, sex, and ethnicity (for additional information, see http://www.mesa-nhlbi.org/CACReference.aspx.); ABI <0.9; or lifetime risk of ASCVD. Additional factors that may aid in individual risk assessment may be identified in the future.
Table 5. Assessment and Management of Muscle Symptoms During Statin Therapy
- Evaluate and treat muscle symptoms, including pain, tenderness, stiffness, cramping, weakness, or fatigue, in statin-treated patients according to the following management algorithm (IIa-B)
- A. To avoid unnecessary discontinuation of statins, obtain a history of prior or current muscle symptoms to establish a baseline before initiating statin therapy.
- B. If unexplained severe muscle symptoms or fatigue develop during statin therapy, promptly discontinue the statin and address the possibility of rhabdomyolysis by evaluating CK, creatinine, and a urinalysis for myoglobinuria.
- C. If mild to moderate muscle symptoms develop during statin therapy:
- Discontinue the statin until the symptoms can be evaluated.
- Evaluate the patient for other conditions that might increase the risk for muscle symptoms (e.g., hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases.)
- If muscle symptoms resolve, and if no contraindication exists, give the patient the original or a lower dose of the same statin to establish a causal relationship between the muscle symptoms and statin therapy.
- If a causal relationship exists, discontinue the original statin. Once muscle symptoms resolve, use a low dose of a different statin.
- Once a low dose of a statin is tolerated, gradually increase the dose as tolerated.
- If, after 2 months without statin treatment, muscle symptoms or elevated CK levels do not resolve completely, consider other causes of muscle symptoms listed above.
- D. If persistent muscle symptoms are determined to arise from a condition unrelated to statin therapy, or if the predisposing condition has been treated, resume statin therapy at the original dose.
- CK, creatine kinase, a test of muscle injury
Table 6. Statin Safety Recommendations
|Recommendations||ACC/AHA COR||ACC/AHA LOE|
|1. To maximize the safety of statins, selection of the appropriate statin and dose in men and nonpregnant/nonnursing women should be based on patient characteristics, level of ASCVDa risk, and potential for adverse effects.|
Moderate-intensity statin therapy should be used in individuals in whom high-intensity statin therapy would otherwise be recommended when characteristics predisposing them to statin-associated adverse effects are present.
Characteristics predisposing individuals to statin adverse effects include, but are not limited to:
|2a. CK should not be routinely measured in individuals receiving statin therapy.||III: No Benefit||A|
|2b. Baseline measurement of CK is reasonable for individuals believed to be at increased risk for adverse muscle events based on a personal or family history of statin intolerance or muscle disease, clinical presentation, or concomitant drug therapy that might increase the risk of myopathy.||IIa||C|
|2c. During statin therapy, it is reasonable to measure CK in individuals with muscle symptoms, including pain, tenderness, stiffness, cramping, weakness, or generalized fatigue.||IIa||C|
|3a. Baseline measurement of hepatic transaminase levels (ALT) should be performed before initiaton of statin therapy.||Ib||B|
|3b. During statin therapy, it is reasonable to measure hepatic function if symptoms suggesting hepatotoxicity arise (e.g., unusual fatigue or weakness, loss of appetite, abdominal pain, dark-colored urine or yellowing of the skin or sclera).||IIa||C|
|4. Decreasing the statin dose may be considered when|
2 consecutive values of LDL-C levels are <40 mg/dL.
|5. It may be harmful to initiate simvastatin at 80 mg daily or increase the dose of simvastatin to 80 mg daily.||III: Harm||A|
|6. Individuals receiving statin therapy should be evaluated for new-onset diabetes according to the current diabetes screening guidelines. Those who develop diabetes during statin therapy should be encouraged to adhere to a heart-healthy dietary pattern, engage in physical activity, achieve and maintain a healthy body weight, cease tobacco use, and continue statin therapy to reduce their risk of ASCVD events.||Ic||B|
|7. For individuals taking any dose of statins, it is reasonable to use caution in individuals >75 years of age, as well as in individuals who are taking concomitant medications that alter drug metabolism, taking multiple drugs, or taking drugs for conditions that require complex medication regimens (e.g., those who have undergone solid organ transplantation or are receiving treatment for HIV). A review of the manufacturerâs prescribing information may be useful before initiating any cholesterol-lowering drug.||IIa||C|
|8. It is reasonable to evaluate and treat muscle symptoms, including pain, tenderness, stiffness, cramping, weakness, or fatigue, in statin-treated patients according to the following management algorithm:||IIa||B|
|9. For individuals presenting with a confusional state or memory impairment while on statin therapy, it may be reasonable to evaluate the patient for nonstatin causes, such as exposure to other drugs, as well as for systemic and neuropsychiatric causes, in addition to the possibility of adverse effects associated with statin drug therapy.||IIb||C|
|a Based on the presence of clinical ASCVD, diabetes mellitus, LDL-C â¥190 mg/dL, or level of estimated 10-year ASCVD risk.|
b Individuals with elevated ALT levels (usually â¥1.5 or 2 times ULN) were excluded from RCT participation. Unexplained ALT â¥3 times ULN is a contraindication to statin therapy as listed in manufacturerâs prescribing information.
c Statin use is associated with a very modest excess risk of new onset diabetes in RCTs and meta-analyses of RCTs (i.e., ~0.1 excess cases per 100 individuals treated 1 year with moderate-intensity statin therapy and ~0.3 excess cases per 100 individuals treated for 1 year with high-intensity statin therapy). The increased risk of new onset diabetes appears to be confined to those with risk factors for diabetes. These individuals are also at higher risk of ASCVD due to these risk factors. Therefore, if a statin-treated individual develops diabetes as detected by current diabetes screening guidelines, they should be counseled to adhere to a heart healthy dietary pattern, engage in physical activity, achieve and maintain a healthy body weight, cease tobacco use, and continue statin therapy to reduce their risk of ASCVD events.
Table 7. Nonstatin Safety Recommendations
|Recommendations||ACC/AHA COR||ACC/AHA LOE|
|Safety of Niacin|
|1. Baseline hepatic transaminases, fasting blood glucose or hemoglobin A1c, and uric acid should be obtained before initiating niacin, and again during up-titration to a maintenance dose and every 6 months thereafter.||I||B|
|2. Niacin should NOT be used if:||III: Harm||B|
|3. In individuals with adverse effects from niacin, the potential for ASCVD benefits and the potential for adverse effects should be reconsidered before reinitiating niacin therapy.||I||B|
|4. To reduce the frequency and severity of adverse cutaneous symptoms, it is reasonable to:||IIa||C|
|Safety of Bile Acid Sequestrants (BAS)|
|1. BAS should not be used in individuals with baseline fasting triglyceride levels â¥300 mg/dL or type III hyperlipoproteinemia, because severe triglyceride elevations might occur. (A fasting lipid panel should be obtained before BAS is initiated, 3 months after initiation, and every 6 to 12 months thereafter.)||III: Harm||B|
|2. It is reasonable to use BAS with caution if baseline triglyceride levels are 250-299 mg/dL, and evaluate a fasting lipid panel in 4-6 weeks after initiation. Discontinue the BAS if triglycerides exceed 400 mg/dL.||IIa||C|
|Safety of Cholesterol-Absorption Inhibitors|
|1. It is reasonable to obtain baseline hepatic transaminases before initiating ezetimibe. When ezetimibe is coadministered with a statin, monitor transaminase levels as clinically indicated, and discontinue ezetimibe if persistent ALT elevations â¥3 times ULN occur.||IIa||B|
|Safety of Fibrates|
|1. Gemfibrozil should not be initiated in patients on statin therapy because of an increased risk for muscle symptoms and rhabdomyolysis.||III: Harm||B|
|2. Fenofibrate may be considered concomitantly with a low- or moderate-intensity statin only if the benefits from ASCVD risk reduction or triglyceride lowering when triglycerides are â¥500 mg/dL are judged to outweigh the potential risk for adverse effects.||IIb||C|
|3. Renal status should be evaluated before fenofibrate initiation, within 3 months after initiation, and every 6 months thereafter. Assess renal safety with both a serum creatinine level and an eGFR based on creatinine.||I||B|
|Safety of Omega-3 Fatty Acids|
|1. If EPA and/or DHA are used for the management of severe hypertriglyceridemia, defined as triglycerides â¥500 mg/dL, it is reasonable to evaluate the patient for gastrointestinal disturbances, skin changes, and bleeding.||IIa||B|
|a Consult the manufacturer's prescribing information as there are several forms of fenofibrate available.|