A

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)

Executive 

Summary 

High Blood Cholesterol Evaluation

Treatment

Detection

NATIONAL INSTITUTES OF HEALTH

NATIONAL HEART, LUNG, AND BLOOD INSTITUTE

National Cholesterol Education Program
B

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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) 

Executive 

Summary 

National Cholesterol Education Program

National Heart, Lung, and Blood Institute

National Institutes of Health

NIH Publication No. 01-3670

May 2001

Evaluation

Treatment

Detection

High Blood Cholesterol

i

Acknowledgements

National Cholesterol Education Program Expert Panel on Detection, Evaluation, and

Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)

Members:

Scott M. Grundy, M.D., Ph.D. – Chair of the Panel

Diane Becker, R.N., M.P.H., Sc.D. 

Luther T. Clark, M.D. 

Richard S. Cooper, M.D.

Margo A. Denke, M.D. 

Wm. James Howard, M.D.

Donald B. Hunninghake, M.D.

D. Roger Illingworth, M.D., Ph.D.

Russell V. Luepker, M.D., M.S. 

Patrick McBride, M.D., M.P.H. 

James M. McKenney, Pharm.D. 

Richard C. Pasternak, M.D., F.A.C.C. 

Neil J. Stone, M.D. 

Linda Van Horn, Ph.D, R.D.

Ex-officio Members:

H. Bryan Brewer, Jr., M.D. 

James I. Cleeman, M.D. – Executive Director of the Panel

Nancy D. Ernst, Ph.D., R.D. 

David Gordon, M.D., Ph.D. 

Daniel Levy, M.D. 

Basil Rifkind, M.D.

Jacques E. Rossouw, M.D. 

Peter Savage, M.D.

Consultants:

Steven M. Haffner, M.D. 

David G. Orloff, M.D. 

Michael A. Proschan, Ph.D. 

J. Sanford Schwartz, M.D. 

Christopher T. Sempos, Ph.D.

Staff:

Susan T. Shero, R.N., M.S.

Elaine Z. Murray
Executive Committee Liaison and Reviewers of the Full Report

Executive Committee Liaison to the Panel:

Stephen Havas, M.D., M.P.H., M.S.

Reviewers of the Full Report of ATP III:

Eugene Braunwald, M.D., W. Virgil Brown, M.D., Alan Chait, M.D., 

James E. Dalen, M.D., Valentin Fuster, M.D., Ph.D., Henry N. Ginsberg, M.D.,

Antonio M. Gotto, M.D., D.Phil., Ronald M. Krauss, M.D., 

John C. LaRosa, M.D., F.A.C.P., Thomas H. Lee, Jr., M.D.,

Linda Meyers, Ph.D., Michael Newman, M.D., Thomas Pearson, M.D., Ph.D.,

Daniel J. Rader, M.D., Frank M. Sacks, M.D., Ernst J. Schaefer, M.D.,

Sheldon G. Sheps, M.D., Lynn A. Smaha, M.D., Ph.D., Sidney C. Smith, Jr., M.D., 

Jeremiah Stamler, M.D., Daniel Steinberg, M.D., Ph.D., Nanette K. Wenger, M.D.

National Cholesterol Education Program Coordinating Committee

The Third Report of the National Cholesterol Education Expert Panel on

Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults was

approved by the National Cholesterol Education Program Coordinating Committee,

which comprises the following organizational representatives:

Member Organizations

National Heart, Lung, and Blood Institute 

Claude Lenfant, M.D. (Chair) 

James I. Cleeman, M.D. (Coordinator) 

American Academy of Family Physicians

Theodore G. Ganiats, M.D.

American Academy of Insurance Medicine 

Gary Graham, M.D.

American Academy of Pediatrics 

Ronald E. Kleinman, M.D.

American Association of Occupational Health Nurses 

Pamela Hixon, B.S.N., R.N., C.O.H.N-S

American College of Cardiology 

Richard C. Pasternak, M.D., F.A.C.C. 

American College of Chest Physicians 

Gerald T. Gau, M.D. 

American College of Nutrition 

Harry Preuss, M.D. 

American College of Obstetricians and Gynecologists 

Thomas C. Peng, M.D. 

American College of Occupational and Environmental Medicine 

Ruth Ann Jordan, M.D. 

American College of Preventive Medicine 

Lewis H. Kuller, M.D., Dr.P.H. 

American Diabetes Association, Inc. 

Alan J. Garber, M.D., Ph.D. 

ii
iii

American Dietetic Association 

Linda Van Horn, Ph.D., R.D.

American Heart Association 

Scott M. Grundy, M.D., Ph.D.

American Hospital Association 

Sandra Cornett, R.N., Ph.D. 

American Medical Association 

Yank D. Coble, Jr., M.D.

American Nurses Association

To be named

American Osteopathic Association 

Michael Clearfield, D.O.

American Pharmaceutical Association 

James M. McKenney, Pharm.D.

American Public Health Association 

Stephen Havas, M.D., M.P.H., M.S.

American Red Cross

Donald Vardell, M.S. 

Association of Black Cardiologists 

Karol Watson, M.D., Ph.D.

Association of State and Territorial Health Officials 

Joanne Mitten, M.H.E.

Citizens for Public Action on Blood Pressure and Cholesterol, Inc. 

Gerald J. Wilson, M.A., M.B.A.

National Black Nurses Association, Inc. 

Linda Burnes-Bolton, Dr.P.H., R.N., M.S.N., F.A.A.N. 

National Medical Association 

Luther T. Clark, M.D. 

Society for Nutrition Education 

Darlene Lansing, M.P.H., R.D. 

Society for Public Health Education 

Donald O. Fedder, Dr.P.H., M.P.H.

Associate Member Organization

American Association of Office Nurses 

Joyce Logan

Federal Agencies 

NHLBI Ad Hoc Committee on Minority Populations 

Yvonne L. Bronner, Sc.D., R.D., L.D.

Agency for Healthcare Research and Quality 

Francis D. Chesley, Jr., M.D.

Centers for Disease Control and Prevention 

Wayne Giles, M.D., M.P.H.

Coordinating Committee for the Community Demonstration Studies 

Thomas M. Lasater, Ph.D.
Department of Agriculture 

Alanna Moshfegh, M.S., R.D.

Department of Defense 

Col. Robert Dana Bradshaw, M.D., M.P.H.

Food and Drug Administration 

Elizabeth Yetley, Ph.D.

Health Resources and Services Administration 

Celia Hayes, M.P.H., R.D.

National Cancer Institute 

Carolyn Clifford, Ph.D.

National Center for Health Statistics 

Clifford Johnson, M.P.H.

Office of Disease Prevention and Health Promotion 

Elizabeth Castro, Ph.D.

Department of Veterans Affairs 

Pamela Steele, M.D.

iv
Introduction

Background

LDL Cholesterol: The Primary Target of Therapy

Risk Assessment: First Step in Risk Management

Method of risk assessment: counting major 

risk factors and estimating 10-year CHD risk 

Role of other risk factors in risk assessment

Metabolic syndrome 

The link between risk assessment and cost 

effectiveness 

Primary Prevention With LDL-Lowering Therapy

Secondary Prevention With LDL-Lowering Therapy

LDL-Lowering Therapy in Three Risk Categories

CHD and CHD risk equivalents 

Multiple (2+) risk factors and 10-year risk ≤20%

Zero to one risk factor 

Therapeutic Lifestyle Changes in LDL-Lowering Therapy

Drug Therapy to Achieve LDL-Cholesterol Goals

Secondary prevention: drug therapy for CHD and 

CHD risk equivalents 

LDL-lowering drug therapy for primary prevention 

Benefit Beyond LDL Lowering: The Metabolic

Syndrome as a Secondary Target of Therapy

Management of underlying causes of the metabolic 

syndrome 

Specific Treatment of Lipid and Non-Lipid Risk 

Factors 

Special Issues

Management of Specific Dyslipidemias 

Special Considerations for Different Population Groups 

Adherence to LDL-Lowering Therapy 

Appendix

Shared Features of ATP III and ATP II

Estimating 10-Year Risk for Men and Women

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Contents
vi
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) 

Executive Summary

Introduction

The Third Report of the Expert Panel on Detection, Evaluation, and

Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III,

or ATP III) constitutes the National Cholesterol Education Program’s

(NCEP’s) updated clinical guidelines for cholesterol testing and management. The full ATP III document is an evidence-based and extensively 

referenced report that provides the scientific rationale for the recommendations contained in the executive summary. ATP III builds on previous

ATP reports and expands the indications for intensive cholesterol-lowering

therapy in clinical practice. It should be noted that these guidelines are

intended to inform, not replace, the physician’s clinical judgment, which

must ultimately determine the appropriate treatment for each individual.

Background

The third ATP report updates the existing recommendations for clinical

management of high blood cholesterol. The NCEP periodically produces

ATP clinical updates as warranted by advances in the science of cholesterol

management. Each of the guideline reports—ATP I, II, and III—has a major

thrust. ATP I outlined a strategy for primary prevention of coronary heart

disease (CHD) in persons with high levels of low density lipoprotein (LDL)

cholesterol (≥160 mg/dL) or those with borderline-high LDL cholesterol

(130-159 mg/dL) and multiple (2+) risk factors. ATP II affirmed the importance of this approach and added a new feature: the intensive management

of LDL cholesterol in persons with established CHD. For CHD patients,

ATP II set a new, lower LDL cholesterol goal of ≤100 mg/dL. ATP III adds

a call for more intensive LDL-lowering therapy in certain groups of people,

in accord with recent clinical trial evidence, but its core is based on ATP I

and ATP II. Some of the important features shared with previous reports are

shown in Table A in the Appendix.

While ATP III maintains attention to intensive treatment of patients with

CHD, its major new feature is a focus on primary prevention in persons

with multiple risk factors. Many of these persons have a relatively high risk

for CHD and will benefit from more intensive LDL-lowering treatment than

recommended in ATP II. Table 1 shows the new features of ATP III.

1
LDL Cholesterol: The Primary Target of Therapy

Research from experimental animals, laboratory investigations, epidemiology,

and genetic forms of hypercholesterolemia indicate that elevated LDL cholesterol is a major cause of CHD. In addition, recent clinical trials robustly 

show that LDL-lowering therapy reduces risk for CHD. For these reasons, 

ATP III continues to identify elevated LDL cholesterol as the primary target of

cholesterol-lowering therapy. As a result, the primary goals of therapy and the

cutpoints for initiating treatment are stated in terms of LDL.

Risk Assessment: First Step in Risk Management

A basic principle of prevention is that the intensity of risk-reduction therapy

should be adjusted to a person’s absolute risk. Hence, the first step in 

selection of LDL-lowering therapy is to assess a person’s risk status. Risk

assessment requires measurement of LDL cholesterol as part of lipoprotein

analysis and identification of accompanying risk determinants. 

2

Focus on Multiple Risk Factors

■ Raises persons with diabetes without CHD, most of whom display multiple 

risk factors, to the risk level of CHD risk equivalent.

■ Uses Framingham projections of 10-year absolute CHD risk (i.e., the percent 

probability of having a CHD event in 10 years) to identify certain patients 

with multiple (2+) risk factors for more intensive treatment.

■ Identifies persons with multiple metabolic risk factors (metabolic syndrome) 

as candidates for intensified therapeutic lifestyle changes. 

Modifications of Lipid and Lipoprotein Classification

■ Identifies LDL cholesterol <100 mg/dL as optimal.

■ Raises categorical low HDL cholesterol from <35 mg/dL to <40 mg/dL 

because the latter is a better measure of a depressed HDL.

■ Lowers the triglyceride classification cutpoints to give more attention to 

moderate elevations.

Support for Implementation

■ Recommends a complete lipoprotein profile (total cholesterol, LDL 

cholesterol, HDL cholesterol, and triglycerides) as the preferred initial test, 

rather than screening for total cholesterol and HDL alone.

■ Encourages use of plant stanols/sterols and viscous (soluble) fiber as 

therapeutic dietary options to enhance lowering of LDL cholesterol.

■ Presents strategies for promoting adherence to therapeutic lifestyle changes 

and drug therapies.

■ Recommends treatment beyond LDL lowering for persons with triglycerides 

≥200 mg/dL.

Table 1. New Features of ATP III
In all adults aged 20 years or older, a fasting lipoprotein profile (total 

cholesterol, LDL cholesterol, high density lipoprotein (HDL) cholesterol,

and triglyceride) should be obtained once every 5 years. If the testing opportunity is nonfasting, only the values for total cholesterol and HDL cholesterol will be usable. In such a case, if total cholesterol is ≥200 mg/dL or

HDL is <40 mg/dL, a followup lipoprotein profile is needed for appropriate

management based on LDL. The relationship between LDL cholesterol 

levels and CHD risk is continuous over a broad range of LDL levels from

low to high. Therefore, ATP III adopts the classification of LDL cholesterol

levels shown in Table 2, which also shows the classification of total and

HDL cholesterol levels. 

Risk determinants in addition to LDL-cholesterol include the presence or

absence of CHD, other clinical forms of atherosclerotic disease, and the

major risk factors other than LDL (see Table 3). (LDL is not counted

among the risk factors in Table 3 because the purpose of counting those

risk factors is to modify the treatment of LDL.) Based on these other risk

determinants, ATP III identifies three categories of risk that modify the

goals and modalities of LDL-lowering therapy. Table 4 defines these 

categories and shows corresponding LDL-cholesterol goals. 

3

Table 2. ATP III Classification of LDL, Total, and HDL Cholesterol (mg/dL)

LDL Cholesterol 

<100 Optimal 

100-129 Near optimal/above optimal 

130-159 Borderline high 

160-189 High 

≥190 Very high 

Total Cholesterol 

<200 Desirable 

200-239 Borderline high 

≥240 High 

HDL Cholesterol 

<40 Low 

≥60 High 

Table 3. Major Risk Factors (Exclusive of LDL Cholesterol) That Modify LDL Goals*

■ Cigarette smoking

■ Hypertension (BP ≥140/90 mmHg or on antihypertensive medication)

■ Low HDL cholesterol (<40 mg/dL)†

■ Family history of premature CHD (CHD in male first degree relative <55 

years; CHD in female first degree relative <65 years)

■ Age (men ≥45 years; women ≥55 years)*

* In ATP III, diabetes is regarded as a CHD risk equivalent.

† HDL cholesterol ≥60 mg/dL counts as a “negative” risk factor; its presence removes one risk factor from the 

total count.
The category of highest risk consists of CHD and CHD risk equivalents.

The latter carry a risk for major coronary events equal to that of established

CHD, i.e., >20% per 10 years (i.e., more than 20 of 100 such individuals

will develop CHD or have a recurrent CHD event within 10 years). CHD

risk equivalents comprise: 

■ Other clinical forms of atherosclerotic disease (peripheral arterial disease,

abdominal aortic aneurysm, and symptomatic carotid artery disease);

■ Diabetes;

■ Multiple risk factors that confer a 10-year risk for CHD >20%.

Diabetes counts as a CHD risk equivalent because it confers a high risk of

new CHD within 10 years, in part because of its frequent association with

multiple risk factors. Furthermore, because persons with diabetes who 

experience a myocardial infarction have an unusually high death rate either

immediately or in the long term, a more intensive prevention strategy is

warranted. Persons with CHD or CHD risk equivalents have the lowest

LDL cholesterol goal (<100 mg/dL). 

The second category consists of persons with multiple (2+) risk factors in

whom 10-year risk for CHD is ≤20%. Risk is estimated from Framingham

risk scores (see Appendix). The major risk factors, exclusive of elevated

LDL cholesterol, are used to define the presence of multiple risk factors that

modify the goals and cutpoints for LDL-lowering treatment, and these are

listed in Table 3. The LDL cholesterol goal for persons with multiple (2+)

risk factors is <130 mg/dL.

The third category consists of persons having 0-1 risk factor; with few

exceptions, persons in this category have a 10-year risk <10%. Their LDL

cholesterol goal is <160 mg/dL.

Method of risk assessment: counting major risk factors and estimating 10-year

CHD risk

Risk status in persons without clinically manifest CHD or other clinical

forms of atherosclerotic disease is determined by a 2-step procedure. 

4

Table 4. Three Categories of Risk that Modify LDL Cholesterol Goals

Risk Category LDL Goal (mg/dL)

CHD and CHD risk equivalents <100

Multiple (2+) risk factors* <130

Zero to one risk factor <160

* Risk factors that modify the LDL goal are listed in Table 3
First, the number of risk factors is counted (Table 3). Second, for persons

with multiple (2+) risk factors, 10-year risk assessment is carried out 

with Framingham scoring (see Appendix) to identify individuals whose

short-term (10-year) risk warrants consideration of intensive treatment.

Estimation of the 10-year CHD risk adds a step to risk assessment beyond

risk factor counting, but this step is warranted because it allows better 

targeting of intensive treatment to people who will benefit from it. When

0-1 risk factor is present, Framingham scoring is not necessary because 

10-year risk rarely reaches levels for intensive intervention; a very high

LDL level in such a person may nevertheless warrant consideration of drug

therapy to reduce long-term risk. Risk factors used in Framingham scoring

include age, total cholesterol, HDL cholesterol, blood pressure, and 

cigarette smoking. Total cholesterol is used for 10-year risk assessment

because of a larger and more robust Framingham database for total than

for LDL cholesterol, but LDL cholesterol is the primary target of therapy.

Framingham scoring divides persons with multiple risk factors into those

with 10-year risk for CHD of >20%, 10-20%, and <10%. It should be

noted that this 2-step sequence can be reversed with essentially the same

results.* Initial risk assessment in ATP III uses the major risk factors to

define the core risk status. Only after the core risk status has been 

determined should any other risk modifiers be taken into consideration for

adjusting the therapeutic approach.

Role of other risk factors in risk assessment

ATP III recognizes that risk for CHD is influenced by other factors not

included among the major, independent risk factors (Table 3). Among these

are life-habit risk factors and emerging risk factors. The former include 

obesity, physical inactivity, and atherogenic diet; the latter consist of

lipoprotein (a), homocysteine, prothrombotic and proinflammatory factors,

impaired fasting glucose, and evidence of subclinical atherosclerotic disease.

The life-habit risk factors are direct targets for clinical intervention, but are

not used to set a lower LDL cholesterol goal of therapy. The emerging risk 

factors do not categorically modify LDL cholesterol goals; however, they

appear to contribute to CHD risk to varying degrees and can have utility in

selected persons to guide intensity of risk-reduction therapy. Their presence

can modulate clinical judgment when making therapeutic decisions. 

Metabolic syndrome

Many persons have a constellation of major risk factors, life-habit risk 

factors, and emerging risk factors that constitute a condition called the

5

*If Framingham scoring is carried out before risk factor counting, persons with <10 percent risk are then divided into

those with 2+ risk factors and 0-1 risk factor by risk factor counting to determine the appropriate LDL goal (see Table 4).
metabolic syndrome. Factors characteristic of the metabolic syndrome are

abdominal obesity, atherogenic dyslipidemia (elevated triglyceride, small

LDL particles, low HDL cholesterol), raised blood pressure, insulin 

resistance (with or without glucose intolerance), and prothrombotic and

proinflammatory states. ATP III recognizes the metabolic syndrome as a 

secondary target of risk-reduction therapy, after the primary target—LDL 

cholesterol. Diagnosis and treatment of the metabolic syndrome is described

beginning on page 15 under “Benefit Beyond LDL Lowering: The

Metabolic Syndrome as a Secondary Target of Therapy.”

The link between risk assessment and cost effectiveness

In ATP III, a primary aim is to match intensity of LDL-lowering therapy

with absolute risk. Everyone with elevated LDL cholesterol is treated with

lifestyle changes that are effective in lowering LDL levels. Persons at 

relatively high risk are also candidates for drug treatment, which is very

effective but entails significant additional expense. The cutpoints for drug

treatment are based primarily on risk-benefit considerations: those at higher

risk are likely to get greater benefit. However, cutpoints for recommended

management based on therapeutic efficacy are checked against currently

accepted standards for cost effectiveness. Lifestyle changes are the most

cost-effective means to reduce risk for CHD. Even so, to achieve maximal

benefit, many persons will require LDL-lowering drugs. Drug therapy is the

major expense of LDL-lowering therapy, and it dominates cost-effectiveness

analysis. However, the costs of LDL-lowering drugs are currently in flux

and appear to be declining. This report recognizes that as drug prices

decline it will be possible to extend drug use to lower risk persons and still

be cost effective. In addition, ATP III recognizes that some persons with

high long-term risk are candidates for LDL-lowering drugs even though use

of drugs may not be cost effective by current standards.

Primary Prevention With LDL-Lowering Therapy

Primary prevention of CHD offers the greatest opportunity for reducing

the burden of CHD in the United States. The clinical approach to 

primary prevention is founded on the public health approach that calls 

for lifestyle changes, including: 1) reduced intakes of saturated fat and

cholesterol, 2) increased physical activity, and 3) weight control, to lower

population cholesterol levels and reduce CHD risk, but the clinical

approach intensifies preventive strategies for higher risk persons. One aim

of primary prevention is to reduce long-term risk (>10 years) as well as

short-term risk (≤10 years). LDL goals in primary prevention depend on

a person’s absolute risk for CHD (i.e., the probability of having a CHD

6
event in the short term or the long term)—the higher the risk, the lower

the goal. Therapeutic lifestyle changes are the foundation of clinical 

primary prevention. Nonetheless, some persons at higher risk because of

high or very high LDL cholesterol levels or because of multiple risk 

factors are candidates for LDL-lowering drugs. Recent primary prevention

trials show that LDL-lowering drugs reduce risk for major coronary

events and coronary death even in the short term. 

Secondary Prevention With LDL-Lowering Therapy

Recent clinical trials demonstrate that LDL-lowering therapy reduces total

mortality, coronary mortality, major coronary events, coronary artery 

procedures, and stroke in persons with established CHD. As shown in

Table 2, an LDL cholesterol level of <100 mg/dL is optimal; therefore, 

ATP III specifies an LDL cholesterol <100 mg/dL as the goal of therapy in 

secondary prevention. This goal is supported by clinical trials with both

clinical and angiographic endpoints and by prospective epidemiological

studies. The same goal should apply for persons with CHD risk equivalents. When persons are hospitalized for acute coronary syndromes or

coronary procedures, lipid measures should be taken on admission or 

within 24 hours. These values can guide the physician on initiation of

LDL-lowering therapy before or at discharge. Adjustment of therapy 

may be needed after 12 weeks. 

LDL-Lowering Therapy in Three Risk Categories

The two major modalities of LDL-lowering therapy are therapeutic lifestyle

changes (TLC) and drug therapy. Both are described in more detail later.

The TLC Diet stresses reductions in saturated fat and cholesterol intakes.

When the metabolic syndrome or its associated lipid risk factors (elevated

7

Any person with elevated LDL cholesterol or other form of hyperlipidemia should

undergo clinical or laboratory assessment to rule out secondary dyslipidemia before

initiation of lipid-lowering therapy. Causes of secondary dyslipidemia include:

• Diabetes 

• Hypothyroidism 

• Obstructive liver disease 

• Chronic renal failure 

• Drugs that increase LDL cholesterol and decrease HDL cholesterol 

(progestins, anabolic steroids, and corticosteroids). 

Once secondary causes have been excluded or, if appropriate, treated, the goals for LDL-lowering therapy in

primary prevention are established according to a person’s risk category (Table 4).
triglyceride or low HDL cholesterol) are present, TLC also stresses weight

reduction and increased physical activity. Table 5 defines LDL cholesterol

goals and cutpoints for initiation of TLC and for drug consideration for

persons with three categories of risk: CHD and CHD risk equivalents; multiple (2+) risk factors (10-year risk 10-20% and <10%); and 0-1 risk factor.

CHD and CHD risk equivalents

For persons with CHD and CHD risk equivalents, LDL-lowering therapy

greatly reduces risk for major coronary events and stroke and yields highly

favorable cost-effectiveness ratios. The cut-points for initiating lifestyle and

drug therapies are shown in Table 5. 

■ If baseline LDL cholesterol is ≥130 mg/dL, intensive lifestyle therapy and

maximal control of other risk factors should be started. Moreover, for 

most patients, an LDL-lowering drug will be required to achieve an LDL 

cholesterol <100 mg/dL; thus an LDL cholesterol lowering drug can be 

started simultaneously with TLC to attain the goal of therapy.

■ If LDL cholesterol levels are 100-129 mg/dL, either at baseline or on 

LDL-lowering therapy, several therapeutic approaches are available: 

8

Table 5: LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle 

Changes (TLC) and Drug Therapy in Different Risk Categories.

Risk Category LDL Goal LDL Level LDL Level 

at Which to Initiate at Which to

Therapeutic Lifestyle Consider Drug 

Changes (TLC) Therapy

CHD or CHD Risk <100 mg/dL ≥100 mg/dL ≥130 mg/dL

Equivalents (100-129 mg/dL:

(10-year risk >20%) drug optional)* 

10-year risk 10-20%:

≥130 mg/dL

10-year risk <10%:

≥160 mg/dL 

0-1 Risk Factor† <160 mg/dL ≥160 mg/dL ≥190 mg/dL

(160-189 mg/dL: 

LDL-lowering drug 

optional) 

* Some authorities recommend use of LDL-lowering drugs in this category if an LDL cholesterol <100 mg/dL 

cannot be achieved by therapeutic lifestyle changes. Others prefer use of drugs that primarily modify triglycerides and HDL, e.g., nicotinic acid or fibrate. Clinical judgment also may call for deferring drug therapy 

in this subcategory.

† Almost all people with 0-1 risk factor have a 10-year risk <10%, thus 10-year risk assessment in people with

0-1 risk factor is not necessary.

2+ Risk Factors

(10-year risk ≤20%) 

<130 mg/dL ≥130 mg/dL
• Initiate or intensify lifestyle and/or drug therapies specifically to 

lower LDL.

• Emphasize weight reduction and increased physical activity in persons 

with the metabolic syndrome.

• Delay use or intensification of LDL-lowering therapies and institute 

treatment of other lipid or nonlipid risk factors; consider use of other 

lipid-modifying drugs (e.g., nicotinic acid or fibric acid) if the patient 

has elevated triglyceride or low HDL cholesterol. 

■ If baseline LDL cholesterol is <100 mg/dL, further LDL-lowering 

therapy is not required. Patients should nonetheless be advised to follow 

the TLC Diet on their own to help keep the LDL level optimal. Several 

clinical trials are currently underway to assess benefit of lowering LDL 

cholesterol to well below 100 mg/dL. At present, emphasis should be 

placed on controlling other lipid and nonlipid risk factors and on 

treatment of the metabolic syndrome, if present.

Multiple (2+) risk factors and 10-year risk ≤20%

For persons with multiple (2+) risk factors and 10-year risk ≤ 20%, intensity of therapy is adjusted according to 10-year risk and LDL cholesterol

level. The treatment approach for each category is summarized in Table 5. 

■ Multiple (2+) risk factors and a 10-year risk of 10-20%. In this category, 

the goal for LDL cholesterol is <130 mg/dL. The therapeutic aim is to 

reduce short-term risk as well as long-term risk for CHD. If baseline 

LDL cholesterol is ≥130 mg/dL, TLC is initiated and maintained for 

3 months. If LDL remains ≥130 mg/dL after 3 months of TLC, 

consideration can be given to starting an LDL-lowering drug to achieve 

the LDL goal of <130 mg/dL. Use of LDL-lowering drugs at this risk 

level reduces CHD risk and is cost-effective. If the LDL falls to less than 

130 mg/dL on TLC alone, TLC can be continued without adding drugs. 

In older persons (≥65 years), clinical judgment is required for how

intensively to apply these guidelines; a variety of factors, including concomitant illnesses, general health status, and social issues may influence 

treatment decisions and may suggest a more conservative approach.

■ Multiple (2+) risk factors and a 10-year risk of <10%. In this 

category, the goal for LDL cholesterol also is <130 mg/dL. The 

therapeutic aim, however, is primarily to reduce longer-term risk. If 

baseline LDL cholesterol is ≥130 mg/dL, the TLC Diet is initiated to 

reduce LDL cholesterol. If LDL is <160 mg/dL on TLC alone, it should 

be continued. LDL-lowering drugs generally are not recommended 

because the patient is not at high short-term risk. On the other hand, if 

9
LDL cholesterol is ≥160 mg/dL, drug therapy can be considered to 

achieve an LDL cholesterol <130 mg/dL; the primary aim is to reduce 

long-term risk. Cost-effectiveness is marginal, but drug therapy can be 

justified to slow development of coronary atherosclerosis and to reduce 

long-term risk for CHD. 

Zero to one risk factor

Most persons with 0-1 risk factor have a 10-year risk <10%. They are 

managed according to Table 5. The goal for LDL cholesterol in this risk

category is <160 mg/dL. The primary aim of therapy is to reduce long-term

risk. First-line therapy is TLC. If after 3 months of TLC the LDL cholesterol is <160 mg/dL, TLC is continued. However, if LDL cholesterol is 

160-189 mg/dL after an adequate trial of TLC, drug therapy is optional

depending on clinical judgment. Factors favoring use of drugs include:

■ A severe single risk factor (heavy cigarette smoking, poorly controlled 

hypertension, strong family history of premature CHD, or very low 

HDL cholesterol);

■ Multiple life-habit risk factors and emerging risk factors (if measured);

■ 10-year risk approaching 10% (if measured; see Appendix). 

If LDL cholesterol is ≥190 mg/dL despite TLC, drug therapy should be 

considered to achieve the LDL goal of <160 mg/dL. 

The purpose of using LDL-lowering drugs in persons with 0-1 risk factor

and elevated LDL cholesterol (≥160 mg/dL) is to slow the development of

coronary atherosclerosis, which will reduce long-term risk. This aim may

conflict with cost-effectiveness considerations; thus, clinical judgment is

required in selection of persons for drug therapy, although a strong case can

be made for using drugs when LDL cholesterol is ≥190 mg/dL after TLC. 

For persons whose LDL cholesterol levels are already below goal levels

upon first encounter, instructions for appropriate changes in life habits,

periodic followup, and control of other risk factors are needed. 

Therapeutic Lifestyle Changes in LDL-Lowering Therapy

ATP III recommends a multifaceted lifestyle approach to reduce risk for

CHD. This approach is designated therapeutic lifestyle changes (TLC).

Its essential features are:

10
■ Reduced intakes of saturated fats (<7% of total calories) and cholesterol 

(<200 mg per day) (see Table 6 for overall composition of the TLC Diet)

■ Therapeutic options for enhancing LDL lowering such as plant 

stanols/sterols (2 g/day) and increased viscous (soluble) fiber (10-25 g/day)

■ Weight reduction 

■ Increased physical activity

A model of steps in TLC is shown in Figure 1. To initiate TLC, intakes of

saturated fats and cholesterol are reduced first to lower LDL cholesterol.

To improve overall health, ATP III’s TLC Diet generally contains the 

recommendations embodied in the Dietary Guidelines for Americans 2000.

One exception is that total fat is allowed to range from 25-35% of total

calories provided saturated fats and trans fatty acids are kept low. A higher

intake of total fat, mostly in the form of unsaturated fat, can help to reduce

triglycerides and raise HDL cholesterol in persons with the metabolic 

syndrome. In accordance with the Dietary Guidelines, moderate physical

activity is encouraged. After 6 weeks, the LDL response is determined; if the

LDL cholesterol goal has not been achieved, other therapeutic options for

LDL lowering such as plant stanol/sterols and viscous fiber can be added. 

After maximum reduction of LDL cholesterol with dietary therapy, 

emphasis shifts to management of the metabolic syndrome and associated

lipid risk factors. The majority of persons with these latter abnormalities 

are overweight or obese and sedentary. Weight reduction therapy for overweight or obese patients will enhance LDL lowering and will provide other

health benefits including modifying other lipid and nonlipid risk factors.

11

Table 6. Nutrient Composition of the TLC Diet

Nutrient Recommended Intake 

Saturated fat* Less than 7% of total calories 

Polyunsaturated fat Up to 10% of total calories 

Monounsaturated fat Up to 20% of total calories 

Total fat 25-35% of total calories 

Carbohydrate† 50-60% of total calories 

Fiber 20-30 g/day 

Protein Approximately 15% of total calories 

Cholesterol Less than 200 mg/day 

Total calories (energy)‡ Balance energy intake and expenditure to 

maintain desirable body weight/prevent 

weight gain

* Trans fatty acids are another LDL-raising fat that should be kept at a low intake. 

† Carbohydrate should be derived predominantly from foods rich in complex carbohydrates including grains, 

especially whole grains, fruits, and vegetables. 

‡ Daily energy expenditure should include at least moderate physical activity (contributing approximately 

200 Kcal per day).
Assistance in the management of overweight and obese persons is provided

by the Clinical Guidelines on the Identification, Evaluation, and Treatment

of Overweight and Obesity in Adults from the NHLBI Obesity Education

Initiative (1998). Additional risk reduction can be achieved by simultaneously increasing physical activity.

At all stages of dietary therapy, physicians are encouraged to refer patients

to registered dietitians or other qualified nutritionists for medical nutrition

therapy, which is the term for the nutritional intervention and guidance 

provided by a nutrition professional.

Drug Therapy to Achieve LDL Cholesterol Goals

A portion of the population whose short-term or long-term risk for CHD is

high will require LDL-lowering drugs in addition to TLC to reach the designated goal for LDL cholesterol (see Table 5). When drugs are prescribed,

attention to TLC should always be maintained and reinforced. Currently

available drugs that affect lipoprotein metabolism and their major characteristics are listed in Table 7.

Some cholesterol-lowering agents are currently available over-the-counter

(OTC) (e.g., nicotinic acid), and manufacturers of several classes of LDLlowering drugs (e.g., statins, bile acid sequestrants) have applied to the

12

Figure 1. A Model of Steps in Therapeutic Lifestyle Changes (TLC) 

Visit 1

Begin Lifestyle 

Therapies

Visit 2

Evaluate LDL

response

If LDL goal not

achieved, intensify

LDL-lowering Tx

Visit 3

Evaluate LDL

response

If LDL goal not

achieved, consider

adding drug Tx

Visit N

Monitor

Adherence to

TLC

■ Emphasize 

reduction in 

saturated fat and 

cholesterol

■ Encourage 

moderate physical 

activity

■ Consider referral 

to dietitian

■ Reinforce 

reduction in 

saturated fat and 

cholesterol

■ Consider adding 

plant stanols/sterols

■ Increase fiber intake

■ Consider referral 

to dietitian

■ Initiate Tx for

Metabolic 

Syndrome

■ Intensify weight 

management and

physical activity

■ Consider referral to dietitian

6 wks 6 wks Q 4-6 mos
13

Table 7. Drugs Affecting Lipoprotein Metabolism

Drug Class, Agents Lipid/Lipoprotein Side Effects Contraindications Clinical Trial 

and Daily Doses Effects Results

* Lovastatin (20-80 mg), pravastatin (20-40 mg), simvastatin (20-80 mg), fluvastatin (20-80 mg), atorvastatin (10-80 mg), 

cerivastatin (0.4-0.8 mg).

† Cyclosporine, macrolide antibiotics, various antifungal agents and cytochrome P-450 inhibitors (fibrates and niacin should be 

used with appropriate caution).

‡ Cholestyramine (4-16 g), colestipol (5-20 g), colesevelam (2.6-3.8 g).

¥ Immediate release (crystalline) nicotinic acid (1.5-3 g), extended release nicotinic acid (Niaspan ®) (1-2 g), sustained release 

nicotinic acid (1-2 g). 

§ Gemfibrozil (600 mg BID), fenofibrate (200 mg), clofibrate (1000 mg BID).

HMG CoA reductase

inhibitors (statins)* 

Bile acid

Sequestrants‡

Nicotinic acid¥

Fibric acids§

LDL ↓18-55%

HDL ↑5-15%

TG ↓7-30% 

LDL ↓15-30%

HDL ↑3-5%

TG No 

change or 

increase 

LDL ↓ 5-25%

HDL ↑15-35%

TG ↓20-50% 

LDL ↓5-20%

(may be increased in 

patients with high TG)

HDL ↑10-20%

TG ↓20-50% 

Myopathy

Increased liver 

enzymes 

Gastrointestinal

distress

Constipation

Decreased 

absorption of 

other drugs 

Flushing

Hyperglycemia

Hyperuricemia

(or gout)

Upper GI 

distress

Hepatotoxicity 

Dyspepsia

Gallstones

Myopathy

Unexplained 

non-CHD 

deaths in 

WHO study 

Absolute: 

• Active or chronic liver disease

Relative:

• Concomitant 

use of certain 

drugs†

Absolute:

• dysbetalipoproteinemia

• TG >400 mg/dL

Relative:

• TG >200 mg/dL 

Absolute:

• Chronic liver 

disease

• Severe gout

Relative:

• Diabetes

• Hyperuricemia

• Peptic ulcer 

disease 

Absolute:

• Severe renal 

disease

• Severe hepatic 

disease 

Reduced major 

coronary 

events, CHD 

deaths, need 

for coronary 

procedures, 

stroke, and 

total mortality 

Reduced major 

coronary events 

and CHD 

deaths 

Reduced major 

coronary 

events, and 

possibly total 

mortality 

Reduced major 

coronary events
Food and Drug Administration (FDA) to allow these agents to become

OTC medications. At the time of publication of ATP III, the FDA has not

granted permission for OTC status for statins or bile acid sequestrants. If an

OTC cholesterol-lowering drug is or becomes available, patients should

continue to consult with their physicians about whether to initiate drug

treatment, about setting the goals of therapy, and about monitoring for

therapeutic responses and side effects.

Secondary prevention: drug therapy for CHD and CHD risk equivalents

For persons with CHD and CHD risk equivalents, the goal is to attain an

LDL cholesterol level <100 mg/dL. The cutpoints for initiating lifestyle and

drug therapies are shown in Table 5, and the approach to treatment is 

discussed immediately after Table 5. Most CHD patients will need LDLlowering drug therapy. Other lipid risk factors may also warrant consideration of drug treatment. Whether or not lipid-modifying drugs are used, 

nonlipid risk factors require attention and favorable modification. 

In persons admitted to the hospital for a major coronary event, LDL 

cholesterol should be measured on admission or within 24 hours. This

value can be used for treatment decisions. In general, persons hospitalized

for a coronary event or procedure should be discharged on drug therapy if

the LDL cholesterol is ≥130 mg/dL. If the LDL is 100–129 mg/dL, clinical

judgment should be used in deciding whether to initiate drug treatment at

discharge, recognizing that LDL cholesterol levels begin to decline in the

first few hours after an event and are significantly decreased by 24-48 hours

and may remain low for many weeks. Thus, the initial LDL cholesterol level

obtained in the hospital may be substantially lower than is usual for the

patient. Some authorities hold drug therapy should be initiated whenever 

a patient hospitalized for a CHD-related illness is found to have an LDL

cholesterol >100 mg/dL. Initiation of drug therapy at the time of hospital

discharge has two advantages. First, at that time patients are particularly

motivated to undertake and adhere to risk-lowering interventions; and 

second, failure to initiate indicated therapy early is one of the causes of a

large “treatment gap,” because outpatient followup is often less consistent

and more fragmented. 

LDL-lowering drug therapy for primary prevention

Table 5 shows the cutpoints for considering drug treatment in primary prevention. The general approach to management of drug therapy for primary

prevention is outlined in Figure 2.

14
When drug therapy for primary prevention is a consideration, the third visit

of dietary therapy (see Figure 1) will typically be the visit to initiate drug

treatment. Even if drug treatment is started, TLC should be continued. As

with TLC, the first priority of drug therapy is to achieve the goal for LDL

cholesterol. For this reason, an LDL-lowering drug should be started. The

usual drug will be a statin, but alternatives are a bile acid sequestrant or

nicotinic acid. In most cases, the statin should be started at a moderate

dose. In many patients, the LDL cholesterol goal will be achieved, and higher doses will not be necessary. The patient’s response should be checked

about 6 weeks after starting drug therapy. If the goal of therapy has been

achieved, the current dose can be maintained. However, if the goal has not

been achieved, LDL-lowering therapy can be intensified, either by increasing

the dose of statin or by combining a statin with a bile acid sequestrant or

nicotinic acid. 

After 12 weeks of drug therapy, the response to therapy should again be

assessed. If the LDL cholesterol goal is still not achieved, consideration can

be given to further intensification of drug therapy. If the LDL goal cannot

be attained by standard lipid-lowering therapy, consideration should be

given to seeking consultation from a lipid specialist. Once the goal for LDL

cholesterol has been attained, attention can turn to other lipid risk factors

and nonlipid factors. Thereafter, patients can be monitored for response to

therapy every 4 to 6 months, or more often if considered necessary. 

Benefit Beyond LDL Lowering: The Metabolic Syndrome as a Secondary Target

of Therapy

Evidence is accumulating that risk for CHD can be reduced beyond 

LDL-lowering therapy by modification of other risk factors. One potential 

15

Figure 2. Progression of Drug Therapy in Primary Prevention

Initiate 

LDL-lowering

drug therapy

If LDL goal not

achieved, intensify

LDL-lowering 

therapy

If LDL goal not

achieved, intensify

drug therapy or

refer to a lipid 

specialist

Monitor

response and

adherence to

therapy

■ Start statin or 

bile acid

sequestrant or

nicotinic acid

■ Consider higher 

dose of statin or 

add bile acid 

sequestrant or 

nicotinic acid

■ If LDL goal 

achieved, treat 

other lipid risk 

factors

6 wks 6 wks Q 4-6 mos
secondary target of therapy is the metabolic syndrome, which represents a

constellation of lipid and nonlipid risk factors of metabolic origin. This 

syndrome is closely linked to a generalized metabolic disorder called insulin

resistance in which the normal actions of insulin are impaired. Excess body

fat (particularly abdominal obesity) and physical inactivity promote the

development of insulin resistance, but some individuals also are genetically

predisposed to insulin resistance. 

The risk factors of the metabolic syndrome are highly concordant; in 

aggregate they enhance risk for CHD at any given LDL cholesterol level.

For purposes of ATP III, the diagnosis of the metabolic syndrome is made

when three or more of the risk determinants shown in Table 8 are present.

These determinants include a combination of categorical and borderline risk

factors that can be readily measured in clinical practice.

Management of the metabolic syndrome has a two-fold objective: (1) to

reduce underlying causes (i.e., obesity and physical inactivity), and (2) to

treat associated nonlipid and lipid risk factors. 

Management of underlying causes of the metabolic syndrome

First-line therapies for all lipid and nonlipid risk factors associated with the

metabolic syndrome are weight reduction and increased physical activity,

which will effectively reduce all of these risk factors. Therefore, after 

16

Table 8. Clinical Identification of the Metabolic Syndrome

Risk Factor Defining Level 

Abdominal Obesity* Waist Circumference†

Men >102 cm (>40 in)

Women >88 cm (>35 in) 

Triglycerides ≥150 mg/dL 

HDL cholesterol

Men <40 mg/dL

Women <50 mg/dL 

Blood pressure ≥130/≥85 mmHg 

Fasting glucose ≥110 mg/dL 

* Overweight and obesity are associated with insulin resistance and the metabolic syndrome. However, the 

presence of abdominal obesity is more highly correlated with the metabolic risk factors than is an elevated 

body mass index (BMI). Therefore, the simple measure of waist circumference is recommended to identify the 

body weight component of the metabolic syndrome. 

† Some male patients can develop multiple metabolic risk factors when the waist circumference is only 

marginally increased, e.g., 94-102 cm (37-39 in). Such patients may have a strong genetic contribution to 

insulin resistance. They should benefit from changes in life habits, similarly to men with categorical increases 

in waist circumference.
appropriate control of LDL cholesterol, TLC should stress weight reduction

and physical activity if the metabolic syndrome is present. 

Weight control. In ATP III overweight and obesity are recognized as major,

underlying risk factors for CHD and identified as direct targets of intervention. Weight reduction will enhance LDL lowering and reduce all of the risk

factors of the metabolic syndrome. The recommended approaches for

reducing overweight and obesity are contained in the clinical guidelines of

the NHLBI Obesity Education Initiative. 

Physical activity. Physical inactivity is likewise a major, underlying risk 

factor for CHD. It augments the lipid and nonlipid risk factors of the metabolic syndrome. It further may enhance risk by impairing cardiovascular fitness and coronary blood flow. Regular physical activity reduces very low

density lipoprotein (VLDL) levels, raises HDL cholesterol, and in some 

persons, lowers LDL levels. It also can lower blood pressure, reduce insulin

resistance, and favorably influence cardiovascular function. Thus, ATP III

recommends that regular physical activity become a routine component 

in management of high serum cholesterol. The evidence base for this 

recommendation is contained in the U.S. Surgeon General’s Report on

Physical Activity.

Specific Treatment of Lipid and Non-Lipid Risk Factors

Beyond the underlying risk factors, therapies directed against the lipid and

nonlipid risk factors of the metabolic syndrome will reduce CHD risk.

These include treatment of hypertension, use of aspirin in patients with

CHD to reduce the prothrombotic state (guidelines for aspirin use in 

primary prevention have not been firmly established), and treatment of 

elevated triglycerides and low HDL cholesterol as discussed below under

Management of Specific Dyslipidemias.

Special Issues

Management of Specific Dyslipidemias

Very high LDL cholesterol (≥190 mg/dL). Persons with very high LDL 

cholesterol usually have genetic forms of hypercholesterolemia: monogenic

familial hypercholesterolemia, familial defective apolipoprotein B, and 

polygenic hypercholesterolemia. Early detection of these disorders through

cholesterol testing in young adults is needed to prevent premature CHD.

Family testing is important to identify similarly affected relatives. These 

17
disorders often require combined drug therapy (statin + bile acid sequestrant) to achieve the goals of LDL-lowering therapy.

Elevated serum triglycerides. Recent meta-analyses of prospective studies

indicate that elevated triglycerides are also an independent risk factor for

CHD. Factors contributing to elevated (higher than normal) triglycerides in

the general population include: obesity and overweight, physical inactivity,

cigarette smoking, excess alcohol intake, high carbohydrate diets (>60% of

energy intake), several diseases (e.g., type 2 diabetes, chronic renal failure,

nephrotic syndrome), certain drugs (e.g., corticosteroids, estrogens,

retinoids, higher doses of beta-adrenergic blocking agents), and genetic 

disorders (familial combined hyperlipidemia, familial hypertriglyceridemia,

and familial dysbetalipoproteinemia). 

In clinical practice, elevated serum triglycerides are most often observed in

persons with the metabolic syndrome, although secondary or genetic factors

can heighten triglyceride levels. ATP III adopts the following classification

of serum triglycerides: 

■ Normal triglycerides: <150 mg/dL 

■ Borderline-high triglycerides: 150-199 mg/dL 

■ High triglycerides: 200-499 mg/dL 

■ Very high triglycerides: ≥500 mg/dL

The finding that elevated triglycerides are an independent CHD risk factor

suggests that some triglyceride-rich lipoproteins are atherogenic. The latter

are partially degraded VLDL, commonly called remnant lipoproteins. In

clinical practice, VLDL cholesterol is the most readily available measure of

atherogenic remnant lipoproteins. Thus, VLDL cholesterol can be a target

of cholesterol-lowering therapy. ATP III identifies the sum of LDL+VLDL

cholesterol [termed non-HDL cholesterol (total cholesterol minus HDL 

cholesterol)] as a secondary target of therapy in persons with high 

triglycerides (≥200 mg/dL). The goal for non-HDL cholesterol in persons

with high serum triglycerides can be set at 30 mg/dL higher than that for

LDL cholesterol (Table 9) on the premise that a VLDL cholesterol level ≤30

mg/dL is normal. 

The treatment strategy for elevated triglycerides depends on the causes of

the elevation and its severity. For all persons with elevated triglycerides, the

primary aim of therapy is to achieve the target goal for LDL cholesterol.

When triglycerides are borderline high (150-199 mg/dL), emphasis should

also be placed on weight reduction and increased physical activity. For high

triglycerides (200-499 mg/dL), non-HDL cholesterol becomes a secondary

18
target of therapy. Aside from weight reduction and increased physical activity, drug therapy can be considered in high-risk persons to achieve the nonHDL cholesterol goal. There are two approaches to drug therapy. First, the

non-HDL cholesterol goal can be achieved by intensifying therapy with an

LDL-lowering drug; or second, nicotinic acid or fibrate can be added, if

used with appropriate caution, to achieve the non-HDL cholesterol goal by

further lowering of VLDL cholesterol. In rare cases in which triglycerides

are very high (≥500 mg/dL), the initial aim of therapy is to prevent acute

pancreatitis through triglyceride lowering. This approach requires very low

fat diets (≤15% of calorie intake), weight reduction, increased physical

activity, and usually a triglyceride-lowering drug (fibrate or nicotinic acid).

Only after triglyceride levels have been lowered to <500 mg/dL should

attention turn to LDL lowering to reduce risk for CHD. 

Low HDL cholesterol. Low HDL cholesterol is a strong independent 

predictor of CHD. In ATP III, low HDL cholesterol is defined categorically

as a level <40 mg/dL, a change from the level of <35 mg/dL in ATP II. In

the present guidelines, low HDL cholesterol both modifies the goal for

LDL-lowering therapy and is used as a risk factor to estimate 10-year risk

for CHD. 

Low HDL cholesterol levels have several causes, many of which are 

associated with insulin resistance, i.e., elevated triglycerides, overweight and

obesity, physical inactivity, and type 2 diabetes. Other causes are cigarette

smoking, very high carbohydrate intakes (>60% of calories), and certain

drugs (e.g., beta-blockers, anabolic steroids, progestational agents)

ATP III does not specify a goal for HDL raising. Although clinical trial

results suggest that raising HDL will reduce risk, the evidence is insufficient

to specify a goal of therapy. Furthermore, currently available drugs do not

robustly raise HDL cholesterol. Nonetheless, a low HDL should receive

clinical attention and management according to the following sequence. In

all persons with low HDL cholesterol, the primary target of therapy is LDL

19

Table 9. Comparison of LDL Cholesterol and Non-HDL Cholesterol Goals for 

Three Risk Categories

Risk Category LDL Goal (mg/dL) Non-HDL-C Goal (mg/dL)

CHD and CHD Risk Equivalent <100 <130 

(10-year risk for CHD >20%)

Multiple (2+) Risk Factors and <130 <160 

10-year risk ≤20%

0-1 Risk Factor <160 <190 
cholesterol; ATP III guidelines should be followed to achieve the LDL cholesterol goal. Second, after the LDL goal has been reached, emphasis shifts

to weight reduction and increased physical activity (when the metabolic

syndrome is present). When a low HDL cholesterol is associated with high

triglycerides (200-499 mg/dL), secondary priority goes to achieving the nonHDL cholesterol goal, as outlined before. Also, if triglycerides are <200

mg/dL (isolated low HDL cholesterol), drugs for HDL raising (fibrates or

nicotinic acid) can be considered; however, treatment for isolated low HDL

is mostly reserved for persons with CHD and CHD risk equivalents. 

Diabetic dyslipidemia. This disorder is essentially atherogenic dyslipidemia

(high triglycerides, low HDL, and small dense LDL) in persons with type 2

diabetes. Although elevated triglycerides and/or low HDL cholesterol are

common in persons with diabetes, clinical trial results support the identification of LDL cholesterol as the primary target of therapy, as it is in those

without diabetes. Since diabetes is designated a CHD risk equivalent in ATP

III, the LDL cholesterol goal of therapy for most persons with diabetes will

be <100 mg/dL. Furthermore, when LDL cholesterol is ≥130 mg/dL, most

persons with diabetes will require initiation of LDL-lowering drugs simultaneously with TLC to achieve the LDL goal. When LDL cholesterol levels

are in the range of 100-129 mg/dL at baseline or on treatment, several therapeutic options are available: increasing intensity of LDL-lowering therapy,

adding a drug to modify atherogenic dyslipidemia (fibrate or nicotinic acid),

or intensifying control of other risk factors including hyperglycemia. When

triglyceride levels are ≥200 mg/dL, non-HDL cholesterol becomes a secondary target of cholesterol-lowering therapy. Several ongoing clinical trials

(e.g., Antihypertensive and Lipid Lowering Heart Attack Trial [ALLHAT])

will better quantify the magnitude of the benefit of LDL-lowering treatment

in older individuals with diabetes. In older persons (≥65 years of age) with

diabetes but no additional CHD risk factors other than age, clinical judgment is required for how intensively to apply these guidelines; a variety of

factors, including concomitant illnesses, general health status, and social

issues may influence treatment decisions and may suggest a more conservative approach.

Special Considerations for Different Population Groups

Middle-aged men (35-65 years). In general, men have a higher risk for CHD

than do women. Middle-aged men in particular have a high prevalence of

the major risk factors and are predisposed to abdominal obesity and the

metabolic syndrome. A sizable fraction of all CHD in men occurs in middle

age. Thus, many middle-aged men carry a relatively high risk for CHD, and

for those who do, intensive LDL-lowering therapy is needed. 

20
Women (ages 45-75 years). In women, onset of CHD generally is delayed

by some 10-15 years compared with that in men; thus most CHD in

women occurs after age 65. All risk factors contribute to CHD in women,

and most premature CHD in women (<65 years) occurs in those with multiple risk factors and the metabolic syndrome. Despite the previous belief

that the gender difference in risk for CHD reflects a protective effect of

estrogen in women, recent secondary and primary prevention trials cast

doubt on the use of hormone replacement therapy to reduce CHD risk in

postmenopausal women. In contrast, the favorable effects of statin therapy

in women in clinical trials make a cholesterol-lowering drug preferable to

hormone replacement therapy for CHD risk reduction. Women should be

treated similarly to men for secondary prevention. For primary prevention,

ATP III’s general approach is similarly applicable for women and men.

However, the later onset of CHD for women in general should be factored

into clinical decisions about use of cholesterol-lowering drugs.

Older adults (men ≥ 65 years and women ≥ 75 years). Overall, most new

CHD events and most coronary deaths occur in older persons (≥ 65 years).

A high level of LDL cholesterol and low HDL cholesterol still carry predictive power for the development of CHD in older persons. Nevertheless, the

finding of advanced subclinical atherosclerosis by noninvasive testing can be

helpful for confirming the presence of high risk in older persons. Secondary

prevention trials with statins have included a sizable number of older persons, mostly in the age range of 65 to 75 years. In these trials, older persons

showed significant risk reduction with statin therapy. Thus, no hard-andfast age restrictions appear necessary when selecting persons with established CHD for LDL-lowering therapy. For primary prevention, TLC is the

first line of therapy for older persons. However, LDL-lowering drugs can

also be considered when older persons are at higher risk because of multiple

risk factors or advanced subclinical atherosclerosis. 

Younger adults (men 20-35 years; women 20-45 years). CHD is rare except

in those with severe risk factors, e.g., familial hypercholesterolemia, heavy

cigarette smoking, or diabetes. Even though clinical CHD is relatively rare

in young adults, coronary atherosclerosis in its early stages may progress

rapidly. The rate of development of coronary atherosclerosis earlier in life

correlates with the major risk factors. In particular, long-term prospective

studies reveal that elevated serum cholesterol detected in young adulthood

predicts a higher rate of premature CHD in middle age. Thus, risk factor

identification in young adults is an important aim for long-term prevention.

The combination of early detection and early intervention on elevated LDL

cholesterol with life-habit changes offers the opportunity for delaying or

preventing onset of CHD later in life. For young adults with LDL cholesterol levels ≥130 mg/dL, TLC should be instituted and emphasized.

21
Particular attention should be given to young men who smoke and have a

high LDL cholesterol (160-189 mg/dL); they may be candidates for 

LDL-lowering drugs. When young adults have very high LDL cholesterol

levels (≥190 mg/dL), drug therapy should be considered, as in other adults.

Those with severe genetic forms of hypercholesterolemia may require 

LDL-lowering drugs in combination (e.g., statin + bile acid sequestrant). 

Racial and ethnic groups. African Americans have the highest overall CHD

mortality rate and the highest out-of-hospital coronary death rates of any

ethnic group in the United States, particularly at younger ages. Although the

reasons for the excess CHD mortality among African Americans have not

been fully elucidated, it can be accounted for, at least in part, by the high

prevalence of coronary risk factors. Hypertension, left ventricular hypertrophy, diabetes mellitus, cigarette smoking, obesity, physical inactivity, and

multiple CHD risk factors all occur more frequently in African Americans

than in whites. Other ethnic groups and minority populations in the United

States include Hispanics, Native Americans, Asian and Pacific Islanders, and

South Asians. Although limited data suggest that racial and ethnic groups

vary somewhat in baseline risk for CHD, this evidence did not appear 

sufficient to lead the ATP III panel to modify general recommendations for

cholesterol management in these populations.

Adherence to LDL-Lowering Therapy

Adherence to the ATP III guidelines by both patients and providers is a key

to approximating the magnitude of the benefits demonstrated in clinical 

trials of cholesterol lowering. Adherence issues have to be addressed in

order to attain the highest possible levels of CHD risk reduction. Thus, 

ATP III recommends the use of state-of-the-art multidisciplinary methods

targeting the patient, providers, and health delivery systems to achieve the

full population effectiveness of the guidelines for primary and secondary

prevention (Table 10).

22
23

Focus on the Patient

■ Simplify medication regimens

■ Provide explicit patient instruction and use good counseling techniques to 

teach the patient how to follow the prescribed treatment

■ Encourage the use of prompts to help patients remember treatment 

regimens

■ Use systems to reinforce adherence and maintain contact with the patient

■ Encourage the support of family and friends

■ Reinforce and reward adherence

■ Increase visits for patients unable to achieve treatment goal

■ Increase the convenience and access to care

■ Involve patients in their care through self-monitoring 

Focus on the Physician and Medical Office

■ Teach physicians to implement lipid treatment guidelines

■ Use reminders to prompt physicians to attend to lipid management

■ Identify a patient advocate in the office to help deliver or prompt care

■ Use patients to prompt preventive care

■ Develop a standardized treatment plan to structure care

■ Use feedback from past performance to foster change in future care

■ Remind patients of appointments and follow-up missed appointments 

Focus on the Health Delivery System

■ Provide lipid management through a lipid clinic

■ Utilize case management by nurses

■ Deploy telemedicine

■ Utilize the collaborative care of pharmacists

■ Execute critical care pathways in hospitals 

Table 10. Interventions to Improve Adherence
Appendix

Shared Features of ATP III and ATP II

ATP III shares a set of core features with ATP II. These are shown in Table A.

24

■ Continued identification of LDL cholesterol lowering as the primary goal of therapy

■ Consideration of high LDL cholesterol (≥160 mg/dL) as a potential target for 

LDL-lowering drug therapy, specifically as follows:

• For persons with multiple risk factors whose LDL levels are high (≥160 

mg/dL) after dietary therapy, consideration of drug therapy is recommended

• For persons with 0-1 risk factor, consideration of drug therapy (after dietary 

therapy) is optional for LDL 160-189 mg/dL and recommended for 

LDL ≥190 mg/dL 

■ Emphasis on intensive LDL-lowering therapy in persons with established CHD

■ Identification of three categories of risk for different LDL goals and different 

intensities of LDL-lowering therapy:

• CHD and CHD risk equivalents* (other forms of clinical atherosclerotic 

disease)

• Multiple (2+) risk factors†

• 0-1 risk factor 

■ Identification of subpopulations, besides middle-aged men, for detection of high

LDL cholesterol (and other lipid risk factors) and for clinical intervention. These

include:

• Young adults

• Postmenopausal women

• Older persons 

■ Emphasis on weight loss and physical activity to enhance risk reduction in persons

with elevated LDL cholesterol

Table A. Shared Features of ATP III and ATP II

* A CHD risk equivalent is a condition that carries an absolute risk for developing new CHD equal to the risk for

having recurrent CHD events in persons with established CHD.

† Risk factors that continue to modify the LDL goal include cigarette smoking, hypertension, low HDL 

cholesterol, family history of premature CHD, age (male >45 years and female >55 years), and diabetes 

(in ATP III diabetes is regarded as a CHD risk equivalent).
Estimating 10-Year Risk for Men and Women

Risk assessment for determining the 10-year risk for developing CHD is

carried out using Framingham risk scoring (Table B1 for men and Table B2

for women). The risk factors included in the Framingham calculation of 

10-year risk are: age, total cholesterol, HDL cholesterol, systolic blood 

pressure, treatment for hypertension, and cigarette smoking. The first step is

to calculate the number of points for each risk factor. For initial assessment,

values for total cholesterol and HDL cholesterol are required. Because of a

larger database, Framingham estimates are more robust for total cholesterol

than for LDL cholesterol. Note, however, that the LDL cholesterol level

remains the primary target of therapy. Total cholesterol and HDL 

cholesterol values should be the average of at least two measurements

obtained from lipoprotein analysis. The blood pressure value used is that

obtained at the time of assessment, regardless of whether the person is on

anti-hypertensive therapy. However, if the person is on antihypertensive

treatment, an extra point is added beyond points for the blood pressure

reading because treated hypertension carries residual risk (see Tables B1 and

B2). The average of several blood pressure measurements, as recommended

by the Joint National Committee (JNC), is needed for an accurate measure

of baseline blood pressure. The designation “smoker” means any cigarette

smoking in the past month. The total risk score sums the points for each

risk factor. The 10-year risk for myocardial infarction and coronary death

(hard CHD) is estimated from total points, and the person is categorized

according to absolute 10-year risk as indicated above (see Table 5).

25
Table B1. Estimate of 10-Year Risk for Men (Framingham Point Scores)

Point Total 10-Year Risk %

<0 < 1 

0 1 

1 1 

2 1 

3 1 

4 1 

5 2 

6 2 

7 3 

8 4 

9 5 

10 6 

11 8 

12 10 

13 12

14 16 

15 20 

16 25 

≥17 ≥ 30 

26

<160 0 0 0 0 0

160-199 4 3 2 1 0

200-239 7 5 3 1 0

240-279 9 6 4 2 1

≥280 11 8 5 3 1

Total

Cholesterol

Age 20-39 Age 40-49 Age 50-59 Age 60-69 Age 70-79

Age 20-39 Age 40-49 Age 50-59 Age 60-69 Age 70-79

Points 

Nonsmoker 00 000

Smoker 85 311

Points 

HDL (mg/dL) Points

≥60 -1

50-59 0

40-49 1

<40 2

Systolic BP (mmHg) If Untreated If Treated

<120 0 0

120-129 0 1

130-139 1 2

140-159 1 2

≥160 2 3

Age Points

20-34 -9

35-39 -4

40-44 0

45-49 3

50-54 6

55-59 8

60-64 10

65-69 11

70-74 12

75-79 13
27

Table B2. Estimate of 10-Year Risk for Women (Framingham Point Scores)

Point Total 10-Year Risk %

<9 < 1 

9 1 

10 1 

11 1 

12 1 

13 2 

14 2 

15 3 

16 4 

17 5 

18 6 

19 8 

20 11 

21 14 

22 17 

23 22 

24 27 

≥25 ≥ 30 

<160 0 0 0 0 0

160-199 4 3 2 1 1

200-239 8 6 4 2 1

240-279 11 8 5 3 2

≥280 13 10 7 4 2

Total

Cholesterol

Age 20-39 Age 40-49 Age 50-59 Age 60-69 Age 70-79

Age 20-39 Age 40-49 Age 50-59 Age 60-69 Age 70-79

Points 

Nonsmoker 00 000

Smoker 97 421

Points 

HDL (mg/dL) Points

≥60 -1

50-59 0

40-49 1

<40 2

Systolic BP (mmHg) If Untreated If Treated

<120 0 0

120-129 1 3

130-139 2 4

140-159 3 5

≥160 4 6

Age Points

20-34 -7

35-39 -3

40-44 0

45-49 3

50-54 6

55-59 8

60-64 10

65-69 12

70-74 14

75-79 16
28

30

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

Public Health Service

National Institutes of Health

National Heart, Lung, and Blood Institute

NIH Publication No. 01-3670

May 2001