John Barron

Vincent J. Willey

Hyperlipidemia is a blood disorder characterized by elevations in blood cholesterol levels. The term is often used synonymously with dyslipidemia and hypercholesterolemia. Hyperlipidemia is one of the major contributing risk factors in the development of coronary heart disease (CHD). It is estimated that approximately 15.5 million people in the United States have CHD, with approximately 375,000 deaths each year (American Heart Association, 2015). In addition, approximately $215 billion is spent each year on direct and indirect costs from CHD.

Informed estimates indicate that approximately greater than 100 million adults aged 20 and older had total cholesterol levels above 200 mg/dL using data from 2009 to 2012, representing approximately 47% of adults in the United States (American Heart Association, 2015). However, data from the National Health and Nutrition Examination Survey (NHANES) suggest that the percentage of patients with elevated cholesterol may be decreasing.

Numerous large studies have shown that reducing elevated cholesterol levels reduces morbidity and mortality rates in patients with and without existing CHD (Downs et al., 1998; Frick et al., 1987; Heart Protection Study Collaborative Group, 2002; Lewis et al., 1998; Long-Term Intervention With Pravastatin in Ischaemic Disease [LIPID] Study Group, 1998; Ridker et al., 2008; Scandinavian Simvastatin Survival Study Group, 1994; Shepherd et al., 1995). Although these and other trials have clearly shown the benefits of treating high cholesterol levels and other preventive measures, including the use of aspirin, beta-blockers, and angiotensin-converting enzyme inhibitors in the treatment of patients with coronary artery disease, long-term use of these medications across the population is still suboptimal (Newby et al., 2006).


In hyperlipidemia, serum cholesterol levels may be elevated as a result of an increased level of any of the lipoproteins. (See the section on Pathophysiology: Lipoproteins and Lipid Metabolism.) The mechanisms for hyperlipidemia appear to be genetic (primary) and environmental (secondary). In fact, the most common cause of hyperlipidemia (95% of all those with hyperlipidemia) is a combination of genetic and environmental factors.

Some individuals are genetically predisposed to elevated cholesterol levels. They may inherit defective genes that lead to abnormalities in the synthesis or breakdown of cholesterol. These may include abnormalities in low-density lipoprotein (LDL) receptors and mutations in apolipoproteins that lead to increased production of cholesterol or decreased clearance of cholesterol from the bloodstream. (See the section on Pathophysiology: Lipoproteins and Lipid Metabolism.)

Secondary factors may include medications (e.g., beta-blockers and oral contraceptives), concomitant disease states or other conditions (e.g., diabetes mellitus and pregnancy), diets high in fat and cholesterol, lack of exercise, obesity, and smoking (Box 20.1).


In 2013, the American College of Cardiology and the American Heart Association released guidelines on the assessment of CV risk (2013 ACC/AHA CV risk guidelines). While these guidelines encompass more than just assessment based on lipid levels, lipids are still an important part of the overall CV risk assessment for a patient. The workgroup echoed a well-established but important framework that the intensity of an intervention should be proportional to the individual’s absolute risk for having a future atherosclerotic cardiovascular disease (ASCVD) event (Box 20.2). Health care practitioners can then utilize this framework by assessing a patient’s ASCVD risk, discussing benefits and risks associated with potential therapies, and reviewing the patient’s goals and preferences for treatment.

The 2013 ACC/AHA CV risk guidelines recommend assessment of traditional ASCVD risk factors in patients age 20 to 79 without a history of CVD every 4 to 6 years. In addition to lipid levels, these traditional risk factors include age, gender, systolic blood pressure, antihypertensive therapy use, presence of diabetes, and smoking status. While for the estimation of 10-year risk for ASCVD only total and HDL cholesterol levels are required, a full lipid panel, which also contains LDL cholesterol and triglycerides, should be obtained to fully evaluate a patient’s ASCVD risk. A past medical history should also be obtained to determine if the patient has already had an ASCVD event such as an MI or thromboembolic stroke. Those patients with a past medical history of ASCVD, labeled as secondary prevention patients, are at a higher risk for a future ASCVD event than are those without a history of ASCVD, labeled as primary prevention.

To quantify the ASCVD risk in a primary prevention patient, the 2013 ACC/AHA CV risk guidelines recommend the use of the Pooled Cohort Equations that are race and gender specific. This risk assessment tool estimates the 10-year ASCVD risk for patients 40 to 79 years of age and the lifetime ASCVD risk for patients 20 to 59 years of age. The Pooled Cohort Equations are based off of multiple studies beyond the original Framingham study and were hoped to be an improvement on the Framingham risk calculator because the equations were developed in a broader population, including African Americans, and a fuller definition of ASCVD was utilized (CHD death, nonfatal MI, and fatal/nonfatal stroke). Patients with a 10-year ASCVD risk ≥7.5% are considered at elevated risk for a future ASCVD event. Some individuals have criticized the accuracy of the results the Pooled Cohort Equations generate for some patients and the use of a cut point for elevated risk of ≥7.5%. In order to potentially improve the ASCVD risk assessment in patients with borderline risk based on the traditional risk factors and to help inform treatment decisions, the 2013 ACC/AHA CV risk guidelines also addressed the use of several novel risk markers. Although the workgroup responsible for the development of these guidelines reviewed multiple novel risk markers, they identified the following four that were considered to show promise for clinical utility: family history of CVD, high-sensitivity C-reactive protein (hs-CRP), coronary artery calcium (CAC) score, and ankle-brachial index (ABI). hs-CRP is a marker for inflammation, and levels ≥2 mg/L have been associated with an increased risk of ASCVD.

Lifestyle Modification

In 2013, the American College of Cardiology and the American Heart Association also released guidelines on lifestyle management to reduce CV risk (2013 ACC/AHA lifestyle guidelines). These guidelines focused primarily on dietary therapy, exercise, weight loss, moderation of alcohol intake, and smoking cessation.


The guidelines recommend a diet that is high in fruits, vegetables, whole grains, low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts. It also
recommends limiting sweets, sugar-sweetened beverages, and red meats. Individuals should try to limit caloric intake of saturated fat to no more that 5% to 6% of total calories. Additionally, it is recommended to limit intake of trans fats. Diets that are recommended include the Dietary Approaches to Stop Hypertension (DASH) dietary pattern, the USDA Food Pattern, or the AHA Diet.

In addition, overweight patients should attempt to lose weight. The ability to lose weight depends on the amount of calories consumed and the amount of calories burned. The goal for overweight patients should be a realistic, gradual, and steady loss of weight. Once an ideal weight is achieved, caloric intake is adjusted to maintain that weight.

Moderation of Alcohol Intake and Smoking Cessation

Excessive alcohol intake may elevate serum lipid levels, specifically triglyceride levels, but in moderation (no more than one drink per day for women and two drinks per day for men), alcohol may improve HDL levels and has been associated with lower ASCVD rates (Brien et al., 2011). Despite these benefits, alcohol should not be recommended for ASCVD prevention because the consequences associated with excessive alcohol use outweigh any benefits.

Cigarette smoking is an independent risk factor in the development of ASCVD (Huxley & Woodward, 2011). Although smoking minimally affects cholesterol levels, it contributes to the development of ASCVD by damaging the vascular endothelium and promoting platelet aggregation, which results in increased risk of clot formation. Smoking cessation can reduce this risk and should be encouraged by all health care professionals. The risk of developing ASCVD decreases by approximately 50% within 1 to 2 years of smoking cessation.


The 2013 ACC/AHA treatment guidelines recommend use of HMG-CoA reductase inhibitors (statins) for ASCVD prevention in four groups of patients, termed “statin benefit groups.” The statin benefit groups include individuals who are (1) ≥21 years of age and have clinical ASCVD or (2) do not have ASCVD but have LDL-C values ≥190 mg/dL or (3) are 40 to 75 years old with type 1 or type 2 diabetes mellitus and have LDL-C values of 70 to 189 mg/dL, or (4) are 40 to 75 years old with LDL-C values of 70 to 189 mg/dL and have a 10-year risk of ASCVD of ≥7.5% (Table 20.1).

TABLE 20.1 Four Major Statin Benefit Groups

Statin Benefit Group

Statin Dose Intensity

1. Have clinical ASCVD

High intensity ages ≤75

Moderate intensity >75 y

2. No ASCVD but have LDL-C values ≥190 mg/dL

High intensity unless contraindicated or unable to tolerate

3. No ASCVD and 40-75 y old with type 1 or type 2 diabetes mellitus and have LDL-C values of 70-189 mg/dL

Moderate-intensity statin if 10-year ASCVD risk is <7.5%

High-intensity statin if 10-year ASCVD risk is ≥7.5%

4. No ASCVD or diabetes mellitus and are 40-75 y old with LDL-C values of 70-189 mg/dL and have a 10-year risk of ASCVD of ≥7.5%

Moderate-intensity statin if 10-year ASCVD risk is ≥7.5%.

The recommended statin and dose to use are based upon the expected reduction in LDL-C levels. High-intensity statins are those that can lower LDL-C by 50% or more, on average. Moderate-intensity statins reduce LDL-C by about 30% to 49%, and low-intensity statins typically reduce LDL-C by less than 30%. Specific medications and doses for each category are listed in Table 20.2.

In individuals with clinical ASCVD, a high-intensity statin is recommended in those ≤75 years of age, unless contraindicated (known hypersensitivity, active liver disease, women who are pregnant or may become pregnant, or nursing mothers) or unable to tolerate dose, in which a moderate-intensity statin should be used. For individuals with ASCVD who are greater than 75 years of age, a moderate-dose statin is recommended.

TABLE 20.2 Statin Dose Intensity (Daily Dose)

Generic Name (Trade Name)

High Intensity

Moderate Intensity

Low Intensity

atorvastatin (Lipitor)

40-80 mg

10-20 mg


rosuvastatin (Crestor)

20-40 mg

5-10 mg


simvastatin (Zocor)


20-40 mg

10 mg

lovastatin (Mevacor)


40 mg

20 mg

pravastatin (Pravachol)


40-80 mg

10-20 mg

fluvastatin (Lescol)


80 mg

20-40 mg

pitavastatin (Livalo)


2-4 mg

1 mg

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Nov 11, 2018 | Posted by in PHARMACY | Comments Off on Hyperlipidemia
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