Executive Summary of the Third Report of the National Cholesterol Education
Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult Treatment Panel III)


Author Information <http://jama.ama-assn.org/issues/v285n19/ffull/#aainfo>
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults
JSC10094
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 reportsATP I, II, and IIIhas 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 patients
with CHD, 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_ta.html>  in the
APPENDIX <http://jama.ama-assn.org/issues/v285n19/ffull/#box1> .
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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t1.html>  shows
the new features of ATP III. (Note: To convert cholesterol to mmol/L, divide
values by 38.7).



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.
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 follow-up 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t2.html> , 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 ( Table 3
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t3.html> ). (LDL
is not counted among the risk factors in Table 3
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t3.html>  because
the purpose of counting those risk factors is to modify the treatment of
LDL.) Based on these other risk determinants, ATP III identifies 3
categories of risk that modify the goals and modalities of LDL-lowering
therapy. Table 4
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t4.html>  defines
these categories of risk and shows corresponding LDL cholesterol goals.
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, ie, >20% per 10 years (ie, 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
<http://jama.ama-assn.org/issues/v285n19/ffull/#box1> ). 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t3.html> . 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. First,
the number of risk factors is counted ( Table 3
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t3.html> ).
Second, for persons with multiple (2+) risk factors, 10-year risk assessment
is carried out with Framingham scoring (see Appendix
<http://jama.ama-assn.org/issues/v285n19/ffull/#box1> ) 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. (If Framingham scoring is carried out before risk factor counting,
persons with <10% 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 [ Table 4
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t4.html> ].)
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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t3.html> ). 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
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 targetLDL
cholesterol. Diagnosis and treatment of the metabolic syndrome is described
below 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-effective
ness 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 (ie, the probability of having a CHD 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t2.html> , an LDL
cholesterol level of <100 mg/dL is optimal; therefore, ATP III specifies an
LDL cholesterol level of <100 mg/dL as the goal of therapy in secondary
prevention. This goal is supported by clinical trials with both clinical and
angiographic end points 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 3 RISK CATEGORIES



The 2 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
triglyceride or low HDL cholesterol) are present, TLC also stresses weight
reduction and increased physical activity. Table 5
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html>  defines
LDL cholesterol goals and cutpoints for initiation of TLC and for drug
consideration for persons with 3 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 cutpoints for initiating lifestyle
and drug therapies are shown in Table 5
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html> .
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 level of <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 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 (eg, 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 under way 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 of 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html> .
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 LDL cholesterol is 160 mg/dL,
drug therapy can be considered to achieve an LDL cholesterol level of <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.
0-1 Risk Factor

Most persons with 0-1 risk factor have a 10-year risk <10%. They are managed
according to Table 5
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html> . 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
<http://jama.ama-assn.org/issues/v285n19/ffull/#box1> ). 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 follow-up, 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:
*         Reduced intakes of saturated fats (<7% of total calories) and
cholesterol (<200 mg/d) (see Table 6
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t6.html>  for
overall composition of the TLC Diet)
*         Therapeutic options for enhancing LDL lowering such as plant
stanols/sterols (2 g/d) and increased viscous (soluble) fiber (10-25 g/d)
*         Weight reduction
*         Increased physical activity.
A model of steps in TLC is shown in Figure 1
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_f1.html> . 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 accord 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.
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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html> ). 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t7.html> .
Some cholesterol-lowering agents are currently available over-the-counter
(OTC) (eg, nicotinic acid), and manufacturers of several classes of
LDL-lowering drugs (eg, statins, bile acid sequestrants) have applied to the
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 of <100 mg/dL. The cutpoints for initiating lifestyle and
drug therapies are shown in Table 5
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html> . Most
patients with CHD will need LDL-lowering 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 patients 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 to 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 that 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 2 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 follow-up
is often less consistent and more fragmented.
LDL-Lowering Drug Therapy for Primary Prevention

Table 5 <http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html>
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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_f2.html> .
When drug therapy for primary prevention is a consideration, the third visit
of dietary therapy (see Figure 1
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_f1.html> ) 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 evaluated 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
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 3
or more of the risk determinants shown in Table 8
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t8.html>  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 2-fold objective: (1) to reduce
underlying causes (ie, 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
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 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 US Surgeon General's Report on Physical Activity.
Specific Treatment of Lipid and Nonlipid 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 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 (eg, type 2 diabetes, chronic renal failure,
nephrotic syndrome), certain drugs (eg, 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
(To convert triglyceride values to mmol/L, divide by 88.6.)
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 - 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t9.html> ) 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 borderline high or high
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 target of therapy. Aside from weight reduction and
increased physical activity, drug therapy can be considered in high-risk
persons to achieve the non-HDL cholesterol goal. There are 2 approaches to
drug therapy. First, the non-HDL cholesterol goal can be achieved by
intensifying therapy with an LDL-lowering drug; second, nicotinic acid or
fibrate can be added, if used with appropriate caution, to achieve the
non-HDL cholesterol goal by further lowering 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, ie, 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 (eg, 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 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 non-HDL cholesterol goal, as outlined earlier. 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 in persons with type 2
diabetes. Although elevated triglycerides, low HDL cholesterol, or both 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 (eg, 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) 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.
Women Aged 45-75 Years
In women, onset of CHD generally is delayed by some 10 to 15 years compared
with that in men; thus, most CHD in women occurs after age 65 years. 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 sex 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-and-fast 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)
In this age group, CHD is rare except in those with severe risk factors, eg,
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 of 130
mg/dL, TLC should be instituted and emphasized. 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 (eg,
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 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, clinicians, and health delivery systems to achieve the full
population effectiveness of the guidelines for primary and secondary
prevention ( Table 10
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t10.html> ).



Author/Article Information


Corresponding Author and Reprints: James I. Cleeman, MD, National
Cholesterol Education Program, National Heart, Lung, and Blood Institute
(NHLBI), 31 Center Dr, Room 4A16, MSC 2480, Bethesda, MD 20892-2480 (e-mail:
[log in to unmask] <mailto:[log in to unmask]> ).
The Full Report of ATP III is available online on the NHLBI Web site at
http://www.nhlbi.nih.gov <http://www.nhlbi.nih.gov> .


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, MD, PhD (Chair of the panel), Diane Becker, RN,
MPH, ScD, Luther T. Clark, MD, Richard S. Cooper, MD, Margo A. Denke, MD,
Wm. James Howard, MD, Donald B. Hunninghake, MD, D. Roger Illingworth, MD,
PhD, Russell V. Luepker, MD, MS, Patrick McBride, MD, MPH, James M.
McKenney, PharmD, Richard C. Pasternak, MD, Neil J. Stone, MD, Linda Van
Horn, PhD, RD
Ex-officio Members: H. Bryan Brewer, Jr, MD, James I. Cleeman, MD (Executive
Director of the panel), Nancy D. Ernst, PhD, RD, David Gordon, MD, PhD,
Daniel Levy, MD, Basil Rifkind, MD, Jacques E. Rossouw, MD, Peter Savage, MD
Consultants: Steven M. Haffner, MD, David G. Orloff, MD, Michael A.
Proschan, PhD, J. Sanford Schwartz, MD, Christopher T. Sempos, PhD
Staff: Susan T. Shero, RN, MS, Elaine Z. Murray




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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t4.html> ).


Financial Disclosure: Dr Grundy has received honoraria from Merck, Pfizer,
Sankyo, Bayer, and Bristol-Myers Squibb. Dr Hunninghake has current grants
from Merck, Pfizer, Kos Pharmaceuticals, Schering Plough, Wyeth Ayerst,
Sankyo, Bayer, AstraZeneca, Bristol-Myers Squibb, and G. D. Searle; he has
also received consulting honoraria from Merck, Pfizer, Kos Pharmaceuticals,
Sankyo, AstraZeneca, and Bayer. Dr McBride has received grants and/or
research support from Pfizer, Merck, Parke-Davis, and AstraZeneca; has
served as a consultant for Kos Pharmaceuticals, Abbott, and Merck; and has
received honoraria from Abbott, Bristol-Myers Squibb, Novartis, Merck, Kos
Pharmaceuticals, Parke-Davis, Pfizer, and DuPont. Dr Pasternak has served as
a consultant for and received honoraria from Merck, Pfizer, and Kos
Pharmaceuticals, and has received grants from Merck and Pfizer. Dr Stone has
served as a consultant and/or received honoraria for lectures from Abbott,
Bayer, Bristol-Myers Squibb, Kos Pharmaceuticals, Merck, Novartis,
Parke-Davis/Pfizer, and Sankyo. Dr Schwartz has served as a consultant for
and/or conducted research funded by Bristol-Myers Squibb, AstraZeneca,
Merck, Johnson & Johnson-Merck, and Pfizer.
Executive Committee Liaison to the Panel: Stephen Havas, MD, MPH, MS
Reviewers of the Full Report of ATP III: Eugene Braunwald, MD, W. Virgil
Brown, MD, Alan Chait, MD, James E. Dalen, MD, Valentin Fuster, MD, PhD,
Henry N. Ginsberg, MD, Antonio M. Gotto, MD, DPhil, Ronald M. Krauss, MD,
John C. LaRosa, MD, Thomas H. Lee, Jr, MD, Linda Meyers, PhD, Michael
Newman, MD, Thomas Pearson, MD, PhD, Daniel J. Rader, MD, Frank M. Sacks,
MD, Ernst J. Schaefer, MD, Sheldon G. Sheps, MD, Lynn A. Smaha, MD, PhD,
Sidney C. Smith, Jr, MD, Jeremiah Stamler, MD, Daniel Steinberg, MD, PhD,
Nanette K. Wenger, MD
National Cholesterol Education Program Coordinating Committee: The Third
Report of the 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, MD (Chair), James I. Cleeman, MD (Coordinator); American Academy of
Family Physicians: Theodore G. Ganiats, MD; American Academy of Insurance
Medicine: Gary Graham, MD; American Academy of Pediatrics: Ronald E.
Kleinman, MD; American Association of Occupational Health Nurses: Pamela
Hixon, BSN, RN, COHN-S; American College of Cardiology: Richard C.
Pasternak, MD; American College of Chest Physicians: Gerald T. Gau, MD,
American College of Nutrition: Harry Preuss, MD; American College of
Obstetricians and Gynecologists: Thomas C. Peng, MD; American College of
Occupational and Environmental Medicine: Ruth Ann Jordan, MD; American
College of Preventive Medicine: Lewis H. Kuller, MD, DrPH; American Diabetes
Association, Inc: Alan J. Garber, MD, PhD; American Dietetic Association:
Linda Van Horn, PhD, RD; American Heart Association: Scott M. Grundy, MD,
PhD; American Hospital Association: Sandra Cornett, RN, PhD; American
Medical Association: Yank D. Coble, Jr, MD; American Nurses Association: to
be named; American Osteopathic Association: Michael Clearfield, DO; American
Pharmaceutical Association: James M. McKenney, PharmD; American Public
Health Association: Stephen Havas, MD, MPH, MS; American Red Cross: Donald
Vardell, MS; Association of Black Cardiologists: Karol Watson, MD, PhD;
Association of State and Territorial Health Officials: Joanne Mitten, MHE;
Citizens for Public Action on Blood Pressure and Cholesterol, Inc: Gerald J.
Wilson, MA, MBA; National Black Nurses Association, Inc: Linda
Burnes-Bolton, DrPH, RN, MSN; National Medical Association: Luther T. Clark,
MD; Society for Nutrition Education: Darlene Lansing, MPH, RD; Society for
Public Health Education: Donald O. Fedder, DrPH, MPH.
Associate Member Organization: American Association of Office Nurses: Joyce
Logan.
Federal Agencies: NHLBI Ad Hoc Committee on Minority Populations: Yvonne L.
Bronner, ScD, RD, LD; Agency for Healthcare Research and Quality: Francis D.
Chesley, Jr, MD; Centers for Disease Control and Prevention: Wayne Giles,
MD, MPH; Coordinating Committee for the Community Demonstration Studies:
Thomas M. Lasater, PhD; Department of Agriculture: Alanna Moshfegh, MS, RD;
Department of Defense: Col Robert Dana Bradshaw, MD, MPH; Food and Drug
Administration: Elizabeth Yetley, PhD; Health Resources and Services
Administration: Celia Hayes, MPH, RD; National Cancer Institute: Carolyn
Clifford, PhD; National Center for Health Statistics: Clifford Johnson, MPH;
Office of Disease Prevention and Health Promotion: Elizabeth Castro, PhD;
Department of Veterans Affairs: Pamela Steele, MD.



APPENDIX



Shared Features of ATP III and ATP II
Adult Treatment Panel (ATP) III shares a set of core features with ATP II,
shown in Table A
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_ta.html> .
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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_tb1.html>  for men
and Table B2
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_tb2.html>  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 2 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 antihypertensive
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 ( Table B1
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_tb1.html>  and
Table B2
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_tb2.html> ). 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
<http://jama.ama-assn.org/issues/v285n19/fig_tab/jsc10094_t5.html> ).


Edward E. Rylander, M.D.
Diplomat American Board of Family Practice.
Diplomat American Board of Palliative Medicine.