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Lipid Panel

Elevated LDL cholesterol is a major cause of coronary heart disease (CHD). Recent clinical trials have convincingly demonstrated that LDL lowering therapy reduces the risk for CHD. The National Cholesterol Education Program’s (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults recently published their updated clinical guideline for cholesterol testing and management (JAMA 2001; 285:2486), which is referred to as the Adult Treatment Panel III (ATP III). ATP III recommends intensive treatment for patients with CHD and primary prevention in persons with multiple risk factors.

The new guideline recommends that a fasting lipid panel should be obtained once every 5 years for all adults aged 20 years or older. The panel should include total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides. The new guideline also states that a lipid panel should be ordered within 24 hours of admission when patients are hospitalized for acute coronary syndromes or coronary procedures to guide initiation of LDL lowering therapy prior to discharge.

ATP III differs significantly from ATPII, which was published in 1993, in the interpretation of lipid levels.

  • The optimal LDL cholesterol level was lowered from 130 to 100 mg/dL.
  • The lower limit of normal for HDL cholesterol was raised from 35 to 40 mg/dL.
  • The optimal triglyceride level was decreased from 200 to 150 mg/dL.

Because of these changes, lipid values are now interpreted as follows:


Total cholesterol


200 – 239



Borderline high


LDL cholesterol


100 – 129

130 – 159

160 – 189



Above optimal

Borderline High


Very High

HDL cholesterol







150 – 199

200 – 499



Borderline High


Very High

Consistent with the two previous consensus statements, ATP III continues to identify elevated LDL cholesterol as the primary target of cholesterol lowering therapy. Thus, the first step in assessing a patient’s risk is to determine their LDL cholesterol level. The second step is to determine if the patient has any additional risk determinants such as the presence or absence of CHD, other clinical forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, & carotid artery disease) diabetes mellitus and the following major risk factors.

  • Cigarette smoking
  • Hypertension (BP >140/90) or anti-hypertensive medication
  • Low HDL cholesterol (<40 mg/dL)
  • Family history of premature CHD (1st degree relative male <55 or female <65 years)
  • Age (men >44 years & women >55 years)

Based on these other risk determinants, ATP III identifies 3 categories of risk that modify the goals of LDL cholesterol lowering therapy.

Risk Category

LDL Goal (mg/dL)

CHD & Equivalents


Multiple (2+) risk factors


0 – 1 risk factor


The relationship between LDL cholesterol levels and CHD risk is continuous over a broad range of LDL levels. An LDL cholesterol level of <100 mg/dL is optimal. Therefore, ATP III specifies that the goal of therapy for secondary prevention in persons with CHD or CHD risk equivalents is <100 mg/dL. Diabetes and peripheral vascular disease are now considered risk equivalents to CHD, because patients with these diseases have at least a 20% chance of experiencing a major coronary event within 10 years.

LDL goals in primary prevention depend on a person’s absolute risk for CHD. Individuals without CHD, diabetes or peripheral vascular disease who have 2 or more risk factors have a 10 to 20% of developing a major coronary event in the next 10 years. Their LDL treatment goal is <130 mg/dL. Persons with 1 or less risk factors have a 10 year coronary risk of <10% and need to reduce their LDL cholesterol below 160 mg/dL.

Many other lifestyle risk factors are known to be independent risk factors for CHD including obesity, physical inactivity, atherogenic diet, impaired glucose tolerance, lipoprotein (a), homocysteine, fibrinogen, and high sensitivity C-reactive protein. However, these factors were not used to set a lower LDL cholesterol goal of therapy.

Non-HDL-C offers several advantages over LDL cholesterol (LDL-C). A practical advantage is that measurement of non-HDL-C does not require collection of a fasting sample. Laboratories use the Friedewald equation to calculate LDL-C:

LDLC = TotalC ? HDLC ? Triglycerides/5

This formula increasingly underestimates the true LDL-C value as triglyceride levels increase. This is why the laboratory does not report LDL levels when triglycerides are above 400 mg/dL. But the calculation is affected to some extent at all triglyceride levels above 100 mg/dL. A falsely low LDL-C level may give a patient and their physician a false sense of reassurance.

Patients with diabetic dyslipidemia and related conditions, such as the metabolic syndrome, often have elevated triglycerides, low HDL, and relatively normal calculated LDL values. Sustained hypertriglyceridemia eventuates in elevated levels of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and small dense atherogenic LDL particles. Non-HDL cholesterol provides a single index of all these apolipoprotein B-containing lipoproteins, essentially acting as a surrogate for direct apolipoprotein B determinations. The bottom line is that the measurement of LDL-C alone is not an adequate measure of atherogenic risk in hypertriglyceridemic patients.

Stated otherwise, non-HDL cholesterol is a stronger predictor of coronary risk than LDL or triglycerides in certain patient populations, since it reflects the sum of serum cholesterol carried by all of the potentially atherogenic lipoproteins including LDL, VLDL, IDL, and other remnant lipoproteins. Moreover, since it is calculated from total cholesterol and HDL cholesterol, both of which are measured directly, it is not affected by the triglyceride level and does not require a fasting specimen.

A recent meta-analysis, which encompassed more than 300,000 patients and 10,000 major adverse events found that calculated LDL cholesterol is no more effective than using the non-HDL cholesterol level to predict the risk of vascular disease (Di Angel­antonio E, et al. JAMA. 2009;302:1993–2000).

NCEP ATP III guidelines recommend lowering non-HDL cholesterol as a secondary goal when triglycerides are > 200 mg/dl. As can be seen in the following table, the target goal for non-HDL is always 30 mg/dl higher than the LDL target for each NCEP Risk Category.

Risk Category

LDL Goal

Non-HDL Goal

CHD & CHD Risk Equivalent

<100 mg/dL

<130 mg/dL

Multiple (2+) Risk Factors

<130 mg/dL

<160 mg/dL

0 – 1 Risk Factor

<160 mg/dL

<190 mg/dL

The concept of good and bad cholesterol is still correct. However, non-HDL cholesterol is becoming the new bad cholesterol.

Low HDL cholesterol is a strong independent predictor of CHD and is considered to be a major risk factor. In ATP III, low HDL cholesterol is defined as a level below 40 mg/dL, which is a change from the level of <35 mg/dL specified in ATP II. Most commonly, low HDL cholesterol is combined with high triglycerides. This combination is most often associated with insulin resistance. ATP III does not specify a therapeutic goal for raising HDL; instead the emphasis is on reducing LDL cholesterol. Treatment of isolated low HDL is mostly reserved for persons with CHD or CHD risk equivalents.

Reference ranges are:



Total cholesterol


LDL cholesterol


HDL cholesterol




Specimen requirement is one SST tube of blood collected after an overnight fast

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