The Role of the Pharmacist in Managing Hyperlipidemia

Release Date: February 1, 2013

Expiration Date: February 28, 2015


Muideen Adigun, PharmD, BCPS
Assistant Professor, Howard University
College of Pharmacy

Department of Clinical and
Administrative Pharmacy Sciences
Program Director, PGY-1 Pharmacy

Practice Residency
Howard University Hospital
Washington, D.C.

Mia N. Barnes, PharmD
PGY-1 Pharmacy Resident
Howard University Hospital

Sharika Johnson, PharmD
PGY-1 Pharmacy Resident
Howard University Hospital

Jinwi Ghogomu, PharmD
PGY-1 Pharmacy Resident
Howard University Hospital


Drs. Adigun, Barnes, Johnson, and Ghogomu have no actual or potential conflicts of interest in relation to this activity.

Postgraduate Healthcare Education, LLC does not view the existence of relationships as an implication of bias or that the value of the material is decreased. The content of the activity was planned to be balanced, objective, and scientifically rigorous. Occasionally, authors express opinions that represent their own viewpoint. Conclusions drawn by participants should be derived from objective analysis of scientific data.


Pharmacy acpe
Postgraduate Healthcare Education, LLC is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education.
UAN: 0430-0000-13-002-H01-P
Credits: 2.0 hours (0.20 ceu)
Type of Activity: Knowledge


Payment of $6.50 required for exam to be graded.


This accredited activity is targeted to pharmacists. Estimated time to complete this activity is 120 minutes.

Exam processing and other inquiries to:
CE Customer Service: (800) 825-4696 or


Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible contraindications or dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities.


To educate community pharmacists on the appropriate management of patients with hyperlipidemia and its importance in reducing the incidence of cardiovascular-related diseases.


After completing this activity, the participant should be able to:

  1. Define specific classes of lipoproteins and their potential roles in hyperlipidemia.
  2. Identify risk factors associated with hyperlipidemia.
  3. Understand the role that various risk factors play in the incidence of coronary heart disease.
  4. Outline the goals of therapy of patients who present with hyperlipidemia.
  5. Describe the mechanism of action, adverse effects, potential drug interactions, and specific effects on the lipoprotein component of various medications used in the management of hyperlipidemia.
  6. Define strategies to improve patient adherence to lipid-lowering medications and to improve patient-centered therapeutic outcomes.

ABSTRACT: The management of plasma cholesterol levels is of utmost importance in reducing the risk of cardiovascular-related diseases. Elevations in plasma cholesterol levels, particularly of LDL cholesterol (LDL-C), has proven to be a significant risk factor in the incidence of coronary heart disease. Furthermore, lipid-related risk factors produce additive effects when combined with other nonlipid-related risk factors. The National Cholesterol Education Program Adult Treatment Panel III (ATP III) encourages the management of hyperlipidemia to be inclusive of targeting both lipid-related and modifiable nonlipid-related risk factors. In addition, ATP III identifies several pharmacologic and nonpharmacologic therapies to target cholesterol levels, with reductions in LDL-C being the primary target of therapy. Community pharmacists may play a unique role in the management of hyperlipidemia by educating practitioners about available therapies, assessing potential drug interactions, and counseling patients about the appropriate use of medications and side-effect management.

Coronary heart disease (CHD) is the leading cause of death for both men and women and accounts for approximately 600,000 deaths in the United States every year.1 Although the mortality rates of CHD have declined over the years, patient-specific risk-factor modification is of critical importance in reducing the risk of cardiovascular-related death.

Numerous clinical studies have established that the management of plasma cholesterol levels is of utmost importance in reducing the risk of cardiovascular-related diseases. However, available data have demonstrated that there are numerous individuals who are inadequately treated.2-4 It is estimated that nearly 33.5 million adults over 20 years of age have total serum cholesterol levels above 240 mg/dL.5 Specifically, a prospective study of 1,017 young, healthy, low-risk Caucasian men (mean age 22 years) were studied over a period of 27 to 42 years. Researchers concluded that participants with higher serum cholesterol levels at baseline had a higher incidence of cardiovascular-related death during follow-up as compared to those with the lowest cholesterol levels at baseline (37.7 vs. 9.7; P < .001).4

The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) has established guidelines that summarize significant data and recommendations in the management of hyperlipidemia in adult populations.2 Throughout the guidelines, the NCEP has communicated the importance of early identification of risk, lifestyle modification, and pharmacologic treatment as the mainstay of therapy for hyperlipidemia and in the prevention of cardiovascular-related death.2


One of the key focuses of ATP III is to outline specific risk factors associated with increased risk of CHD, which is inclusive of both lipid-related (triglycerides, elevated LDL-C, HDL, and non-HDL) and nonlipid-related risk factors.2 Nonlipid-related risk factors can be further classified into two categories, modifiable or nonmodifiable. Modifiable risk factors are inclusive of the presence of hypertension, obesity, cigarette smoking, physical inactivity, and diabetes.2

Nonmodifiable risk factors are inclusive of patient-specific characteristics such as age, male sex, and family history of CHD.2 Elevations in cholesterol produce additive effects when combined with other nonlipid risk factors for CHD and have proven to increase the incidence of cardiovascular diseases.2 Therefore, clinicians should provide focused attention on encouraging the management of modifiable risk factors.

Lipid-Related Risk Factors: Importance of LDL-C

Evidence from numerous epidemiologic, genetic, and controlled clinical trials implicates LDL-C as a major atherogenic lipoprotein and further supports a strong contributory relationship between elevated LDL-C and CHD.2,5 The strongest supporting evidence available that demonstrates the role of LDL-C as a major atherogenic protein can be seen in patients with elevations of LDL-C due to genetic causes. Genetic studies have concluded that high LDL-C levels, even in the absence of other known risk factors, increase the incidence of advanced coronary atherosclerosis and premature CHD.2,5

Lipid-Related Risk Factors: Role of Triglycerides and HDL

While LDL-C has proven to be the greatest indicator of CHD risk, it is evident that other circulating lipoproteins, specifically triglycerides and HDL, also play important roles in predisposing patients to cardiovascular-related diseases (TABLE 1).


In previous studies and guidelines, elevated triglycerides were not indicated as an independent risk factor of CHD.2,6 On the contrary, current prospective clinical studies have confirmed that a significant relationship does in fact exist between elevations of triglycerides and CHD risk.6,7 Analysis of clinical data has theorized that some forms of triglyceride-rich lipoproteins, chylomicrons, and very low-density lipoproteins may in fact carry the same athrogenic potential as that of LDL-C.6 However, clinicians should also note that increased risk of CHD is not limited to merely an increase in triglycerides, but is also inclusive of various relationships that exist between triglycerides and other nonlipid-related risk factors.2,6

Nonlipid risk factors appear to be consistent factors that are often present in conjunction with elevated serum triglycerides.2,6 Metabolic syndrome, a syndrome that is inclusive of both nonlipid risk factors and the presence of a prothrombotic state, is also most commonly associated with hypertriglyceridemia.2,6 Because of these evident and established relationships, it is recommended that the management of hypertriglyceridemia be approached at a broader metabolic level rather than specifically focusing on elevations of triglycerides.

When assessing the roles of HDL in CVD risk, it appears that HDL plays a dual role in the risk of CHD development. Epidemiologic studies have indicated that both low and high HDL cholesterol (HDL-C) levels affect a patient's risk of coronary artery disease (CAD). Elevated levels of HDL are established to be of benefit in lowering CAD risk; however, in contrast, low levels of serum HDL cholesterol independently increase the risk of CAD.2,8,9 Although there are available data to support these theories, the specific underlying relationship that exists between low HDL cholesterol levels and the incidence of CHD has yet to be fully understood.2


Secondary causes of hyperlipidemia should be considered in patients with elevation in lipoprotein(s), in addition to cardiovascular risk assessment. Pharmacists may serve as a valuable resource in determining the presence of drug-induced causes of hyperlipidemia. Potential causes of drug-induced hyperlipidemia include, but are not limited to, HIV protease inhibitors, thiazide diuretics, atypical antipsychotics—particularly clozapine and olan-zapine—and glucocorticoids.13 If potential drug-induced causes of hyperlipidemia are noted, therapeutic interventions should be aimed at encouraging physicians to consider therapy discontinuation. However, effort should be made to assess the benefits of discontinuation versus the risk. Once the offending agents are discontinued, plasma lipid levels should be reassessed to determine the need for further interventions.13


Current guidelines recommend a fasting lipid panel be completed at least once every 5 years in adults aged 20 years and older, since many patients will appear to be asymptomatic upon presentation.2 Total cholesterol, LDL-C, HDL-C, and triglyceride levels should be mea sured.2 The NCEP suggests that more frequent measurement be required in patients who present with multiple risk factors that confer a higher risk of developing CHD.


The goals of therapy for treating hyperlipidemia are to reduce the LDL-C levels to goal and reduce the risk of first cardiovascular-related events or recurrent events such as myocardial infarction, angina, heart failure, ischemic stroke, and other forms of peripheral artery disease.14

According to the ATP III guidelines, the target lipid for treatment of hyperlipidemia is LDL-C.2 The guidelines provided classifications of LDL-C, total cholesterol, HDL-C, and triglyceride levels so that clinicians may properly assess the need for treatment in patients with suspected hyperlipidemia (TABLE 2).


In addition to the assessment of lipid levels in patients, major risk factors and potential CHD risk equivalents, which modify LDL-C goals, should be taken into account. The ATP III classifies CHD risk equivalents as presence of specific disease states such as diabetes mellitus, peripheral artery disease, abdominal aortic aneurysm, symptomatic carotid artery disease, and multiple risk factors with a 10-year risk for CHD >20%. A Framingham risk score should also be calculated. The Framingham Risk Assessment assigns numerical values to patient-specific categories: age, systolic blood pressure, cigarette smoking, total cholesterol, and HDL-C. The resulting score can then be utilized to determine the 10-year risk for CHD as greater than 20%, 10% to 20%, or less than 10%.2

If after utilization of the Framingham Risk Assessment a patient's 10-year risk for CHD is greater than 20% and multiple other risk factors are present, the clinician should then consider the patient as having a CHD risk equivalent.2

The presence of major risk factors, CHD risk equivalents, and the Framingham risk score are used to guide the initiation of therapeutic lifestyle changes (TLC) or drug therapy in patients with hyperlipidemia (TABLE 3).



Currently, there are many classes of medications that may be utilized in the pharmacologic management of hyperlipidemia. These classes are inclusive of HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reduc-tase inhibitors, fibrates, ezetimibe, nicotinic acid, bile acid sequestrants, fish oils, and OTC herbal products. However, TLC should be considered first-line therapy in the management of individuals diagnosed with hyper-lipidemia.2 If TLC fail and pharmacologic therapy is required, the specific drug therapy used should be determined by an assessment of patient-specific LDL-C goals (FIGURE 1). Although LDL-C levels are the primary targets of therapy, secondary goals of therapy should be aimed at the reduction of elevated triglyceride levels as well as attainment of HDL-C goals.


HMG-CoA Reductase Inhibitors

The HMG-CoA reductase inhibitors, commonly known as statins, are the most effective and practical class of drugs for reducing LDL-C concentrations.2 HMG-CoA reductase inhibitors work by inhibiting the rate-limiting step of endogenous cholesterol synthesis and are structurally similar to HMG-CoA.

The mechanism by which statins reduce LDL-C is seen first in the partial inhibition of HMG-CoA reductase. The inhibition of HMG-CoA reductase leads to the increased expression of LDL-C receptors, which increases catabolism of LDL-C and liver extraction of LDL-C precursors (VLDL-C [very low-density lipoprotein cholesterol] remnants) from blood, thus reducing blood levels of LDL-C. Other effects of statins include decreased oxidative stress and vascular inflammation with increased stability of atherosclerotic lesions.15

Currently, seven statins are available in the United States: atorvastatin (Lipitor), fluvastatin (Lescol, Lescol XL), lovastatin (Mevacor, Altoprev), pitavastatin (Livalo), pravastatin (Pravachol), rosuvastatin (Crestor), and sim-vastatin (Zocor) (TABLE 4).


Because HMG-CoA is most active at night when dietary intake is low, it is suggested that statins be generally administered with the evening meal or at bedtime in order to provide optimal decreases in LDL-C. However, due to their longer half-lives, atorvastatin, rosuvastatin, and pitavastatin do not require evening dosing and provide equivalent efficacy when administered as morning or afternoon doses.2,16,20,23

Side effects of statins include elevated liver transaminases and myalgia/myopathy, which could progress to rhabdomyolysis. Risk of rhabdomyolysis is generally increased with administration of other drug/substances that can increase statin concentrations or carry an independent risk for rhabdomyolysis, such as fibrates.

Statins are considered pregnancy Category X and should be avoided by both pregnant women and people with active or chronic liver diseases. Furthermore, women of childbearing age should be counseled on the teratogenic effects of statins. The ATP III guidelines recommend caution be exercised when using statins with other medications such as cyclosporine, macrolide antibiotics, various antifungal agents, CYP-450 inhibitors, fibrates, and nicotinic acid, as the incidence of myopathy has been found to be more likely.2


Fenofibric acid is a common adjunct drug product that is used in combination with statins to reduce triglycerides and increase HDL-C in patients with mixed hyperlipidemia and CHD or CHD risk equivalents who are on optimal statin therapy and have achieved their LDL-C goal.26 Fenofibrates may also be utilized as monotherapy in patients with severe hypertriglyc-eridemia, primary hyperlipidemia, or mixed hyperlip-idemia. Available fenofibrate agents include gemfibro-zil and fenofibric acid (TABLE 5). The use of fibrates has proven to be an effective alternative for lipid-lowering therapy and provide a 5% to 20% reduction in LDL-C, a 10% to 35% increase in HDL, and a 20% to 50% reduction in triglycerides.2


Fenofibric acid derivatives exert their effects on lipid metabolism by the activation of peroxisome-proliferator-activated receptor-alpha (PPAR-α) by active fenofibric acid. Fenofibrate reduces triglyceride levels by inhibiting synthesis and stimulating clearance of triglycerides.

The most common adverse effects are dyspepsia, myalgia, gallstones, and moderate elevation of creatinine kinase.26 Close monitoring should be done when using a fibrate in combination with a statin, as this may potentially increase the risk for myopathy (rhabdomyolysis). However, the combination of gemfibrozil and any statin is contraindicated, and concomitant use has been associated with a 15-fold higher risk of rhabdomyolysis. Fenofibrate has proven to be a safer alternative for use with statins because both classes of drugs are metabolized via the glucuronidation pathway.26 All fibrates are contraindicated in patients with preexisting gallbladder disease, severe renal disease, and severe hepatic disease.26


Ezetimibe (Zetia) and its glucuronyl metabolite are thought to inhibit a putative cholesterol transporter of enterocytes, located within the brush-border membrane of the small intestine, which leads to reduced absorption of cholesterol and related plant sterols in the intestine.35 Clinical studies have demonstrated significant incremental reductions in LDL-C, incremental increases in HDL-C, as well as reductions in triglyceride levels in patients diagnosed with primary hypercholesterolemia who were initiated on ezetimibe plus a statin or who were already on statin therapy and required the addition of ezetimibe.36 Additionally, studies using low doses of simvastatin, atorvastatin, pravastatin, and/or lovastatin along with ezetimibe proved to be as effective as a two- to threefold upward titration of the corresponding statin dose.37 Utilization of ezetimibe along with a statin allows for lower doses of the statin to be used, therefore reducing the likelihood of dose-related side effects of the statin.


Nicotinic acid (niacin) reduces the mobilization of free fatty acids from adipose tissue, decreasing triglyceride synthesis and VLDL-C. The decrease in available VLDL-C particles, which are converted to LDL-C, results in an overall reduction in LDL-C levels.38 One of the significant advantages of niacin therapy is that it is known to significantly increase HDL-C levels.

The three most commonly used formulations include crystalline/immediate-release nicotinic acid, sustained-release nicotinic acid, and extended-release nicotinic acid (TABLE 6). When compared, these agents differ mainly in dissolution rate, which is the primary cause of variations in each agent's side-effect profile.39 Adverse effects of nicotinic acid include flushing (most common in the immediate-release formulation), hyperuricemia, hyperglycemia, and hepatotoxicity (most common in the slow-release formulation). Gastrointestinal side effects may also occur; these include activation of peptic ulcer, nausea, dyspepsia, flatulence, vomiting, and diarrhea.


When initiating patients on niacin therapy, all patients should be counseled on the potential of flushing. Flushing is prostaglandin mediated, is produced by dilation of small subcutaneous blood vessels, and is characterized by warmth, redness, and itching or tingling in the upper portion of the body. Flushing affects almost all users initially and often leads to therapy discontinuation in 10% to 50% of patients.39 Patients should be educated on the importance pretreatment with 325 mg of aspirin or nonsteroidal anti-inflammatory agents (NSAIDs) 45 to 60 minutes before the first dose to reduce the incidence of flushing symptoms. Also, slow titration of dosage increases will further assist in reducing the incidence of flushing. Avoiding alcohol, hot showers, spicy foods, and hot beverages soon after dosing will also help alleviate flushing.39

Bile Acid Sequestrants

Bile acid sequestrants (BAS) are positively charged nondigestible resins that bind to negatively charged cholesterol containing bile acids in the intestine to form an insoluble complex, which is then excreted in the feces.43,44

Current formulations of BAS include cholestyramine (Questran), colestipol (Coletid), and colesevelam (Welchol). These agents are indicated as adjunctive therapy to diet for reduction of elevated serum LDL-C and cholesterol levels in patients who do not respond adequately to diet.2 Moreover, adding a moderate dose of a BAS may further lower LDL-C by 12% to 16% when combined with statin therapy.2 In addition to offering lipid-lowering advantages, BAS have also been found to improve glycemic control in patients with type 2 diabetes by an unknown mechanism.45 However, one of the major disadvantages of BAS is that they have been noted to raise serum triglyceride levels and are thus contraindicated as monotherapy in persons with triglycerides >400 mg/dL.

Notable adverse effects associated with BAS include constipation, abdominal pain, bloating, fullness, nausea, and flatulence. In addition, due to the localized action of BAS within the gut, these agents may also alter or inhibit the absorption of substances. Pharmacists should educate patients to separate other medications by at least 1 hour before or 4 hours after the administration of cholestyramine and colestipol. However, colesevelam is not known to have these same drug-binding mechanisms.


In cases of hypertriglyceridemia, Lovaza (formerly available as Omacor), an omega-3-acid ethyl ester, is indicated as adjunct therapy to diet in patients with triglyceride levels greater than or equal to 500 mg/dL. The specific mechanism of action of Lovaza is unclear; however, proposed mechanisms include decreasing lipogenesis in the liver, increasing plasma lipoprotein lipase activity, and increasing mitochondrial and perixosomal lipase activity. Omega-3-acid ethyl esters provide significant reduction in triglycerides, of approximately 44.9%, making Lovaza an ideal drug choice in patients with high triglycerides.46

Lovaza is available in a 1-g gel capsule formulation that contains approximately 900 mg of the ethyl esters of omega-3 fatty acids derived from fish oils.46 The drug consists of a combination of the ethyl esters eicosapen-taenoic acid (EPA) and docosahexaenoic acid (DHA). Each capsule contains roughly 465 mg of EPA and 375 mg of DHA. The daily dose of Lovaza is 4 g, which patients can take as four capsules once daily or two capsules twice daily. Dosing schedules should be determined by assessment of potential patient compliance. Common adverse effects associated with Lovaza include eructation, altered sense of taste, and upset stomach.

Manufacturer's recommendations indicate Lovaza should be avoided in patients with a shellfish allergy, as its components are derived from fish products. In addition, Lovaza should also be used with caution in patients with hepatic impairment, as it may increase aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Periodic monitoring of AST and ALT may be warranted. Lovaza is categorized as pregnancy Category C and should only be used if the potential benefit to the patient justifies the potential risk to the fetus. Lastly, Lovaza has also been known to prolong bleeding time and should be used with caution in patients receiving anticoagulant therapy.46

Herbal Products

One of the most studied herbal supplements used for lipid-lowering effects is red yeast rice (RYR). RYR is made by fermenting Monascus purpureus, a form of yeast, on rice, which is then dried, pulverized, and encapsulated. This process leads to the formation of 14 monacolins, which are compounds that inhibit HMG-CoA reductase, or the rate-limiting step in cholesterol biosynthesis, as seen with the statins. One of the mona-colins, monacolin K, referred to as lovastatin or mev-inolin, was the first synthesized HMG-CoA reductase inhibitor, Mevacor. The similarity of the mechanisms of action of RYR and the statins have led to the conduction of a number of studies to determine the efficacy of RYR as an herbal alternative for patients with hyperlipidemia.47

RYR is commercially available in 600-mg capsules that may vary in consistency when comparing different brands.47 The amount of monacolin K in each capsule may range anywhere from 0.1 mg to 10 mg, which may lead to an unpredictable response. Serious adverse effects of RYR include myopathy, rhabdomyolysis, hepatotoxicity, and anaphylaxis. In addition, loose stools, dizziness, headache, and rash have also been reported. Patients should be educated that RYR should only be used under a physician's supervision and should be monitored frequently for muscle symptoms and elevation in liver enzymes.47

Fish oil is another common OTC product that provides an alternative to the prescription product Lovaza. However, as with many other OTC herbal products, components of EPA and DHA vary in consistency when comparing various product brands, which may lead to unpredictable responses.48


According to the ATP III guidelines, the initial step in lowering LDL-C levels to goal is the initiation of TLC. These include reduced intake of saturated fat and cholesterol, incorporating plant sterols and stanols and soluble fiber into the diet, increased physical activity, and weight reduction (TABLE 7).2


Several dietary options such as soluble fiber, plant sterols and stanols, soy protein, and nuts may be incorporated into the diet and may provide significant reduction in LDL-C. Soluble fibers act by binding bile acids during the intraluminal formation of micelles, leading to increased bile acid synthesis, reduction in hepatic cholesterol content, up-regulation of LDL-C receptors, and increased LDL-C clearance.49 An increase in fiber intake by as little as 5 to 10 g per day has proven to reduce LDL-C by 3% to 5%; therefore, recommended daily intake of soluble fiber is 10 to 25 g.50 Common sources of fiber include oats, psyllium, guar gum, pectin, barley, dried beans, and fruits and vegetables.49,51

The use of plant sterols and stanols also assists in the reduction of LDL-C. Plant sterols reduce cholesterol absorption by competing with cholesterol for space within bile salt micelles in the intestinal lumen.49 The plant stanols, which are the result of the hydrogenation of sterols, are not absorbed as well as sterols. It is recommended that patients ingest about 2 g per day of plant sterols or stanols, with an expected LDL-C reduction of 6% to 15%1,50


It is evident that management of plasma cholesterol levels is imperative in reducing the risk of cardiovascular diseases; hence, the role of pharmacists in lipid management is great.2-4 LDL-C has been identified as the most important target of lipid management, as it has been identified to carry the greatest artherogenic potential and has been associated with increasing the incidence of advanced coronary atherosclerosis, premature CHD, and cardiovascular-related death.2,5 Pharmacists play an important role in educating practitioners about appropriate therapies and patients about appropriate use of medications and herbal products.


  1. Kochanek KD, Xu JQ, Murphy SL, et al. Deaths: final data for 2009. Nat Vital Stat Rep. 2011;60(3):1-117.
  2. 2001 executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285:2486-2497.
  3. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125:e2-e220.
  4. Klag MJ, Ford DE, Mead LA, et al. Serum cholesterol in young men and subsequent cardiovascular disease. N Engl J Med. 1993;328:313-318.
  5. Grundy SM, Cleeman JI, Merz CN, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004;110:227-239.
  6. Grundy SM. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol. 1998;81:18B-25B.
  7. Sarwar N, Danesh J, Eiriksdottir G, et al. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. 2007;115(4):450-458.
  8. Miller M. Raising an isolated low HDL-C level: why, how, and when? Cleve Clin J Med. 2003;70(6):553-560.
  9. Gordon T, Castelli WP, Hjortland MC, et al. High density lipoprotein as a protective factor against coronary artery disease: the Framingham Study. Am J Med. 1977;62:707-714.
  10. Stone NJ. Secondary causes of hyperlipidemia. Med Clin North Am. 1994;78:117-141.
  11. Chait A, Brunzell JD. Acquired hyperlipidemia (secondary dyslipoprotein-emias). Endocrinol Metab Clin North Am. 1990;19:259-278.
  12. Krauss RM. Regulation of high density lipoprotein levels. Med Clin North Am. 1982;66:403-430.
  13. Knopp RH. Drug treatment of lipid disorders. N Engl J Med. 1999;341:498-511.
  14. Dipiro J, Talbert R, Yee G, et al. Pharmacotherapy: A Pathophysiologic Approach. 7th ed. New York, NY: McGraw-Hill Companies, Inc., 2008:385-407. [eBook].
  15. Malloy MJ, Kane JP. Agents used in dyslipidemia. In: Katzung BG, Masters SB, Trevor AJ, eds. Basic & Clinical Pharmacology. 12th ed. New York, NY: McGraw-Hill; 2012. Chapter 35. aspx?aID=55826947. Accessed August 26, 2012.
  16. Lipitor package insert. New York, NY: Pfizer Inc; April 2011.
  17. Lescol and Lescol XL package inserts. East Hanover, NJ: Novartis Pharmaceuticals Corp; July 2011.
  18. Mevacor package insert. Whitehouse Station, NJ: Merck & Co., Inc; May 2010.
  19. Pravachol package insert. Princeton, NJ: Bristol-Myers Squibb Co; May 2011.
  20. Crestor package insert. Wilmington, DE: AstraZeneca Pharmaceuticals LP; May 2011.
  21. Zocor package insert. Whitehouse Station, NJ: Merck & Co., Inc; October 2011.
  22. FDA drug safety communication: new restrictions, contraindications, and dose limitations for Zocor (simvastatin) to reduce the risk of muscle injury. July 18, 2011. Accessed August, 26, 2012.
  23. Livalo package insert. Montgomery, AL: Kowa Pharmaceuticals America, Inc. August 2011.
  24. Vytorin package insert. North Wales, PA: Merck/Schering-Plough Pharmaceuticals; October 2011.
  25. Red Book Online. Greenwood Village, CO: Thomson Healthcare. Accessed September 2, 2012
  26. Moutzouri E, Kei A, Elisaf MS, Milionis HJ. Management of dyslipidemias with fibrates, alone and in combination with statins: role of delayed-release fenofibric acid. Vasc Health Risk Manag. 2010;6:525-539.
  27. Lopid package insert. New York, NY: Pfizer Inc; September 2010.
  28. Triglide package insert. France: Shionogi Pharma, Inc.; January 2010.
  29. Trilipix package insert. North Chicago, IL: Abbott Laboratories; September 2011.
  30. TriCor package insert. North Chicago, IL: Abbott Laboratories; September 2011.
  31. Lofibra package insert. Sellersville, PA: Teva Pharmaceuticals USA; January 2010.
  32. Lipofen package insert. Montgomery, AL: Kowa Pharmaceuticals America, Inc; October 2011.
  33. Fenoglide package insert. Stamford, CT: Shore Therapeutics, Inc; October 2010.
  34. Antara package insert. Baltimore, MD: Lupin Pharma; November 2009.
  35. Malcolm JM, Darkes RM, et al. Ezetimibe. Am J Cardiovasc Drugs. 2003;3(1):67-76.
  36. Patel SB. Ezetimibe: a novel cholesterol-lowering agent that highlights novel physiologic pathways. Curr Cardiol Rep. 2004;6:439-442.
  37. Lipka L. Ezetimibe: a first-in-class, novel cholesterol absorption inhibitor. Cardiovasc Drug Rev. 2003;21(4):293-312.
  38. McKenney J. Niacin for dyslipidemia: considerations in product selection. Am J Health Syst Pharm. 2003;60(10):995-1005.
  39. Pieper J. Overview of niacin formulations: differences in pharmacokinetics, efficacy, and safety. Am J Health Syst Pharm. 2003;60(13 suppl 2):S9-S14.
  40. Niacor oral tablet package insert. Minneapolis, MN: Upsher-Smith Laboratories Inc; 2000.
  41. Niaspan package insert. North Chicago, IL: Abbott Laboratories; September 2009.
  42. Slo-Niacin package insert. Minneapolis, MN: Upsher-Smith Laboratories, Inc; February 2011.
  43. Scaldaferri F, Pizzoferrato M, Ponziani FR, et al. Use and indications of cholestyramine and bile acid sequestrants. Intern Emerg Med. July 8, 2011 [Epub ahead of print].
  44. Insull W. Clinical utility of bile acid sequestrants in the treatment of dyslipidemia: a scientific review. South Med J. 2006;99(3):257-273.
  45. Out C, Groen AK, Brufau G. Bile acid sequestrants: more than simple resins. Curr Opin Lipidol. 2012;23(1):43-55.
  46. Lovaza package insert. Research Triangle Park, NC: GlaxoSmithKline; December 2010.
  47. Ram G, Becker D. The role of red yeast rice for the physician. Curr Atheroscler Rep. 2011;13:73-80.
  48. Toth P, Dayspring T, Pokrywka G. Drug therapy for hypertriglyceridemia: fibrates and omega-3 fatty acids. Curr Atheroscler Rep. 2009;11:71-79.
  49. Prabhjot N, Burke F, Bloesch A, Rader D. Role of dietary supplements in lowering low-density lipoprotein cholesterol: a review. J Clin Lipidol.2010;4.4:248-258.
  50. Fletcher B, Berra K, Ades P, et al. Managing blood lipids: a collaborative approach. Circulation. 2005;112:3184-3209.
  51. Stone N. The optimal dietary strategy to manage risk associated with various dyslipidemias. Curr Cardiol Rep. 2001;3:391-400.

Back to Top

  Take Test  |  View Questions