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High Blood CholesterolNational Cholesterol Education Program Third Report of the
National Cholesterol
Education Program (NCEP)
Expert Panel on

Detection,Evaluation, and Treatmentof High BloodCholesterol in Adults (Adult TreatmentPanel III) N A T I O N A L I N S T I T U T E S O F H E A L T H N A T I O N A L H E A R T , L U N G , A N D B L O O D I N S T I T U T E Discrimination Prohibited: Under provisions ofapplicable public laws enacted by Congress since1964, no person in the United States shall, on thegrounds of race, color, national origin, handicap,or age, be excluded from participation in, bedenied the benefits of, or be subjected to discrimi-nation under any program or activity (or, on thebasis of sex, with respect to any education programor activity) receiving Federal financial assistance. In addition, Executive Order 11141 prohibits discrimination on the basis of age by contractorsand subcontractors in the performance of Federalcontracts, and Executive Order 11246 states thatno federally funded contractor may discriminateagainst any employee or applicant for employmentbecause of race, color, religion, sex, or national origin. Therefore, the National Heart, Lung, andBlood Institute must be operated in compliancewith these laws and Executive Orders.
Third Report of the
National Cholesterol
Education Program (NCEP)
Expert Panel on

Detection, Evaluation, and Treatmentof High Blood Cholesterol in Adults (Adult TreatmentPanel III) National Cholesterol Education Program National Heart, Lung, and Blood Institute NIH Publication No. 01-3670May 2001 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 PanelDiane 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 PanelNancy 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 onDetection, Evaluation, and Treatment of High Blood Cholesterol in Adults wasapproved 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 PhysiciansTheodore 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. 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 AssociationTo 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 CrossDonald 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.
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 The link between risk assessment and cost Primary Prevention With LDL-Lowering Therapy
Secondary Prevention With LDL-Lowering Therapy
LDL-Lowering Therapy in Three Risk Categories
Multiple (2+) risk factors and 10-year risk ≤20% Therapeutic Lifestyle Changes in LDL-Lowering Therapy
Drug Therapy to Achieve LDL-Cholesterol Goals
Secondary prevention: drug therapy for CHD and 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 Specific Treatment of Lipid and Non-Lipid Risk Special Issues
Special Considerations for Different Population Groups Appendix
Estimating 10-Year Risk for Men and Women 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
The Third Report of the Expert Panel on Detection, Evaluation, andTreatment 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 manage-ment. The full ATP III document is an evidence-based and extensively referenced report that provides the scientific rationale for the recommen-dations contained in the executive summary. ATP III builds on previousATP reports and expands the indications for intensive cholesterol-loweringtherapy in clinical practice. It should be noted that these guidelines areintended to inform, not replace, the physician’s clinical judgment, whichmust ultimately determine the appropriate treatment for each individual.
The third ATP report updates the existing recommendations for clinicalmanagement of high blood cholesterol. The NCEP periodically producesATP clinical updates as warranted by advances in the science of cholesterolmanagement. Each of the guideline reports—ATP I, II, and III—has a majorthrust. ATP I outlined a strategy for primary prevention of coronary heartdisease (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 impor-tance of this approach and added a new feature: the intensive managementof 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 addsa 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 Iand ATP II. Some of the important features shared with previous reports areshown in Table A in the Appendix.
While ATP III maintains attention to intensive treatment of patients withCHD, its major new feature is a focus on primary prevention in personswith multiple risk factors. Many of these persons have a relatively high riskfor CHD and will benefit from more intensive LDL-lowering treatment thanrecommended in ATP II. Table 1 shows the new features of ATP III.
Table 1. New Features of ATP III
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 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 ■ Recommends treatment beyond LDL lowering for persons with triglycerides LDL Cholesterol: The Primary Target of Therapy
Research from experimental animals, laboratory investigations, epidemiology,and genetic forms of hypercholesterolemia indicate that elevated LDL choles-terol 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 ofcholesterol-lowering therapy. As a result, the primary goals of therapy and thecutpoints 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 therapyshould 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. Riskassessment requires measurement of LDL cholesterol as part of lipoproteinanalysis and identification of accompanying risk determinants. 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 oppor-tunity is nonfasting, only the values for total cholesterol and HDL choles-terol will be usable. In such a case, if total cholesterol is ≥200 mg/dL orHDL is <40 mg/dL, a followup lipoprotein profile is needed for appropriatemanagement based on LDL. The relationship between LDL cholesterol levels and CHD risk is continuous over a broad range of LDL levels fromlow to high. Therefore, ATP III adopts the classification of LDL cholesterollevels shown in Table 2, which also shows the classification of total andHDL cholesterol levels. Table 2. ATP III Classification of LDL, Total, and HDL Cholesterol (mg/dL)
LDL Cholesterol
Total Cholesterol
HDL Cholesterol
Risk determinants in addition to LDL-cholesterol include the presence orabsence of CHD, other clinical forms of atherosclerotic disease, and themajor risk factors other than LDL (see Table 3). (LDL is not countedamong the risk factors in Table 3 because the purpose of counting thoserisk factors is to modify the treatment of LDL.) Based on these other riskdeterminants, ATP III identifies three categories of risk that modify thegoals and modalities of LDL-lowering therapy. Table 4 defines these categories and shows corresponding LDL-cholesterol goals. Table 3. Major Risk Factors (Exclusive of LDL Cholesterol) That Modify LDL Goals*
■ 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 Table 4. Three Categories of Risk that Modify LDL Cholesterol Goals
Risk Category
LDL Goal (mg/dL)
* Risk factors that modify the LDL goal are listed in Table 3 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 establishedCHD, i.e., >20% per 10 years (i.e., more than 20 of 100 such individualswill develop CHD or have a recurrent CHD event within 10 years). CHDrisk equivalents comprise: Other clinical forms of atherosclerotic disease (peripheral arterial disease,abdominal aortic aneurysm, and symptomatic carotid artery disease); 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 ofnew CHD within 10 years, in part because of its frequent association withmultiple risk factors. Furthermore, because persons with diabetes who experience a myocardial infarction have an unusually high death rate eitherimmediately or in the long term, a more intensive prevention strategy iswarranted. Persons with CHD or CHD risk equivalents have the lowestLDL cholesterol goal (<100 mg/dL). The second category consists of persons with multiple (2+) risk factors inwhom 10-year risk for CHD is ≤20%. Risk is estimated from Framinghamrisk scores (see Appendix). The major risk factors, exclusive of elevatedLDL cholesterol, are used to define the presence of multiple risk factors thatmodify the goals and cutpoints for LDL-lowering treatment, and these arelisted 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 fewexceptions, persons in this category have a 10-year risk <10%. Their LDLcholesterol 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 clinicalforms of atherosclerotic disease is determined by a 2-step procedure. First, the number of risk factors is counted (Table 3). Second, for personswith multiple (2+) risk factors, 10-year risk assessment is carried out with Framingham scoring (see Appendix) to identify individuals whoseshort-term (10-year) risk warrants consideration of intensive treatment.
Estimation of the 10-year CHD risk adds a step to risk assessment beyondrisk factor counting, but this step is warranted because it allows better targeting of intensive treatment to people who will benefit from it. When0-1 risk factor is present, Framingham scoring is not necessary because 10-year risk rarely reaches levels for intensive intervention; a very highLDL level in such a person may nevertheless warrant consideration of drugtherapy to reduce long-term risk. Risk factors used in Framingham scoringinclude age, total cholesterol, HDL cholesterol, blood pressure, and cigarette smoking. Total cholesterol is used for 10-year risk assessmentbecause of a larger and more robust Framingham database for total thanfor LDL cholesterol, but LDL cholesterol is the primary target of therapy.
Framingham scoring divides persons with multiple risk factors into thosewith 10-year risk for CHD of >20%, 10-20%, and <10%. It should benoted that this 2-step sequence can be reversed with essentially the sameresults.* Initial risk assessment in ATP III uses the major risk factors todefine the core risk status. Only after the core risk status has been determined should any other risk modifiers be taken into consideration foradjusting the therapeutic approach.
Role of other risk factors in risk assessment
ATP III recognizes that risk for CHD is influenced by other factors notincluded among the major, independent risk factors (Table 3). Among theseare life-habit risk factors and emerging risk factors. The former include obesity, physical inactivity, and atherogenic diet; the latter consist oflipoprotein (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 arenot used to set a lower LDL cholesterol goal of therapy. The emerging risk factors do not categorically modify LDL cholesterol goals; however, theyappear to contribute to CHD risk to varying degrees and can have utility inselected persons to guide intensity of risk-reduction therapy. Their presencecan 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 *If Framingham scoring is carried out before risk factor counting, persons with <10 percent risk are then divided intothose 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 areabdominal obesity, atherogenic dyslipidemia (elevated triglyceride, smallLDL particles, low HDL cholesterol), raised blood pressure, insulin resistance (with or without glucose intolerance), and prothrombotic andproinflammatory 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 describedbeginning on page 15 under “Benefit Beyond LDL Lowering: TheMetabolic 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 therapywith absolute risk. Everyone with elevated LDL cholesterol is treated withlifestyle changes that are effective in lowering LDL levels. Persons at relatively high risk are also candidates for drug treatment, which is veryeffective but entails significant additional expense. The cutpoints for drugtreatment are based primarily on risk-benefit considerations: those at higherrisk are likely to get greater benefit. However, cutpoints for recommendedmanagement based on therapeutic efficacy are checked against currentlyaccepted standards for cost effectiveness. Lifestyle changes are the mostcost-effective means to reduce risk for CHD. Even so, to achieve maximalbenefit, many persons will require LDL-lowering drugs. Drug therapy is themajor expense of LDL-lowering therapy, and it dominates cost-effectivenessanalysis. However, the costs of LDL-lowering drugs are currently in fluxand appear to be declining. This report recognizes that as drug pricesdecline it will be possible to extend drug use to lower risk persons and stillbe cost effective. In addition, ATP III recognizes that some persons withhigh long-term risk are candidates for LDL-lowering drugs even though useof drugs may not be cost effective by current standards.
Primary Prevention With LDL-Lowering Therapy
Primary prevention of CHD offers the greatest opportunity for reducingthe 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 andcholesterol, 2) increased physical activity, and 3) weight control, to lowerpopulation cholesterol levels and reduce CHD risk, but the clinicalapproach intensifies preventive strategies for higher risk persons. One aimof primary prevention is to reduce long-term risk (>10 years) as well asshort-term risk (≤10 years). LDL goals in primary prevention depend ona person’s absolute risk for CHD (i.e., the probability of having a CHD event in the short term or the long term)—the higher the risk, the lowerthe goal. Therapeutic lifestyle changes are the foundation of clinical primary prevention. Nonetheless, some persons at higher risk because ofhigh or very high LDL cholesterol levels or because of multiple risk factors are candidates for LDL-lowering drugs. Recent primary preventiontrials show that LDL-lowering drugs reduce risk for major coronaryevents and coronary death even in the short term. Any person with elevated LDL cholesterol or other form of hyperlipidemia shouldundergo clinical or laboratory assessment to rule out secondary dyslipidemia beforeinitiation 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 inprimary prevention are established according to a person’s risk category (Table 4). Secondary Prevention With LDL-Lowering Therapy
Recent clinical trials demonstrate that LDL-lowering therapy reduces totalmortality, coronary mortality, major coronary events, coronary artery procedures, and stroke in persons with established CHD. As shown inTable 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 bothclinical and angiographic endpoints and by prospective epidemiologicalstudies. The same goal should apply for persons with CHD risk equiva-lents. When persons are hospitalized for acute coronary syndromes orcoronary procedures, lipid measures should be taken on admission or within 24 hours. These values can guide the physician on initiation ofLDL-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 lifestylechanges (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 triglyceride or low HDL cholesterol) are present, TLC also stresses weightreduction and increased physical activity. Table 5 defines LDL cholesterolgoals and cutpoints for initiation of TLC and for drug consideration forpersons with three categories of risk: CHD and CHD risk equivalents; multi-ple (2+) risk factors (10-year risk 10-20% and <10%); and 0-1 risk factor.
Table 5: LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle
Changes (TLC) and Drug Therapy in Different Risk Categories.

Risk Category
LDL Level
LDL Level
at Which to Initiate
at Which to
Therapeutic Lifestyle
Consider Drug
Changes (TLC)
≥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 tri-glycerides 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 with0-1 risk factor is not necessary. CHD and CHD risk equivalents
For persons with CHD and CHD risk equivalents, LDL-lowering therapygreatly reduces risk for major coronary events and stroke and yields highlyfavorable cost-effectiveness ratios. The cut-points for initiating lifestyle anddrug therapies are shown in Table 5. If baseline LDL cholesterol is 130 mg/dL, intensive lifestyle therapy andmaximal 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: • Initiate or intensify lifestyle and/or drug therapies specifically to • Emphasize weight reduction and increased physical activity in persons • 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%, intensi-ty of therapy is adjusted according to 10-year risk and LDL cholesterollevel. 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 howintensively to apply these guidelines; a variety of factors, including con-comitant 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 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 riskcategory is <160 mg/dL. The primary aim of therapy is to reduce long-termrisk. First-line therapy is TLC. If after 3 months of TLC the LDL choles-terol 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 optionaldepending 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 factorand elevated LDL cholesterol (≥160 mg/dL) is to slow the development ofcoronary atherosclerosis, which will reduce long-term risk. This aim mayconflict with cost-effectiveness considerations; thus, clinical judgment isrequired in selection of persons for drug therapy, although a strong case canbe made for using drugs when LDL cholesterol is ≥190 mg/dL after TLC. For persons whose LDL cholesterol levels are already below goal levelsupon 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 forCHD. This approach is designated therapeutic lifestyle changes (TLC).
Its essential features are: 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) Table 6. Nutrient Composition of the TLC Diet
Recommended Intake
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 A model of steps in TLC is shown in Figure 1. To initiate TLC, intakes ofsaturated 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 totalcalories provided saturated fats and trans fatty acids are kept low. A higherintake of total fat, mostly in the form of unsaturated fat, can help to reducetriglycerides and raise HDL cholesterol in persons with the metabolic syndrome. In accordance with the Dietary Guidelines, moderate physicalactivity is encouraged. After 6 weeks, the LDL response is determined; if theLDL cholesterol goal has not been achieved, other therapeutic options forLDL 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 associatedlipid risk factors. The majority of persons with these latter abnormalities are overweight or obese and sedentary. Weight reduction therapy for over-weight or obese patients will enhance LDL lowering and will provide otherhealth benefits including modifying other lipid and nonlipid risk factors.
Assistance in the management of overweight and obese persons is providedby the Clinical Guidelines on the Identification, Evaluation, and Treatmentof Overweight and Obesity in Adults from the NHLBI Obesity EducationInitiative (1998). Additional risk reduction can be achieved by simultane-ously increasing physical activity.
At all stages of dietary therapy, physicians are encouraged to refer patientsto registered dietitians or other qualified nutritionists for medical nutritiontherapy, which is the term for the nutritional intervention and guidance provided by a nutrition professional.
Figure 1. A Model of Steps in Therapeutic Lifestyle Changes (TLC)
Begin Lifestyle
Evaluate LDL
Evaluate LDL
Adherence to

If LDL goal not
If LDL goal not
achieved, intensify
achieved, consider
LDL-lowering Tx
adding drug Tx
Drug Therapy to Achieve LDL Cholesterol Goals
A portion of the population whose short-term or long-term risk for CHD ishigh will require LDL-lowering drugs in addition to TLC to reach the desig-nated goal for LDL cholesterol (see Table 5). When drugs are prescribed,attention to TLC should always be maintained and reinforced. Currentlyavailable drugs that affect lipoprotein metabolism and their major charac-teristics 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 LDL-lowering drugs (e.g., statins, bile acid sequestrants) have applied to the Table 7. Drugs Affecting Lipoprotein Metabolism
Drug Class, Agents Lipid/Lipoprotein
Side Effects
Contraindications Clinical Trial
and Daily Doses
↑5-15% Increased liver • Active or chron- coronary ↑15-35% Hyperglycemia • Chronic liver ↑10-20% Unexplained • Severe hepatic * Lovastatin (20-80 mg), pravastatin (20-40 mg), simvastatin (20-80 mg), fluvastatin (20-80 mg), atorvastatin (10-80 mg), Cyclosporine, macrolide antibiotics, various antifungal agents and cytochrome P-450 inhibitors (fibrates and niacin should be 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 § Gemfibrozil (600 mg BID), fenofibrate (200 mg), clofibrate (1000 mg BID). Food and Drug Administration (FDA) to allow these agents to becomeOTC medications. At the time of publication of ATP III, the FDA has notgranted permission for OTC status for statins or bile acid sequestrants. If anOTC cholesterol-lowering drug is or becomes available, patients shouldcontinue to consult with their physicians about whether to initiate drugtreatment, about setting the goals of therapy, and about monitoring fortherapeutic 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 anLDL cholesterol level <100 mg/dL. The cutpoints for initiating lifestyle anddrug therapies are shown in Table 5, and the approach to treatment is discussed immediately after Table 5. Most CHD patients will need LDL-lowering drug therapy. Other lipid risk factors may also warrant considera-tion 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. Thisvalue can be used for treatment decisions. In general, persons hospitalizedfor a coronary event or procedure should be discharged on drug therapy ifthe LDL cholesterol is ≥130 mg/dL. If the LDL is 100–129 mg/dL, clinicaljudgment should be used in deciding whether to initiate drug treatment atdischarge, recognizing that LDL cholesterol levels begin to decline in thefirst few hours after an event and are significantly decreased by 24-48 hoursand may remain low for many weeks. Thus, the initial LDL cholesterol levelobtained in the hospital may be substantially lower than is usual for thepatient. Some authorities hold drug therapy should be initiated whenever a patient hospitalized for a CHD-related illness is found to have an LDLcholesterol >100 mg/dL. Initiation of drug therapy at the time of hospitaldischarge has two advantages. First, at that time patients are particularlymotivated to undertake and adhere to risk-lowering interventions; and second, failure to initiate indicated therapy early is one of the causes of alarge “treatment gap,” because outpatient followup is often less consistentand more fragmented. LDL-lowering drug therapy for primary prevention
Table 5 shows the cutpoints for considering drug treatment in primary pre-vention. The general approach to management of drug therapy for primaryprevention is outlined in Figure 2.
Figure 2. Progression of Drug Therapy in Primary Prevention
If LDL goal not
If LDL goal not
achieved, intensify
achieved, intensify
response and
drug therapy
drug therapy or
adherence to
refer to a lipid
When drug therapy for primary prevention is a consideration, the third visitof dietary therapy (see Figure 1) will typically be the visit to initiate drugtreatment. Even if drug treatment is started, TLC should be continued. Aswith TLC, the first priority of drug therapy is to achieve the goal for LDLcholesterol. For this reason, an LDL-lowering drug should be started. Theusual drug will be a statin, but alternatives are a bile acid sequestrant ornicotinic acid. In most cases, the statin should be started at a moderatedose. In many patients, the LDL cholesterol goal will be achieved, and high-er doses will not be necessary. The patient’s response should be checkedabout 6 weeks after starting drug therapy. If the goal of therapy has beenachieved, the current dose can be maintained. However, if the goal has notbeen achieved, LDL-lowering therapy can be intensified, either by increasingthe dose of statin or by combining a statin with a bile acid sequestrant ornicotinic acid. After 12 weeks of drug therapy, the response to therapy should again beassessed. If the LDL cholesterol goal is still not achieved, consideration canbe given to further intensification of drug therapy. If the LDL goal cannotbe attained by standard lipid-lowering therapy, consideration should begiven to seeking consultation from a lipid specialist. Once the goal for LDLcholesterol has been attained, attention can turn to other lipid risk factorsand nonlipid factors. Thereafter, patients can be monitored for response totherapy 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 secondary target of therapy is the metabolic syndrome, which represents aconstellation of lipid and nonlipid risk factors of metabolic origin. This syndrome is closely linked to a generalized metabolic disorder called insulinresistance in which the normal actions of insulin are impaired. Excess bodyfat (particularly abdominal obesity) and physical inactivity promote thedevelopment of insulin resistance, but some individuals also are geneticallypredisposed 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 madewhen three or more of the risk determinants shown in Table 8 are present.
These determinants include a combination of categorical and borderline riskfactors that can be readily measured in clinical practice.
Table 8. Clinical Identification of the Metabolic Syndrome
Risk Factor
Defining Level
* 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. Management of the metabolic syndrome has a two-fold objective: (1) toreduce underlying causes (i.e., obesity and physical inactivity), and (2) totreat 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 themetabolic syndrome are weight reduction and increased physical activity,which will effectively reduce all of these risk factors. Therefore, after appropriate control of LDL cholesterol, TLC should stress weight reductionand 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 interven-tion. Weight reduction will enhance LDL lowering and reduce all of the riskfactors of the metabolic syndrome. The recommended approaches forreducing overweight and obesity are contained in the clinical guidelines ofthe 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 meta-bolic syndrome. It further may enhance risk by impairing cardiovascular fit-ness and coronary blood flow. Regular physical activity reduces very lowdensity lipoprotein (VLDL) levels, raises HDL cholesterol, and in some persons, lowers LDL levels. It also can lower blood pressure, reduce insulinresistance, and favorably influence cardiovascular function. Thus, ATP IIIrecommends 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 onPhysical Activity. Specific Treatment of Lipid and Non-Lipid Risk Factors
Beyond the underlying risk factors, therapies directed against the lipid andnonlipid risk factors of the metabolic syndrome will reduce CHD risk.
These include treatment of hypertension, use of aspirin in patients withCHD 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 underManagement 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: monogenicfamilial hypercholesterolemia, familial defective apolipoprotein B, and polygenic hypercholesterolemia. Early detection of these disorders throughcholesterol testing in young adults is needed to prevent premature CHD.
Family testing is important to identify similarly affected relatives. These disorders often require combined drug therapy (statin + bile acid seques-trant) to achieve the goals of LDL-lowering therapy.
Elevated serum triglycerides. Recent meta-analyses of prospective studiesindicate that elevated triglycerides are also an independent risk factor forCHD. Factors contributing to elevated (higher than normal) triglycerides inthe general population include: obesity and overweight, physical inactivity,cigarette smoking, excess alcohol intake, high carbohydrate diets (>60% ofenergy 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 inpersons with the metabolic syndrome, although secondary or genetic factorscan heighten triglyceride levels. ATP III adopts the following classificationof serum triglycerides: The finding that elevated triglycerides are an independent CHD risk factorsuggests that some triglyceride-rich lipoproteins are atherogenic. The latterare partially degraded VLDL, commonly called remnant lipoproteins. Inclinical practice, VLDL cholesterol is the most readily available measure ofatherogenic remnant lipoproteins. Thus, VLDL cholesterol can be a targetof cholesterol-lowering therapy. ATP III identifies the sum of LDL+VLDLcholesterol [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 personswith high serum triglycerides can be set at 30 mg/dL higher than that forLDL cholesterol (Table 9) on the premise that a VLDL cholesterol level ≤30mg/dL is normal. The treatment strategy for elevated triglycerides depends on the causes ofthe elevation and its severity. For all persons with elevated triglycerides, theprimary aim of therapy is to achieve the target goal for LDL cholesterol.
When triglycerides are borderline high (150-199 mg/dL), emphasis shouldalso be placed on weight reduction and increased physical activity. For hightriglycerides (200-499 mg/dL), non-HDL cholesterol becomes a secondary 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)
(10-year risk for CHD >20%)Multiple (2+) Risk Factors and target of therapy. Aside from weight reduction and increased physical activi-ty, drug therapy can be considered in high-risk persons to achieve the non-HDL cholesterol goal. There are two approaches to drug therapy. First, thenon-HDL cholesterol goal can be achieved by intensifying therapy with anLDL-lowering drug; or second, nicotinic acid or fibrate can be added, ifused with appropriate caution, to achieve the non-HDL cholesterol goal byfurther lowering of VLDL cholesterol. In rare cases in which triglyceridesare very high (≥500 mg/dL), the initial aim of therapy is to prevent acutepancreatitis through triglyceride lowering. This approach requires very lowfat diets (≤15% of calorie intake), weight reduction, increased physicalactivity, and usually a triglyceride-lowering drug (fibrate or nicotinic acid).
Only after triglyceride levels have been lowered to <500 mg/dL shouldattention 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 categoricallyas a level <40 mg/dL, a change from the level of <35 mg/dL in ATP II. Inthe present guidelines, low HDL cholesterol both modifies the goal forLDL-lowering therapy and is used as a risk factor to estimate 10-year riskfor CHD. Low HDL cholesterol levels have several causes, many of which are associated with insulin resistance, i.e., elevated triglycerides, overweight andobesity, physical inactivity, and type 2 diabetes. Other causes are cigarettesmoking, very high carbohydrate intakes (>60% of calories), and certaindrugs (e.g., beta-blockers, anabolic steroids, progestational agents) ATP III does not specify a goal for HDL raising. Although clinical trialresults suggest that raising HDL will reduce risk, the evidence is insufficientto specify a goal of therapy. Furthermore, currently available drugs do notrobustly raise HDL cholesterol. Nonetheless, a low HDL should receiveclinical attention and management according to the following sequence. Inall persons with low HDL cholesterol, the primary target of therapy is LDL cholesterol; ATP III guidelines should be followed to achieve the LDL cho-lesterol goal. Second, after the LDL goal has been reached, emphasis shiftsto weight reduction and increased physical activity (when the metabolicsyndrome is present). When a low HDL cholesterol is associated with hightriglycerides (200-499 mg/dL), secondary priority goes to achieving the non-HDL cholesterol goal, as outlined before. Also, if triglycerides are <200mg/dL (isolated low HDL cholesterol), drugs for HDL raising (fibrates ornicotinic acid) can be considered; however, treatment for isolated low HDLis 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 2diabetes. Although elevated triglycerides and/or low HDL cholesterol arecommon in persons with diabetes, clinical trial results support the identifi-cation of LDL cholesterol as the primary target of therapy, as it is in thosewithout diabetes. Since diabetes is designated a CHD risk equivalent in ATPIII, the LDL cholesterol goal of therapy for most persons with diabetes willbe <100 mg/dL. Furthermore, when LDL cholesterol is ≥130 mg/dL, mostpersons with diabetes will require initiation of LDL-lowering drugs simulta-neously with TLC to achieve the LDL goal. When LDL cholesterol levelsare in the range of 100-129 mg/dL at baseline or on treatment, several ther-apeutic 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. Whentriglyceride levels are ≥200 mg/dL, non-HDL cholesterol becomes a sec-ondary 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 treatmentin older individuals with diabetes. In older persons (≥65 years of age) withdiabetes but no additional CHD risk factors other than age, clinical judg-ment is required for how intensively to apply these guidelines; a variety offactors, including concomitant illnesses, general health status, and socialissues may influence treatment decisions and may suggest a more conserva-tive approach.
Special Considerations for Different Population Groups
Middle-aged men (35-65 years). In general, men have a higher risk for CHDthan do women. Middle-aged men in particular have a high prevalence ofthe major risk factors and are predisposed to abdominal obesity and themetabolic syndrome. A sizable fraction of all CHD in men occurs in middleage. Thus, many middle-aged men carry a relatively high risk for CHD, andfor those who do, intensive LDL-lowering therapy is needed. Women (ages 45-75 years). In women, onset of CHD generally is delayedby some 10-15 years compared with that in men; thus most CHD inwomen occurs after age 65. All risk factors contribute to CHD in women,and most premature CHD in women (<65 years) occurs in those with mul-tiple risk factors and the metabolic syndrome. Despite the previous beliefthat the gender difference in risk for CHD reflects a protective effect ofestrogen in women, recent secondary and primary prevention trials castdoubt on the use of hormone replacement therapy to reduce CHD risk inpostmenopausal women. In contrast, the favorable effects of statin therapyin women in clinical trials make a cholesterol-lowering drug preferable tohormone replacement therapy for CHD risk reduction. Women should betreated 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 factoredinto clinical decisions about use of cholesterol-lowering drugs.
Older adults (men 65 years and women 75 years). Overall, most newCHD events and most coronary deaths occur in older persons (≥ 65 years).
A high level of LDL cholesterol and low HDL cholesterol still carry predic-tive power for the development of CHD in older persons. Nevertheless, thefinding of advanced subclinical atherosclerosis by noninvasive testing can behelpful for confirming the presence of high risk in older persons. Secondaryprevention trials with statins have included a sizable number of older per-sons, mostly in the age range of 65 to 75 years. In these trials, older personsshowed significant risk reduction with statin therapy. Thus, no hard-and-fast age restrictions appear necessary when selecting persons with estab-lished CHD for LDL-lowering therapy. For primary prevention, TLC is thefirst line of therapy for older persons. However, LDL-lowering drugs canalso be considered when older persons are at higher risk because of multiplerisk factors or advanced subclinical atherosclerosis. Younger adults (men 20-35 years; women 20-45 years). CHD is rare exceptin those with severe risk factors, e.g., familial hypercholesterolemia, heavycigarette smoking, or diabetes. Even though clinical CHD is relatively rarein young adults, coronary atherosclerosis in its early stages may progressrapidly. The rate of development of coronary atherosclerosis earlier in lifecorrelates with the major risk factors. In particular, long-term prospectivestudies reveal that elevated serum cholesterol detected in young adulthoodpredicts a higher rate of premature CHD in middle age. Thus, risk factoridentification in young adults is an important aim for long-term prevention.
The combination of early detection and early intervention on elevated LDLcholesterol with life-habit changes offers the opportunity for delaying orpreventing onset of CHD later in life. For young adults with LDL choles-terol levels ≥130 mg/dL, TLC should be instituted and emphasized.
Particular attention should be given to young men who smoke and have ahigh LDL cholesterol (160-189 mg/dL); they may be candidates for LDL-lowering drugs. When young adults have very high LDL cholesterollevels (≥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 CHDmortality rate and the highest out-of-hospital coronary death rates of anyethnic group in the United States, particularly at younger ages. Although thereasons for the excess CHD mortality among African Americans have notbeen fully elucidated, it can be accounted for, at least in part, by the highprevalence of coronary risk factors. Hypertension, left ventricular hypertro-phy, diabetes mellitus, cigarette smoking, obesity, physical inactivity, andmultiple CHD risk factors all occur more frequently in African Americansthan in whites. Other ethnic groups and minority populations in the UnitedStates include Hispanics, Native Americans, Asian and Pacific Islanders, andSouth Asians. Although limited data suggest that racial and ethnic groupsvary somewhat in baseline risk for CHD, this evidence did not appear sufficient to lead the ATP III panel to modify general recommendations forcholesterol management in these populations.
Adherence to LDL-Lowering Therapy
Adherence to the ATP III guidelines by both patients and providers is a keyto approximating the magnitude of the benefits demonstrated in clinical trials of cholesterol lowering. Adherence issues have to be addressed inorder to attain the highest possible levels of CHD risk reduction. Thus, ATP III recommends the use of state-of-the-art multidisciplinary methodstargeting the patient, providers, and health delivery systems to achieve thefull population effectiveness of the guidelines for primary and secondaryprevention (Table 10).
Table 10. Interventions to Improve Adherence
Focus on the Patient
■ 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 ■ Use systems to reinforce adherence and maintain contact with the patient ■ Encourage the support of family and friends ■ 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 the collaborative care of pharmacists ■ Execute critical care pathways in hospitals Appendix
Shared Features of ATP III and ATP II
ATP III shares a set of core features with ATP III. These are shown in Table A.
Table A. Shared Features of ATP III and ATP II
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 • Multiple (2+) risk factors†• 0-1 risk factor Identification of subpopulations, besides middle-aged men, for detection of highLDL cholesterol (and other lipid risk factors) and for clinical intervention. Theseinclude: • Young adults• Postmenopausal women• Older persons Emphasis on weight loss and physical activity to enhance risk reduction in personswith elevated LDL cholesterol * 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 iscarried out using Framingham risk scoring (Table B1 for men and Table B2for 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 isto calculate the number of points for each risk factor. For initial assessment,values for total cholesterol and HDL cholesterol are required. Because of alarger database, Framingham estimates are more robust for total cholesterolthan for LDL cholesterol. Note, however, that the LDL cholesterol levelremains the primary target of therapy. Total cholesterol and HDL cholesterol values should be the average of at least two measurementsobtained from lipoprotein analysis. The blood pressure value used is thatobtained at the time of assessment, regardless of whether the person is onanti-hypertensive therapy. However, if the person is on antihypertensivetreatment, an extra point is added beyond points for the blood pressurereading because treated hypertension carries residual risk (see Tables B1 andB2). The average of several blood pressure measurements, as recommendedby the Joint National Committee (JNC), is needed for an accurate measureof baseline blood pressure. The designation “smoker” means any cigarettesmoking in the past month. The total risk score sums the points for eachrisk factor. The 10-year risk for myocardial infarction and coronary death(hard CHD) is estimated from total points, and the person is categorizedaccording to absolute 10-year risk as indicated above (see Table 5).
Table B1. Estimate of 10-Year Risk for Men (Framingham Point Scores)

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
HDL (mg/dL)
Systolic BP (mmHg)
If Untreated
If Treated
Point Total
10-Year Risk %
Table B2. Estimate of 10-Year Risk for Women (Framingham Point Scores)

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
HDL (mg/dL)
Systolic BP (mmHg)
If Untreated
If Treated
Point Total
10-Year Risk %
U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICESPublic Health ServiceNational Institutes of HealthNational Heart, Lung, and Blood Institute


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