DON’T FORGET
YOUR PATIENTS! |
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REMEMBER–
LipidManagement™ is certified for CME credit–
see page 2. |
Antonio
M. Gotto, Jr, MD, DPhil
Joan and Sanford I. Weill Medical
College of Cornell University |
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Elizabeth
Barrett-Connor, MD
University of California, San Diego,
School of Medicine
Peter Ganz, MD
Harvard Medical School
Brigham and Women's Hospital
Scott
M. Grundy, MD, PhD
University of Texas Southwestern
Medical Center at Dallas
Steven
M. Haffner, MD
University of Texas Health Science Center
Donald B. Hunninghake, MD
University of Minnesota Medical School
Ronald M. Krauss, MD
Lawrence Berkeley National Laboratory
University of California, Berkeley
John C. LaRosa, MD
SUNY Downstate Medical Center
Peter Libby, MD
Harvard Medical School
Brigham and Women's Hospital
Harry L. Metcalf, MD
SUNY/Buffalo School of Medicine and
Biomedical Sciences
©Professional Postgraduate Services®
(PPS), a division of Physicians World/Thomson Healthcare,
400 Plaza Drive, Secaucus, NJ 07094 USA, 2001. All rights
reserved.
This
material may not be reproduced without the express written
permission of PPS. LipidManagement™ is an
educational initiative of the National Lipid Education
Council™. NLEC, National Lipid Education Council and
LipidManagement are trademarks used herein under
license.
Supported by an unrestricted educational
grant from Pfizer Inc.
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Clinical Application
of ATP III Guidelines
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Scott
M. Grundy,
MD, PhD |
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| Message from ATP III Chair,
Page 2
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The
third Adult Treatment Panel, or ATP III, under the auspices of the
National Cholesterol Education Program (NCEP), has revised its guidelines
for cholesterol testing and management.1
This evidence-based set of guidelines builds on ATP I (1988) and
ATP II (1993), and expands the indications for intensive cholesterol-lowering
in clinical practice.
Key changes in the latest release include earlier
and more precise identification of persons at high risk for coronary
heart disease (CHD) and more aggressive treatment to lower cholesterol
in a much broader segment of the population. In fact, if the guidelines
are fully implemented, the number of American adults who would qualify
for lifestyle therapy for high cholesterol is expected to be approximately
65 million. Of these, about 36 million would also qualify for pharmacologic
therapy—almost triple the 13 million who are currently being
prescribed a lipid-modifying drug.
THE FOLLOWING ARE AREAS HIGHLIGHTED IN THE ATP III
EXECUTIVE SUMMARY:
What are the most important new features of ATP III?
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Emphasis on multiple risk factors. The major new feature
is a focus on primary prevention in persons with multiple (>2)
risk factors for CHD. Clinical evidence suggests that many of
these persons will benefit from a more intensive reduction of
LDL-C than that recommended in ATP II. Physicians can use the
Framingham risk scoring system to ascertain the probability
that such patients will experience a CHD event over the next
10 years. |
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Elevation of diabetes to a "CHD risk equivalent."
A new feature of ATP III is the creation of the CHD risk equivalent
category that includes patients with other clinical forms of
atherosclerotic disease (peripheral arterial disease, abdominal
aortic aneurysm, and symptomatic carotid artery disease) or
a risk-factor profile that confers a >20% risk for a coronary
event in the next 10 years. Diabetes, considered a major risk
factor in ATP II, has been upgraded to this category because
of the exceptionally high coronary event rate in patients with
this condition. |
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Identification of the "metabolic syndrome" as a secondary
target of therapy. This is defined as a constellation of
metabolic risk factors associated with coronary heart disease,
including abdominal obesity, atherogenic dyslipidemia, elevated
blood pressure (BP), insulin resistance, and prothrombotic and
proinflammatory states. |
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New screening recommendation. ATP III calls for a fasting
lipoprotein profile (TC, LDL-C, HDL-C, and TG) every 5 years
in adults aged 20 years or older. (ATP II recommended screening
for only TC and HDL-C.2) |
What features do ATP II and ATP III share?
In both treatment panels, the primary goal of therapy is to lower
LDL-C. High LDL-C (>160 mg/dL) is considered a potential
target for LDL-C–lowering drug therapy, particularly in persons
with multiple CHD risk factors. Both panels emphasize intensive therapy
to lower LDL-C in persons with established CHD, and they identify
special considerations in certain subpopulations (young adults, postmenopausal
women, and the elderly). Finally, both panels recommend weight loss
and physical activity to enhance risk reduction in persons with elevated
LDL-C.
Also the same is the LDL-C goal of <130 mg/dL for
persons with >2 risk factors. LDL-C <160 mg/dL is the goal
for persons with 0 or 1 risk factor (with few exceptions, these persons
have a 10-year CHD risk <10%).
How does ATP III differ from ATP II?
In addition to the new features previously mentioned, lipid/lipoprotein
classes have been updated as follows:
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LDL-C. The optimal LDL-C level is now <100 mg/dL. This
is different from ATP II, which had the desirable level as <130
mg/dL. Also, an LDL-C goal of <100 mg/dL is now the target for
patients with CHD or CHD risk equivalency for whom 10-year CHD
risk is >20%. (ATP II limited this highest-risk category to
adults with CHD only, with the LDL-C goal of <100
mg/dL.) |
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HDL-C. Low HDL-C is redefined as <40 mg/dL
(<35 mg/dL in ATP II). |
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Triglycerides. Normal TG is <150 mg/dL (<200 mg/dL
in ATP II). Borderline-high TG is 150–199 mg/dL (200–400
mg/dL in ATP II). High TG is 200–499 mg/dL (400–1,000
mg/dL in ATP II). Very high TG is >500 mg/dL (>1,000
mg/dL in ATP II). |
How is CHD risk assessed in persons without clinically manifest
CHD?
This is done in two steps. First, count the number of major CHD risk
factors other than LDL-C levels (Table 1). Second, for persons
with multiple (>2) risk factors, use the Framingham risk
scoring system to determine 10-year CHD risk (Tables 2A and 2B).
Recognizing that this adds a step to risk-factor assessment, ATP III
authors maintain that it better targets those who would benefit from
intensive treatment. The Framingham risk scoring system assigns point
values for age, TC, HDL-C, systolic BP, and smoking status.
These are weighted within each category. The total
number of points derived from scores in the five categories corresponds
to a specific 10-year CHD risk. Essentially, the Framingham risk scoring
system indicates whether a person with multiple risk factors is in
the CHD risk-equivalent category (10-year risk for CHD >20%) or the
category where 10-year risk for "hard" CHD events is 10%–20%
("hard" CHD events include myocardial infarction [MI] or coronary
death).
Are any other risk factors taken into account?
ATP III recognizes that other factors also influence CHD risk. These
include life-habit risk factors, such as obesity, physical
inactivity, and an atherogenic diet; as well as emerging risk factors,
such as lipoprotein(a), homocysteine, prothrombotic and proinflammatory
factors, impaired fasting glucose, and evidence of subclinical atherosclerotic
disease. Although they are targets for intervention, life-habit risk
factors are not used to set a lower LDL-C goal. The presence of emerging
risk factors also does not categorically alter LDL-C goals, but their
use may help guide the intensity of risk- reduction therapy.
What are the major modalities of LDL-C–lowering therapy?
ATP III recommends therapeutic lifestyle changes (TLC), which
include:
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reduced intake of saturated fat (<7% of total calories) and
cholesterol (<200 mg/day) |
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therapeutic dietary options for lowering LDL-C,
such as plant stanols/sterols (2 g/day; contained in certain
margarine-like spreads) and increased soluble fiber (10–25
g/day) |
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weight reduction |
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increased physical activity |
If LDL-C goals are not achieved with TLC alone
after 3 months, then LDL-C–lowering drugs may be added.
What are cutpoints for instituting these modalities?
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For persons with CHD or a CHD risk equivalent—including
those with multiple risk factors and a 10-year risk >20%—initiate
TLC for those with LDL-C >100 mg/dL. Consider drug
therapy for those with LDL-C >130 mg/dL (optional
for those with LDL-C 100–129 mg/dL). |
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For persons with multiple risk factors and a
10-year CHD risk <20%, initiate TLC for those with
LDL-C >130 mg/dL. For those with a 10-year CHD risk
of 10% to 20%, consider drug therapy at an LDL-C level of >130
mg/dL; for those with a 10-year CHD risk <10%, consider it at
an LDL-C level of >160 mg/dL. |
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For persons with 0 or 1 risk factor, initiate TLC for those
with LDL-C >160 mg/dL. Consider drug therapy for those
with an LDL-C level of >190 mg/dL (optional for those
with LDL-C 160–189 mg/dL). |
When drugs are prescribed, reinforce the patient's
attention to TLC.
How is LDL-C–lowering therapy initiated?
Patients are usually started on moderate doses of HMG-CoA reductase
inhibitors (statins), bile acid sequestrants, nicotinic acid, or fibric
acids (or, where indicated, a combination of these)—all accompanied
by TLC. After 6 weeks, patient response to the drug therapy is evaluated.
If the LDL-C goal has not been met, dosages can be increased and/or
combined therapy can be initiated. Check the response to this regimen
after 6 weeks; if the LDL-C goal still has not been met, consider
intensification of therapy(ies). Consider a referral to or a consultation
with a lipid specialist if the patient is not responding to this standard
therapy.
How are patients with the metabolic syndrome managed?
Because CHD risk can be reduced by modifying factors other than LDL-C—which
is still the primary goal of therapy—these patients should be
advised to lose weight and to increase physical activity. Also note
that therapies directed against lipid and nonlipid risk factors will
reduce CHD risk; these include treatments to lower TG and raise HDL-C,
as well as antihypertensives and aspirin (for patients with preexisting
CHD).
What about treating patients with hypertriglyceridemia?
Advise patients with borderline-high TG to try to lose weight and
increase physical activity. For those with high TG, TLC should be
accompanied by intensified LDL-C–lowering therapy or a TG-lowering
drug (nicotinic acid or fibrate). For persons with very high TG, the
initial aim of therapy is prevention of pancreatitis through TG-lowering,
which is accomplished with a very-low-fat diet, weight loss, increased
physical activity, and a TG-lowering drug. Once TG drops to <500 mg/dL,
refocus attention on lowering LDL-C. (Refer to earlier section
for levels in TG categories.)
How are patients with low HDL-C treated?
After maximizing efforts to lower LDL-C, manage the metabolic syndrome,
and lower TG, emphasis should be shifted to raising HDL-C, which may
be accomplished by adding a fibrate or nicotinic acid.
Once a patient's CHD risk is assessed and a treatment plan is in
place, how is adherence to the regimen encouraged?
Despite abundant clinical evidence that lipid-lowering therapy can
reduce all major manifestations of atherosclerosis, adherence to prescribed
regimens is generally poor in the United States (Table 3).
To promote adherence, ATP III recommends implementing
two or more of the following strategies for each patient:
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Simplify medication regimens. Patients are more likely
to take once-daily medications than those dosed two or more
times daily. Likewise, the fewer number of drugs in the lipid-lowering
regimen, the better, especially for patients with CHD or a CHD
risk equivalent who may already be taking multiple medications.
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Provide explicit instructions and thoughtful counseling.
Identify patients' concerns and misunderstandings. Determine
the benefits that they expect to receive from treatment. Link
these benefits to their LDL-C level, which provides them with
a measure with which to track progress. Most importantly, make
instructions concise and reinforce them with written materials
or web-based information. |
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Encourage use of prompts to help patients remember their
medications. Integrate drug dosing with other daily activities,
such as meals or bedtime rituals. Suggest the use of clocks,
watches, or alarms to signal dosing times, as well as pillboxes
to organize medications. |
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Encourage support from family and friends. |
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Reinforce and reward adherence. Ask about adherence
at each visit. Review lipid findings and chart progress together.
Avoid giving negative feedback; instead, praise small gains.
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Increase visits for patients unable to achieve treatment
goals. |
What in-office steps can be taken to promote patient adherence?
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Learn to implement lipid-treatment guidelines. Physicians
are encouraged to participate in a training program that teaches
how to incorporate this new knowledge into daily practice. |
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Use reminders to address lipid management. Place brightly
colored stickers on the charts of patients requiring lipid-lowering
interventions. Use electronic medical records to prompt action
on lipid results. |
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Choose a patient advocate to direct care. This person
would review charts, extract critical information, summarize
the information, keep the physicians up-to-date, provide patient
information and consultation, and follow up with patients in
between visits, reminding them to refill prescriptions and to
return for their next visit. |
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Develop a standardized treatment plan to structure care. |
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Use feedback from past performance to foster change in
future care. |
Can the healthcare delivery system promote adherence?
Although interventions focused on physicians or patients are foremost
in thought, those focused on the healthcare delivery system have resulted
in the greatest improvement in patient adherence and have fostered
better outcomes. However, like all intervention methods, this system
can be improved. Some approaches to this include the following:
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Providing lipid management through a lipid clinic.
Larger healthcare systems can especially benefit from this.
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Having specially trained nurses manage some or all elements
of care. They are particularly skilled at effectuating TLC.
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Using telemedicine. Phone calls between scheduled visits
improve adherence to therapeutic regimens and help ensure that
follow-up appointments will be kept. |
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Encouraging collaboration with pharmacists. Pharmacists
can enhance patient knowledge and understanding of drug therapy
as well as answer some related questions that may arise between
physician office visits. |
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Executing critical-care pathways in hospitals. Starting
lipid-lowering therapy during hospitalization for CHD has been
shown to increase the number of patients who are treated as
well as facilitate achievement of treatment goals.
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References
| 1. |
Expert Panel on Detection, Evaluation,
and Treatment of High Blood Cholesterol in Adults. 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).
JAMA. 2001;285:2486-2497. |
| 2. |
National Cholesterol Education
Program. Executive Summary of the Second Report of the Expert
Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults (Adult Treatment Panel II). National Institutes
of Health, National Heart, Lung, and Blood Institute; September
1993. NIH Publication No. 93-3096. |
This article was reviewed for medical accuracy by
Antonio M. Gotto, Jr, MD, DPhil, chairman of the National Lipid Education
Council. Dr Gotto has indicated a financial interest or affiliation
as noted: retained as a consultant for AstraZeneca, Bayer Corporation,
Bristol-Myers Squibb Company, Merck & Co., Inc., Pfizer Inc, and Reliant
Pharmaceuticals.
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